Latest / The Big Mig Show / Ending Aging, Forever Young w/ Dr. Aubrey de Grey |EP411

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Ending Aging, Forever Young w/ Dr. Aubrey de Grey |EP411 · The Big Mig Show

• 0:00
  All men are created equal, that they are endowed by their
• 0:04
  Creator with certain unalienable Rights, by liberty.
• 0:13
  If liberty means anything at all, it means right to tell
• 0:17
  people what they do not want to hear.
• 0:54
  Hey, welcome back to the big big Show.
• 0:55
  I'm your host Lance Miliaccio, of course with my Co host George
• 0:58
  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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  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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  $75,000 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
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  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
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  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
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  made any forward movement. And it looks like you've been
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  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
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  expert so I don't want to say this, but it's got to do with
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  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
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  signed by the same color. I don't know.
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  I'm probably given very remedial version of that.
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  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
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  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
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  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
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  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.
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  It's just, you know, the particular target that I have
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  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
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  and the but big Pharma wanting to keep sick people alive rather
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  than wanting to stop people from getting sick.
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  This is all true. It's very true, but it's not
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  really their fault. It's really the fault of the
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  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
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  implementing the law. They're just doing what our
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  elected representatives tell them to do.
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  And our elected representatives, as we all know, have one goal in
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  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
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  preventative medicine out there, whether it's preventative
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  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.
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  The public are inherently hesitant to embrace medicines
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  that are new and thus experimental, and that they
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  perceive might just make them sick rather than postpone the
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  time at which they get sick. Now, of course, doctors and
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  researchers are constantly, you know, generating evidence that
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  that's not that's probably not going to happen.
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  In fact, overwhelmingly probably.
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  But the public are just not very good at probabilities, and so
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  they focus on the worst case scenario, however outlandishly
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  unlikely it is, and that puts them off preventative medicine,
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  prevention in general, of course, preventative lifestyles
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  and so on, different matter. But when it comes to medicine,
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  that's the problem. And that's a good thing, because
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  I believe that we have a chance of educating the public about
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  this, of going to the point where the public does actually
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  understand that preventative medicine is something they want.
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  And as soon as that happens, the industry will follow the money.
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  The it's not as if different skills are required, different
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  technology to develop preventative medicine versus
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  sick care medicine that we have today.
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  So it's all about educating the public.
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  That's why I spend so much of my time trying to do that.
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  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.
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  Well, I, if I, if I heard you correctly, and I think I did, I
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  want to respectfully disagree with something because there's a
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  lot of holistic cures out there that the FDA will fight against.
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  Why? Because Big Pharma doesn't want
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  it. And for instance, like cures for
• 13:46
  cancer, we'll say there's things out there that can help with
• 13:50
  cancer that has been known to cure cancer, but the FDA and Big
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  Pharma want nothing to do with it because you won't have no
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  more cancer drugs, no more chemo, radiation.
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  So the FDA does play a big role. OK.
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  So you're not actually disagreeing with me that because
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  that's true, but it's a separate question.
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  These medicines that you're talking about are not, not
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  preventative medicines. They are medicines to treat
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  things just the same as the medicines that the FDA does
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  approve and does favour. You're quite right that this is
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  a problem, but it's a different problem.
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  It's a problem that is driven by the economics of the system, by
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  the fact that these holistic medicines typically don't have,
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  you know, they don't have intellectual property that is
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  owned by large companies. And plus, yes, absolutely, this
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  is a function of capitalism. It's, you know, it's, it's a
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  problem, but it's a different problem from what I was talking
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  about. Like if, if you I know I forget
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  the that was a doctor, I believe maybe doctor, but I don't know
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  something to do with apricot teas or something where he he
• 14:48
  actually put out on his site that he had a cure for cancer
• 14:51
  and because he put cure for cancer, they came after him.
• 14:54
  They actually locked him up. So even though it did cure
• 14:57
  cancer, but. Well.
• 15:00
  You got to remember cancer is a tricky 1 because cancers differ
• 15:04
  so much from one person to the next.
• 15:06
  Every cancer is genetically different.
• 15:08
  And that means that there is a wide, a large number of, you
• 15:14
  know, exceptional, you know, miracle moments, you know,
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  people who can report that they've had they've been cured
• 15:20
  of this or that. But if you actually look at the
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  proportion of people who have taken the intervention, whatever
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  it may be, whether it's apricots or whether it's some drug that
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  Big Pharma own, but only a minority of those people
• 15:31
  actually benefit. Yeah, it's complicated,
• 15:35
  obviously, because we're on social media, we see lots of
• 15:38
  people talking about alternative remedies.
• 15:40
  Obviously, there was lots of hoopla about ivermectin and
• 15:44
  parasites and being some of those being the cause of
• 15:46
  people's cancers. There's some recent studies that
• 15:49
  are coming out about high doses of inositol and that's supposed
• 15:51
  to have an impact. We've heard the stories about
• 15:53
  the apricot seeds. Obviously there's lots of, you
• 15:56
  know, material and it's confusing for the public.
• 15:58
  They get confused and of course, their doctor tells them none of
• 16:01
  that's going to work. You have to take this pill.
• 16:03
  You got to get chemo. And again, maybe that puts you
• 16:05
  into remission. Of course, chemo is a poison in
• 16:07
  itself. So the body's reaction to that
• 16:09
  is different for every individual.
• 16:11
  It's much more complicated. I want to bring up a term you,
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  and this is interesting because Methuselah, obviously, according
• 16:17
  to the Bible, he was the grandfather of Noah.
• 16:19
  I think he lived 900 and some odd years, maybe 960 or
• 16:22
  something. And of course that's, I think
• 16:25
  that's, you know, a well known story to a lot of people.
• 16:27
  You coined a term Methuselarity, I believe.
• 16:31
  Am I right? Methuselarity.
• 16:34
  That's not completely correct. That was coined by a friend of
• 16:37
  mine and then going to pull neck the but I coined a very related
• 16:42
  term, the term longevity escape velocity.
• 16:45
  So I can explain to you what longevity escape velocity is
• 16:48
  basically, but basically the methuselarity is the point at
• 16:54
  which we reach longevity escape velocity.
• 16:56
  So shall I explain? I explain both of those terms.
• 16:59
  Please, yes, please do. To the audience, of course.
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  OK. So the concept of longevity
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  escape velocity, which I first started talking about about
• 17:07
  2004, so 20 years ago, is as a consequence of the ideas I had a
• 17:15
  few years before that about how we're going to actually bring
• 17:19
  aging under comprehensive medical control.
• 17:22
  And the key, you know, underpinning of that, that work
• 17:26
  back then was that we're going to do it by reversing aging by
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  bonafide and rejuvenation. Whereas historically people in
• 17:35
  the field had been focusing entirely on the idea of slowing
• 17:38
  aging down rather than reversing it.
• 17:41
  Now, slowing aging down is better than nothing, but
• 17:44
  obviously for people who are already your age or mine, you
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  know, with the same age, right? Yeah.
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  Correct. I'm younger.
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  I'm. George, he had to throw that in.
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  I'm younger. For people, for people our age,
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  you know, we have already accumulated a lot of, you know,
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  molecular and cellular damage in the body.
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  We are already biologically old as well as being chronologically
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  old. And therefore, you know, even if
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  we were to, let's say, half the rate at which more damage would
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  accumulate in the future, still we're going to get to the point
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  of having enough damage that we get sick.
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  Whereas if we take people like you and me and we repair that
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  damage, which is what I've been working on ever since that time,
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  then we actually do benefit a lot.
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  We can take we can, we can take people backwards in biological
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  age. Now, the key thing about that is
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  it buys time for people like me. It means that if we take someone
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  who's, let's say, 61 and we take them back to being biologically
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  41, which we would be able to do with a panel of damage repair
• 18:47
  rejuvenation treatments that was not completely comprehensive.
• 18:52
  If it was completely comprehensive, then we'd get
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  back to, you know, 0, right? But if we get back to, you know,
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  middle, early middle age rather than late middle age, then it's
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  going to be 20 more years before those people are going to be
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  back to being biologically the age they were before we began,
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  right? And in all that time, people
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  like me are going to be able to improve the comprehensiveness of
• 19:15
  the therapies. So if we're not able to improve
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  them, then people would get back to being biologically 60 or
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  whatever and they'd carry on getting biologically older as
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  they got chronologically older. And they'd get sick and die same
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  as now, exhausted, do so a bit later.
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  But if we are improving the therapies fast enough, then we
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  won't have that problem. We can re rejuvenate the same
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  people when they're 80 but biologically 60 for the second
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  time. So they won't be biologically
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  sexy for the third time until they're let's say 100 or 110 and
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  so on. So basically longevity escape
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  velocity is defined as the minimum rate at which scientists
• 19:58
  will need to. Improve the comprehensiveness of
• 20:02
  these damage repair therapies over time in the people who are
• 20:06
  getting the state-of-the-art therapies at any point will stay
• 20:10
  one of one step ahead of the aging problem and never get sick
• 20:13
  as they get old. And I believe that we can hit
• 20:16
  that point when we when we get the 1st 20 years, if we take
• 20:20
  people who are let's say 60 and we give them 20 initial healthy
• 20:24
  life, then that'll be enough for us to be with very high
• 20:29
  probability, you know, improving things faster than time is
• 20:33
  Percy. So that 20 year point is what my
• 20:36
  friend called the particularity. Interesting.
• 20:41
  You know, I, I want to, I want to back up here a little bit
• 20:43
  because obviously that's to where you, I don't think a lot.
• 20:45
  Some of that is where you are now.
• 20:46
  Obviously that's what led you here, George.
• 20:48
  Let's throw up the cover of his book, your first book, this.
• 20:50
  I actually read this in 2010, you know, the mitochondrial free
• 20:54
  radical theory of aging, which I guess was your thesis.
• 20:57
  A bunch of your thesis papers combined, obviously very
• 21:00
  scientific. I had to keep a dictionary and
• 21:03
  a, a lot of other information sitting side by so I could look
• 21:07
  up the information in it, you know, and let me give the
• 21:10
  synopsis for the audience. So this is a, it's a, the, the
• 21:13
  book is proposes a biological explanation for aging based on
• 21:16
  mitochondrial activity and free radical damage.
• 21:20
  You know, we always hear about free radicals.
• 21:22
  That term has been obviously, obviously well used in the
• 21:24
  media. And George, Oh, no, not that
• 21:26
  book, George. It's the other cover.
• 21:28
  It's the Gray and blue one. That's the next book.
• 21:30
  That's the only book. No, you got to look further up,
• 21:33
  buddy. Yeah, is what there's a blue and
• 21:35
  Gray. Oh, I see that now.
• 21:36
  Stuck that in there, Lance maybe?
• 21:41
  Maybe I did. You know, sometimes I do that.
• 21:43
  I'll throw a media in the last half hour when I'm getting
• 21:45
  ready. While that's happening, let me
• 21:49
  just interrupt and say a couple of things.
• 21:51
  So first of all, the whole idea that mitochondrial damage might
• 21:55
  be relevant to aging was by no means original with me.
• 21:59
  It was first put forward in the 19 in the early 1970s, so nearly
• 22:03
  30 years before I did. However, what I, what I did was
• 22:07
  I refined it a lot. You know, I had various, various
• 22:11
  hypotheses. That's the one.
• 22:12
  Yeah, various hypotheses for the, the specific mechanistic
• 22:17
  detail that the molecular level, the cellular level for how the
• 22:20
  thing actually works. And that was all new, and it was
• 22:23
  enough to get me my PhD, as you say.
• 22:26
  You know, so obviously people hear about, you know, outside
• 22:29
  influences in flat influences of what causes that kind of damage.
• 22:34
  And obviously the mitochondria are kind of the engine in the
• 22:36
  body for the cells. But the theory in this is that
• 22:39
  the accumulation of damage is caused by those free radicals
• 22:42
  that are produced. Why the mitochondria are
• 22:44
  producing energy. So maybe you can explain that to
• 22:47
  the audience and kind of how that happens because I think a
• 22:49
  lot of them would not because again, I think this is a term
• 22:51
  they probably haven't heard that reactive oxygen species, they
• 22:54
  don't really know that term, I don't believe.
• 22:56
  So if you could share that with them, that would be great.
• 22:58
  Sure, yes. So first of all, the term
• 22:59
  reactive oxygen species sounds a little bit, you know, technical,
• 23:03
  but really it's just a slightly more general term than the term
• 23:06
  free radical, which is is quite a lot.
• 23:09
  So, yes, so the general idea is that we've got these little
• 23:14
  machines in the cell called mitochondria, which are
• 23:18
  responsible for extracting energy from the stuff that we
• 23:22
  eat, especially from carbohydrates and fats that in a
• 23:28
  way that can be used by the rest of the body.
• 23:32
  So there's a, there's a molecule called ATP that the, that the
• 23:37
  cells that cells use all the time to do pretty much
• 23:39
  everything, everything that takes energy is, is driven by
• 23:44
  extracting, but by, by essentially grabbing a, grabbing
• 23:49
  a molecule or two of ATP and doing something with it and, you
• 23:53
  know, expending that energy and lots and lots of things that the
• 23:56
  cell needs to do take energy, you know, DNA replication,
• 23:59
  synthesis of proteins, things like that.
• 24:02
  So ATP is what's often called the currency of the cell.
• 24:05
  And, and most of the ATP in the cell is generated by
• 24:07
  mitochondria. Now, the particular way it's
• 24:10
  generated is really complicated. It turns out that because of the
• 24:15
  way chemistry works, just getting energy out of a sugar
• 24:18
  molecule, for example, and into, you know, the creation of ATP is
• 24:23
  not a simple thing. And the way in which cells do
• 24:28
  it, the way which mitochondria do it only evolved once a couple
• 24:31
  of billion years ago, and it's been used ever since.
• 24:36
  And it works. It worked well, but it doesn't
• 24:38
  work perfectly. Essentially, it has, you know,
• 24:41
  right effects in the same way that, you know, your engine and
• 24:44
  your car may, you know, accumulate contaminants in the
• 24:47
  oil or whatever. Similarly, there are, sorry, you
• 24:51
  know, toxic byproducts of the way in which the mitochondria
• 24:55
  does what I just described. And those byproducts are called
• 24:59
  free radicals. And free radicals are toxic.
• 25:02
  They can do an awful lot of damage to many different things.
• 25:05
  They can cause mutations in the DNA.
• 25:07
  They can, they can damage proteins, for example, and make
• 25:11
  them make, make them not only non functional but also
• 25:15
  indigestible so that they'll can't get rid of them and
• 25:18
  they're just waste products that accumulate things like that.
• 25:22
  So yeah, so basically I was interested in figuring out what
• 25:27
  to do about that. And first of all, I had to
• 25:29
  figure out a bit more than people had figured out before
• 25:32
  about, about the mechanistic details of all of this.
• 25:35
  Why do, why does this kind of damage accumulate over time?
• 25:42
  It turns out that's not a trivial question to answer.
• 25:45
  And then what? How is this damage actually
• 25:47
  toxic? How does 1 cell poison another
• 25:50
  cell, for example, when the first cell is, you know, has has
• 25:54
  been, you know, damaged too much by this kind of mechanism?
• 25:59
  So I did all that, but I also proposed a way in which we might
• 26:03
  fix it that involve genetic engineering.
• 26:07
  And it turns out this was also not original with me.
• 26:09
  It was first proposed back in the 1980s, in fact, by Albert,
• 26:13
  other people. It turns out to be quite a
• 26:15
  simple idea and people had tried this thing.
• 26:18
  It was basically a case of copying the genetic material
• 26:21
  from the mitochondrion into a normal chromosome in the nucleus
• 26:25
  of cells. And, you know, people had tried
• 26:28
  this and they'd made a little bit of progress, and then they'd
• 26:31
  hit a bunch of roadblocks and they'd given up, largely because
• 26:34
  academia forces people to be very short termists and they
• 26:37
  couldn't work on hard stuff. And I said that won't do, let's
• 26:41
  have another gut. So I've been working on this
• 26:43
  with my research teams over the years and we've made a lot more
• 26:46
  progress. Still we're not there.
• 26:49
  And also some other alternatives have turned out that may
• 26:52
  actually achieve the same thing by very different mechanisms.
• 26:56
  So I'm pursuing a lot of avenues in all of this, but yeah, that's
• 27:00
  the basis of it. You know, it's interesting and,
• 27:03
  and George, you and I have seen this.
• 27:04
  We've seen lots of individuals online that are talking about
• 27:06
  biohacking their age. They're using Cryogenifix,
• 27:09
  hyperbaric chambers, stem cell research, you know, KRP, all
• 27:14
  kinds of other things that they allege works.
• 27:16
  And of course, the, the nutritional world has obviously
• 27:20
  told us that we have to take an, you know, obviously
• 27:22
  antioxidants. Now, I don't know how successful
• 27:25
  those are because you're talking about something that's amplified
• 27:28
  cellular dysfunction when this happens for these age-related
• 27:31
  diseases, correct? Do do antioxidants, for example,
• 27:35
  any of this stuff that you see and you see these individuals
• 27:37
  now online that look pretty young in the pictures.
• 27:40
  I don't know if they've been photoshopped and they're and
• 27:42
  they're, they're going in these crazy regimens.
• 27:44
  Some of them are spending over $1,000,000 a year on these
• 27:47
  thorough regimens. Do do you feel like there's any
• 27:49
  of that stuff that's been effective at all or that you
• 27:51
  found that works in your investigation?
• 27:55
  Well, let me divide what you'd have to ask into two parts,
• 27:58
  because the person you're talking about in the second part
• 28:01
  of your question is undoubtedly Brian Johnson.
• 28:03
  He's a good friend of mine and does spend $4 million on
• 28:06
  everything. So I'll come back to that in a
• 28:08
  moment. First of all, antioxidants.
• 28:10
  This is a really important point because when a guy named Danim
• 28:16
  Harmon thought of the idea that free radicals might be
• 28:19
  instrumental in ageing, that was in the 1950s.
• 28:23
  And it was the very first time that anyone had come up with a
• 28:25
  bona fide mechanistic theory of ageing, an actual, actual
• 28:29
  hypothesis that said, OK, the reason we accumulate damage over
• 28:32
  time is because of this particular type of of chemical
• 28:36
  reaction that's going on in the body.
• 28:38
  And he tried a whole bunch of tricks and gave a lot of
• 28:42
  antioxidants to a bunch of mice and rats in his lab for a while,
• 28:46
  and they didn't really work. They were kind of protective,
• 28:51
  but only for only against early death, basically, you know, like
• 28:55
  any animal, especially back then when we didn't know as much as
• 28:58
  we know now about how to keep mice happy and healthy in the
• 29:00
  laboratory. You know, some of them died
• 29:03
  early. And these antioxidants were
• 29:05
  protective against that. They made the mice more kind of
• 29:08
  resilient, but a lot of them, you know, the ones that were
• 29:11
  dying late, you know, the, the kind of what's called the
• 29:14
  maximum lifespan of the mice, that maximum was not increased
• 29:18
  by antioxidants. And it was actually because of
• 29:21
  that that, you know, Harman carried on thinking, this
• 29:23
  unbelievably smart guy, I'm afraid he he died a few years
• 29:27
  ago, but he got to the age of 98.
• 29:29
  He didn't do too badly. Pretty good, fantastic guy, real
• 29:33
  role model for me. He figured out in the 1970s one
• 29:39
  way in which this could be 111 potential explanation for this,
• 29:43
  which was to do with mitochondria, and he was the
• 29:46
  first person to start talking about mitochondrial damage as
• 29:50
  the Nexus of all of this. And basically it all came down
• 29:54
  to localization. The antioxidants are chemicals,
• 29:59
  chemical molecules. They have to get around.
• 30:01
  They have to be in the right place at the right time to
• 30:05
  essentially sacrifice themselves to a free radical as a way of
• 30:10
  stopping the free radical from reacting in a toxic manner with
• 30:15
  molecule that matters, like DNA. And essentially he figured out
• 30:22
  ways in which it might be that antioxidants just can't get to
• 30:25
  the right place at the right time and the and the free
• 30:28
  radicals do their damage regardless of how many
• 30:33
  antioxidants are being consumed. And that seems to be pretty much
• 30:36
  true. Antioxidants are not very, are
• 30:38
  not very beneficial indeed. If you get wrong, if you take
• 30:41
  the wrong combination of antioxidants, they could be
• 30:43
  actively detrimental. They could become pro oxidants,
• 30:47
  however. Anyway, the point is that's not
• 30:49
  the whole story because there are various other ways in which
• 30:51
  you can manipulate this whole system to, you know, to to do
• 30:57
  less damage or to do damage more slowly.
• 31:00
  One way is people have been looking at ways to slow down the
• 31:04
  rate at which mitochondria create free radicals in the 1st
• 31:07
  place to make make mitochondria run more cleanly, to put it to
• 31:11
  an engine analogy. And there are various tricks to
• 31:14
  do that which work to some extent.
• 31:17
  There's another trick which is to make the molecules around the
• 31:21
  mitochondria, the the rest of the molecules in the cell less
• 31:24
  susceptible to being oxidized by free to being damaged by free
• 31:29
  radicals in the 1st place. And that also has some
• 31:31
  interesting ideas around it, including one involving
• 31:34
  deuterium, heavy hydrogen that we're actually pursuing in our
• 31:38
  in our next experiment. Interesting.
• 31:41
  You know, a lot of people, obviously it's their lifestyles.
• 31:44
  We always talk about stress causing it.
• 31:46
  We talk about smoking and alcohol.
• 31:49
  Do you feel like you know of some of those?
• 31:51
  Because I've seen some reports on nicotine that it maybe isn't
• 31:54
  the enemy that people have described it as the other
• 31:56
  chemicals that are in cigarettes.
• 31:58
  What's out there right now? What do you think's accurate
• 32:01
  when people hear about, oh, well, if you do that, it causes
• 32:04
  inflammation. If you do this, you're causing
• 32:06
  free radicals. And if you get too much sun,
• 32:08
  this isn't good for you. What do you think the biggest
• 32:10
  enemies are right now in people's lifestyles for aging?
• 32:14
  There are really 2 mantras that answer that question in the most
• 32:18
  general way that I can. 1 is different people are different.
• 32:23
  Different people have somewhat different, you know, details of
• 32:27
  their metabolism, different weak links in their metabolism.
• 32:31
  And that that translates into those people needing different
• 32:37
  supplements, different lifestyles, different.
• 32:39
  Now, some people are just more prone to putting on weight than
• 32:41
  others, for example. Yeah, I'm one of those
• 32:43
  repulsively lucky people. I can eat and drink exactly what
• 32:46
  I like and nothing happens, and I don't even need to do any
• 32:48
  exercise. And we hate you for that.
• 32:49
  Yeah, I hate you, doc. Yeah, quite right.
• 32:52
  Wait a minute, Italian. We look at food and we gain
• 32:55
  weight. Wait a minute.
• 32:56
  So since you made that glorious statement.
• 32:59
  I do want to finish. I do want to finish.
• 33:02
  The other critical thing to remember is that even if you
• 33:05
  figure out what's right for you, what's best for you, the amount
• 33:10
  of benefit you're going to get relative to simply living the
• 33:13
  way your mother told you to and just, you know, not smoking and
• 33:16
  not getting seriously overweight and eating a reasonably varied
• 33:18
  diet, you know, is very short, very small indeed.
• 33:22
  You know, you'll get a year if you're lucky, really.
• 33:24
  So, yeah. So we just can't do it yet.
• 33:27
  That's why that's what drives my research.
• 33:30
  My research is all about, you know, breaking that glass
• 33:33
  ceiling earned using more high tech things, cell therapies and
• 33:37
  gene therapies and so on to get far more than what we can do
• 33:42
  with anything that we have today.
• 33:45
  Hold up Lance, I got to ask a question since we're not so
• 33:49
  blessed like you and we, you know, if we pasta, Lance might
• 33:53
  put on a few pounds. What can what can we do?
• 33:55
  Is there any you got any secrets?
• 33:58
  Well, no, like I said, I mean, first of all, for myself, I
• 34:01
  don't need to do anything. Secondly, for anyone who does
• 34:04
  have trouble controlling their weight, you know, I'm, I'm, I'm
• 34:07
  sorry, but I mean, things are better now, you know, Of course,
• 34:09
  the GOP one, agonists like Zenpeg that have come along
• 34:12
  recently are an absolute godsend, but they're not a
• 34:15
  godsend for everybody. Some people have really pretty
• 34:17
  bad negative reactions to them. They just can't take them, but a
• 34:21
  lot of people can. A lot of people are benefiting a
• 34:24
  lot from these things and that's a huge thing.
• 34:27
  It actually comes back to what I was saying earlier about
• 34:29
  medicines and the big Pharma and so on.
• 34:32
  This is a real godsend because Ozempic is a preventative
• 34:37
  medicine. It postpones the age at which
• 34:39
  you're going to get diabetes, and that's really important.
• 34:42
  But that's not why people take it.
• 34:44
  The public are skeptical about preventative medicines, but this
• 34:48
  one got in by the side door because in addition to being
• 34:52
  preventative for diabetes, it's also a treatment for something
• 34:56
  that's not called a disease, but that people really don't like to
• 34:59
  have, namely obesity, right? So, so it's, so it's, it's a,
• 35:05
  it's a huge godsend, but for, you know, a rather complicated
• 35:09
  reason. Yeah, it's interesting.
• 35:12
  Obviously, Ozempic's kind of been a big thing in the news the
• 35:14
  last couple of years. Lots of it out there.
• 35:17
  Of course, hormone replacements, another topic that comes up a
• 35:19
  lot. Let's go into your book.
• 35:21
  Before I talk about that, though, let's talk about ending
• 35:23
  aging. Well, you had one before that
• 35:25
  you had advancing conversations. I did not read this one,
• 35:28
  Advocate for an indefinite human lifespan, which I think is
• 35:31
  interesting. You had lots of artists and
• 35:33
  authors and philosophers and economists, scientists and
• 35:35
  activists who work was aimed at the future of progress.
• 35:38
  It's pretty interesting. And this is where you really
• 35:40
  start to talk about the Cens Research Foundation at that time
• 35:43
  that you were involved with. Maybe give us a little detail on
• 35:45
  that and kind of why you took that project kind of because it
• 35:48
  looks like you wanted some, you really wanted to bring in a
• 35:50
  diverse group to kind of look over everything that you guys
• 35:53
  have been working on it seemed like.
• 35:55
  That one book Advancing Conversation, I think I just had
• 35:58
  one chapter in there right there definitely wasn't something that
• 36:00
  I wrote. But coming back to the rest of
• 36:04
  your question, yeah, I mean, basically as soon as I
• 36:09
  established, you know, with good confidence that I was onto
• 36:12
  something with this whole damage repair approach, I knew that it
• 36:16
  was up to me to bring people together to actually do the
• 36:20
  right research. And that involved getting the
• 36:22
  scientists interested. And it also involves getting the
• 36:24
  money for the scientists to do what they're what I've got them
• 36:27
  interested in. Turned out the first of those
• 36:29
  was really easy scientists. I used to actually have a slide
• 36:33
  in my talks that would be entitled Scientists will do
• 36:36
  anything interesting for food I. Didn't see that one.
• 36:41
  It's it's more or less true. So I never had any trouble
• 36:44
  persuading people that they would do what I wanted them to
• 36:49
  do, just as long as I could pay them.
• 36:51
  So my job was to bring in the money.
• 36:54
  And after I spoke at Ted in 2006 and started speaking at other
• 36:58
  high profile places, you know, I decided to meet, you know, with
• 37:02
  people who were willing to fund the philanthropic venture.
• 37:05
  Philanthropy is an enormously important part of all of this
• 37:09
  because there all I've got to do is get wealthy people to trust
• 37:12
  me, OK? I don't have to do anything
• 37:15
  else. Whereas the other sources of
• 37:17
  money that are available, you've basically got industry or you've
• 37:20
  got academia in the industry. They don't.
• 37:24
  The people who are actually writing the checks don't give a
• 37:26
  flying fuck about whether I'm right.
• 37:29
  They just care whether going to make money and no.
• 37:32
  Surprise there. And in particular, anyone who
• 37:34
  wants to make money wants to make it tomorrow.
• 37:37
  So there is an enormous pressure towards short termism, towards
• 37:41
  the low hanging fruit at the expense of, you know, things
• 37:45
  that are just as vital for this divide and conquer damage repair
• 37:48
  approach. But just in whatever even
• 37:52
  harder. Now it turns out that academia
• 37:54
  is every bit as short term as industry or a bit for a
• 37:57
  completely different reason there.
• 37:59
  The issue is there's never enough money being provided by
• 38:02
  the government or, you know, or institute or whatever to, to,
• 38:09
  to, to support the research. So the researchers are competing
• 38:12
  against each other. And the way that that
• 38:15
  competition is always decided is by this horrible repulsive
• 38:19
  mechanism called peer review, where essentially some of the
• 38:22
  experts in a given field are sequestered, you know, are are
• 38:27
  basically brought together to evaluate the relative quality
• 38:32
  of, you know, ideas for research that are being put forward by
• 38:36
  the others. Why is that so repulsive?
• 38:39
  Because there's never enough money.
• 38:41
  And so the best one in the world, these people are coming
• 38:44
  in and they have to, they're just looking for reasons to say
• 38:47
  no. They're looking for stupid
• 38:50
  reasons to choose one particular grant application over another.
• 38:56
  For example, they're saying, OK, you know, this person's got more
• 38:59
  track record or whatever. It's completely in fact, it's
• 39:05
  not even that. It's not like the track record
• 39:07
  is defined in a stupid way. It's defined by how many times
• 39:11
  papers that the person has published have been referenced
• 39:15
  by other scientists. And and worse than that, it's
• 39:20
  quick, you know, like it doesn't matter how important somebody's
• 39:23
  work was that they did 10 years ago.
• 39:25
  It only matters what they did like two years ago.
• 39:28
  You know, it's like it's. Yeah, it's really, it sounds
• 39:31
  really arbitrary and it's tough for somebody that's obviously
• 39:33
  being innovative, assuming that there is no track record and
• 39:37
  it's obviously a a, a a topic. Well, listen, we're going to
• 39:40
  hold you there for a minute. And when we come back, we're
• 39:41
  going to be talking about his ground breaking book that
• 39:44
  represents obviously a road map for ending the aging process.
• 39:48
  You know, obviously through radical life extension
• 39:50
  techniques. You're going to want to hear
• 39:52
  this when we come back. Doctor Aubrey de Grey, The Big
• 39:55
  Ming Show, George Ballantine, Lance Miliacho.
• 39:57
  Stay tuned. There's a chance for your Lance.
• 39:59
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  They would run up to the bamboo fence and they would be shooting
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  between the bamboo at the buildings, you know, just
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  shooting inside. The Wanted man is Joseph Kony,
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  charged with abducting huge numbers of children, forcing
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  them to kill and mutilate innocent victims.
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  Somebody had to pay the price. Sam did that.
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• 42:31
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  And now God has me in the Congo, you know, So hopefully we'll
• 42:57
  meet up one day. But maybe I can lead him to the
• 43:02
  Lord or send him there. One or the other, huh?
• 43:19
  Welcome back to the Big Big Show.
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  Thank you all. So Dak when, when when it comes
• 45:10
  to like anti aging. So I get the part like you can
• 45:14
  look on the outside, you know, the ageing, you know, you look
• 45:18
  whatever younger. Does it also on the inside of
• 45:20
  your organs too? Or reverse that in a sense?
• 45:23
  Oh for sure, for sure. The outside, you know how you
• 45:26
  look is overwhelmingly a side effect of the inside.
• 45:30
  You know the the skin is a constantly regenerating tissue.
• 45:34
  Remember, we lose skin, we have stem cells at the base of the
• 45:37
  skin that are constantly making new skin cells.
• 45:40
  And that means that the health of the skin, how it looks is
• 45:45
  substantially determined by what's going on in the
• 45:49
  bloodstream that is feeding those those stem cells.
• 45:53
  And of course, the bloodstream is also feeding everything else.
• 45:56
  It's a kind of, you know, information highway between
• 45:59
  everything. But the more below that level of
• 46:02
  the skin, there's another level called the dermis, which is
• 46:06
  largely responsible for the elasticity of the skin.
• 46:09
  So when we get wrinkles, which is obviously one aspect of the
• 46:13
  superficial ageing of the skin, that's because the dermis is
• 46:17
  suffering damage to the lattice of proteins called the
• 46:21
  extracellular matrix that holds those cells together and which
• 46:25
  is supposed to be elastic and becomes less elastic as a result
• 46:28
  of oxidative damage. So I'm feeling pretty good right
• 46:33
  now 'cause I'm looking at my skin, I got good skin, so the
• 46:35
  insides work. Why?
• 46:37
  What are you laughing? I'm being serious.
• 46:38
  It's good genetics. So, you know, at the end of the
• 46:40
  day, I think that's part of it. But yeah, you live pretty well.
• 46:42
  You haven't had a drink and you don't smoke.
• 46:44
  I mean, really. Take care to smoke, I Take care
• 46:46
  of myself, I. Had a drink in about 11 years
• 46:48
  Doc He's been clean and sober for about 11.
• 46:50
  I I myself don't drink very much and I don't smoke and.
• 46:53
  Everything why you look so bad bro what's up?
• 46:55
  Hey, you know this was miles in the sun here if I'm looking at
• 46:57
  aged. I always been in the sun a lot
• 46:59
  more than you probably, but it's OK.
• 47:02
  I don't know, maybe. I still love you, answer my
• 47:04
  brother from another mother, but the same father, so it's all
• 47:06
  good. All right, so Doc, you made a,
• 47:09
  you had a quote that says there is no ticking time bomb.
• 47:11
  I mentioned it backstage, just the accumulation of damage.
• 47:16
  And I want you to go and maybe share with the audience, kind of
• 47:18
  take us through the process of, you know, what are the, the big
• 47:21
  ones, You know, where's the big damage and how's it caused?
• 47:25
  Yeah, sure. OK.
• 47:25
  So first of all, let me amplify on that quite a little bit
• 47:30
  because here's what I'm trying to disabuse people of.
• 47:36
  We see that through, you know, 20 or 30 years of adulthood,
• 47:42
  nothing goes wrong. I mean, yes, a 50 year old can't
• 47:45
  run as fast as a 20 year old necessarily.
• 47:48
  Not usually right, but nearly as fast.
• 47:50
  You know, you know, in terms of normal day-to-day activities,
• 47:54
  whether mental or physical, there's not a lot of difference
• 47:57
  between a 20 year old and a 50 year old.
• 48:01
  And then after that, things start to go wrong.
• 48:03
  And when they do start to go wrong, they go wrong at a
• 48:05
  progressive, you know, an accelerating rate.
• 48:07
  So on the face of it, it looks like, you know, the body's got
• 48:12
  some, you know, timer in there, you know, that says, you know,
• 48:16
  that the body can just get on and do what it likes for a
• 48:18
  while. And then eventually, you know,
• 48:22
  there's something that times up, so to speak, and, and the body
• 48:25
  kind of, you know, a whistle gets blown and, and everything
• 48:28
  starts to go to hell in a handbasket.
• 48:31
  And I want to make sure that people understand that that's
• 48:34
  not the case. That's why I often use analogies
• 48:38
  where simple man made machines like cars or aeroplanes or
• 48:41
  whatever. You know, a car doesn't have one
• 48:44
  of them either, right? It's just got a warranty period
• 48:47
  that arises from how it was built, from the quality of the
• 48:52
  components, from the, you know, the which, what type of metal
• 48:54
  they saw that thing was made out of themselves.
• 48:57
  And it's exactly the same for the human body.
• 48:59
  The quality of how how we're built, how well we are capable
• 49:04
  of holding ourselves together is something that's built into our
• 49:09
  genetics. But there's nothing built in
• 49:12
  that says, OK, now stop trying, so to speak.
• 49:16
  Now you know, you know, just go downhill on purpose.
• 49:19
  That's something that people really need to understand.
• 49:21
  And it's helpful because it's what underpins the whole idea
• 49:25
  that all we need to do in order to keep ourselves healthy for a
• 49:29
  lot longer, maybe indefinitely longer, is preventative
• 49:33
  maintenance. Just as long as the preventative
• 49:35
  maintenance is comprehensive enough.
• 49:38
  Because all of us do preventative maintenance on our
• 49:40
  cars, but nearly all of us only do the minimum amount of
• 49:44
  preventative maintenance that the law requires.
• 49:46
  Because we're perfectly happy with the idea that eventually
• 49:48
  the car will fall apart and we'll get a new one.
• 49:50
  Right. You can't do that with the with
• 49:52
  your own body. You know, you can't get a new
• 49:54
  one, not yet anyway. So we've got to do proper
• 49:58
  preventative maintenance. And that of course is inspired
• 50:01
  by what we can do with cars, with vintage cars.
• 50:04
  There are cars around right now that are, that were built 100
• 50:08
  years ago or more. And if you ask how come, how,
• 50:12
  how did they get that way? The answer is not because they
• 50:16
  were built for the last 100 years.
• 50:17
  They were built for the last 10 or 15 years at the outside, but
• 50:21
  just by periodic, comprehensive preventative maintenance, here
• 50:25
  they are. And of course, they'll be here
• 50:27
  in another 100 years. Yeah, it's, it's interesting and
• 50:31
  I think people are always wondering what does that, you
• 50:33
  know, to prevent aging. They're obviously looking for
• 50:35
  that fix. And you're right, people
• 50:37
  obviously want the quick fix. They don't want to do what's
• 50:40
  necessary. You, you mentioned that
• 50:42
  preventing aging is a really complex issue when it comes to
• 50:45
  maintenance. I guess the regimen of that is
• 50:48
  what's, how far along are you with that?
• 50:50
  Because you talk about something that I knew nothing about AG, ES
• 50:54
  and zombie cells and that accumulation of waste that
• 50:58
  builds up. Have you, Have you.
• 51:00
  So let's, let's make sure the audience understands that first
• 51:02
  'cause you and I are talking straight out of the book.
• 51:04
  So they may not even understand unless they've read the book.
• 51:06
  So let's talk about that first. But then have you found
• 51:09
  processes to help clear that out of your system to shut down the
• 51:12
  zombie cells and actually at the same time get rid of that
• 51:14
  intracellular an extracellular waste?
• 51:17
  So, sure. I mean, everything that I've
• 51:19
  been working on over all these years has been precisely to
• 51:22
  develop ways to eliminate these various types of damage that I
• 51:26
  enumerated back in the year 2000.
• 51:30
  Now I want to start one thing. First of all, that the number of
• 51:34
  types of damage that we need to repair in a machine that's so
• 51:37
  insanely complicated as a human body is very large.
• 51:41
  And So what I did in the year 2000 was simply to classify
• 51:45
  those many types of damage into 7 categories.
• 51:49
  The first question that I need to explain that for is why is
• 51:53
  that classification useful? You know, how did that change
• 51:55
  anything? The answer is because for each
• 51:57
  of those seven categories, I can actually describe a generic
• 52:02
  approach to fixing it, something that says, OK, you know,
• 52:07
  different examples within a category may need slightly
• 52:10
  different approaches, but they'll all have a lot in
• 52:12
  common. And so as we get one or two of
• 52:14
  them working, it will be much quicker to get the next one
• 52:16
  working and the one after that. That was the real, the real
• 52:20
  inspiration. All right, so let's look at what
• 52:23
  the the examples that you just mentioned.
• 52:26
  Zombie cells I wouldn't call senescent cells in the technical
• 52:29
  community. So actually I haven't done much
• 52:32
  work on them. I've done some, but basically
• 52:35
  that's one that I've been able to leave to other people simply
• 52:38
  because it got going, you know, pretty quickly.
• 52:41
  Maybe 2025 years ago, people figured out good, good ideas for
• 52:45
  how to move it forward. But yeah, it had moved forward
• 52:48
  very well. We now have ways to eliminate
• 52:51
  such cells pretty selectively, you know, to give drugs to
• 52:55
  animals that will make those cells die without making too
• 53:00
  many other cells die. And and that's extremely
• 53:04
  helpful. In fact, it's been shown in
• 53:05
  various experiments to actually extend life.
• 53:08
  So we're very, we're very much focused on that as one of the
• 53:11
  things we want to do the elimination of waste products
• 53:15
  and especially the elimination of these things called AG ES
• 53:18
  that you mentioned, which is a convenient acronym for something
• 53:21
  extremely complicated and. Can you share with the audience
• 53:23
  talk? I don't want to step on you
• 53:24
  there, but can you share with them?
• 53:25
  Because I hate to say this, I've eaten browned and blackened meat
• 53:28
  many times, not realizing that I was probably doing myself some
• 53:31
  real harm in eating meat like that.
• 53:33
  But go ahead. All right.
• 53:36
  So remember you're talking about 3 of my categories
• 53:39
  simultaneously there. So let me just focus on the one
• 53:41
  you're focusing on, which is 80. The the thing there that gives
• 53:45
  the problem is something called stiffening, lots of elasticity.
• 53:50
  And this happens because of chemical reactions that that
• 53:53
  occurred between proteins in the outside of the cell, what's
• 53:57
  called the extracellular matrix and sugar that's in the
• 54:01
  circulation, just that's wandering around.
• 54:04
  Sometimes those reactions cause new chemical bonds to form
• 54:07
  between proteins that are not supposed to be joined together.
• 54:10
  And that that causes the, the stiffening I'm talking about.
• 54:14
  So we want to break those things.
• 54:17
  Now. Don't worry too much about
• 54:19
  eating stuff with that's brown. You're, you're quite right that
• 54:23
  at the chemical level, what you're eating has a bunch of
• 54:25
  those, those cross links in it, those, those links between
• 54:29
  protein. But those cross-linked proteins
• 54:32
  don't get into cells. They don't get into the, well,
• 54:35
  they probably don't get into the body at all really.
• 54:37
  Maybe it's to the extent that they get into the bloodstream
• 54:39
  even a little bit. It doesn't matter because they
• 54:42
  won't get into cells hardly at all.
• 54:44
  And if they do get into cells, they won't be incorporated into
• 54:47
  new proteins. So one way or another, my view,
• 54:52
  and you know, I've been looking at this for a while because
• 54:54
  people have been espousing the contrary view, my view, my sperm
• 55:01
  view is that this is the red herring.
• 55:03
  But we don't need to worry about any kind of toxicity around.
• 55:10
  Yeah. So.
• 55:13
  So yeah, basically, you know, each of these types of damage
• 55:15
  needs it's own approach. So look, if we look at that
• 55:19
  particular one, we do need to get rid of these cross links,
• 55:22
  just not the ones in the diet. We just need to get rid of the
• 55:24
  ones that spontaneously arise in the body.
• 55:27
  And I was able to support a project, one of my, my previous
• 55:32
  foundation was able to support for several years, an important
• 55:35
  project at Yale University, which led to some real
• 55:38
  breakthroughs publishing science magazine.
• 55:41
  And that led to the spinning out of a company which is now
• 55:43
  pushing that forward quite effectively.
• 55:46
  It's, you know, but it's really tough research.
• 55:48
  Now there's just this one company.
• 55:49
  I don't know of any other company looking at this problem
• 55:52
  as you know, thoroughly as this one is.
• 55:55
  And you know, we definitely need a dozen such companies.
• 55:57
  They don't exist because there's not enough money in buying this
• 56:00
  this field at this point. Yeah, it's and I and I get that,
• 56:06
  you know, when I, when I look at research, obviously this is,
• 56:09
  this seems to be on the cutting edge.
• 56:10
  Of course they spend, there are companies that spend exorbitant
• 56:14
  amounts of money on researching the possibility of creating a
• 56:17
  cream that will make you look younger.
• 56:20
  But of course that's from the outside and not the inside out.
• 56:23
  And I don't know that that solves anything, you know.
• 56:26
  So we talked about, you've got 7 topics here and you talk about
• 56:29
  cell loss and atrophy, which obviously I don't know what the
• 56:33
  solution. One of the things for atrophy,
• 56:35
  we hear a lot of people talking about hormone replacement.
• 56:37
  Has that had any positive effect in those areas?
• 56:39
  Growth hormone? Testosterone.
• 56:42
  So there are various ways to address cell loss in accuracy.
• 56:46
  The one that I talked about the most back 20 odd years ago was
• 56:50
  stem cell therapy. And that's definitely the way to
• 56:53
  go in certain cases. So one very important case of
• 56:57
  this is Parkinson's disease, which is caused by the loss of a
• 57:01
  particular type of brain cells, the particular neuron called a
• 57:04
  dopaminergic neuron. Dopaminergic neurons are really
• 57:09
  hard work horses. They, they, they, they, they do
• 57:13
  stuff that's that's energetically very demanding.
• 57:17
  Basically they make the chemical called dopamine, of course, and
• 57:22
  that result, the result is they die a lot more frequently than
• 57:25
  your average neuron does, and they're not replaced.
• 57:29
  So all of us by our age have lost maybe 2 thirds, 3/4 of
• 57:33
  that's right, about one third, one quarter of the of the
• 57:38
  dopaminergic neurons that we had in young adulthood.
• 57:42
  That's fine though. We don't have Parkinson's
• 57:44
  disease because the system is set up to tolerate that amount
• 57:46
  of loss. Well, it's not set up to
• 57:48
  tolerate losing 2/3 or three courses.
• 57:50
  And some people lose them faster and they're by the time they're
• 57:54
  in their old age, they have lost that number.
• 57:56
  And those are the people who get Parkinson's.
• 57:59
  All right. So what you do to fix this is
• 58:00
  very straightforward. You just put stem cells back
• 58:02
  into the relevant part of the brain that have been programmed
• 58:07
  in the right way to divide and create the replacements for the
• 58:13
  cells that the body's not replacing on it's own.
• 58:15
  And it works. It works spectacularly well.
• 58:18
  Now can I stop? You does that work for dementia,
• 58:21
  Alzheimer's also or just Parkinson's?
• 58:23
  Not exactly, but I'll come to that in a moment.
• 58:25
  Oh, great. OK.
• 58:26
  Parkinson's. This was tried 30 years ago, but
• 58:30
  then it only occasionally worked because people didn't really
• 58:32
  know what to do with preparing the stem cells into the right
• 58:36
  state before they injected them. Now we know all about that, and
• 58:41
  there's half a dozen clinical trials going on right now doing
• 58:44
  this, and everyone's very optimistic this will be a real
• 58:46
  cure for Parkinson's. Because back then, 30 years ago,
• 58:49
  when it did work, on those rare occasions when it did work, it
• 58:52
  worked spectacularly well. People were completely cured for
• 58:55
  like 10 or 15 years, all right? And that was just one injection.
• 59:01
  All right, So you asked an excellent question, whether the
• 59:05
  same kind of thing could work for Alzheimer's disease.
• 59:08
  It's a lot harder for Alzheimer's disease because the
• 59:13
  cells that die in Alzheimer's disease are spread across most
• 59:17
  of the brain. There are certain places that
• 59:19
  are more affected than others, but a lot of places that are
• 59:22
  affected. Whereas in Parkinson's, it's
• 59:23
  just one teeny tiny part of the brain called the substantial
• 59:26
  nigra. And that matters because when
• 59:29
  you inject cells into the brain, they don't move around.
• 59:33
  If you inject cells into the bloodstream, they of course move
• 59:36
  all over the all over body, but the, the, the equivalent of the
• 59:40
  bloodstream in the brain is called the cerebrospinal fluid
• 59:44
  and it's sticky, it's viscous, and so things don't move around.
• 59:49
  But we founded a group, I founded a group for several
• 59:52
  years looking at a really elegant and ingenious solution
• 59:56
  to that that essentially involves genetically engineering
• 59:58
  these dopaminergic precursors, as they're called, so they know
• 1:00:02
  how to swim, so they know how to actually distribute themselves
• 1:00:06
  around the body. You don't use, but for
• 1:00:09
  Alzheimer's, you don't use dopaminergic precursors, you use
• 1:00:12
  cholinergic or Gabaergic or whatever.
• 1:00:14
  But the point is you, you can make them swim so you can
• 1:00:17
  overcome this problem. And that's still very much a
• 1:00:20
  research area, but it's, it's promising then.
• 1:00:23
  So you were asking more generally about about cell loss
• 1:00:27
  and cell atrophy and you were asking about growth hormones and
• 1:00:30
  such like. So they're, so there's been some
• 1:00:34
  very exciting work on one really one other really important area
• 1:00:38
  of cell loss in ageing, which is called thymic involution, where
• 1:00:42
  this organ called the thymus loses cells and the result is
• 1:00:46
  eventually the immune system doesn't work so well.
• 1:00:49
  It's been found that you can use growth hormone along with a
• 1:00:53
  couple of other things that effectively address the side
• 1:00:56
  effects of growth hormone and you can get a rejuvenation of
• 1:01:00
  this thing called the thymus, this organ near the heart.
• 1:01:04
  And it looks like it does actually restore immune function
• 1:01:06
  to some significant extent early stage, but at least it's being
• 1:01:10
  done. It's being done in human beings.
• 1:01:11
  You know, it's not just in in, in mice or anything.
• 1:01:14
  So it's very exciting. And then the third thing that I
• 1:01:17
  want to mention, the last thing in this area is partial
• 1:01:21
  reprogramming. So what the hell is that?
• 1:01:23
  Well, about 18 years ago, a group in Japan figured out a way
• 1:01:29
  to make normal cells from you and me into the most primitive
• 1:01:34
  cells we know about, cells called embryonic stem cells,
• 1:01:37
  like into into things that behave almost exactly like
• 1:01:40
  embryonic stem cells. And this was, this is very
• 1:01:42
  useful because if you've got those cells, you can make other
• 1:01:45
  cells from them really well. Now thing is though, you don't
• 1:01:50
  want to put those cells into the body because they won't know
• 1:01:53
  what to do. They're too primitive.
• 1:01:55
  They know what to do in the early embryo.
• 1:01:57
  They don't want to know what to do in you and me.
• 1:01:59
  So what you do is you want to make them into other cells
• 1:02:02
  before you do that. Now, why is that interesting?
• 1:02:05
  Because you might be able to use the same factors, the same
• 1:02:08
  things that are used in a Petri dish to create those cells.
• 1:02:12
  You might be able to use them in the body, but you use them in a
• 1:02:16
  very delicate way. You only just, you know, you
• 1:02:18
  know, do it transiently for a day or two or something like
• 1:02:22
  that. And that might slightly push
• 1:02:26
  cells back into that direction, but only slightly.
• 1:02:28
  And that might be useful. It might make them more
• 1:02:31
  regenerative. People have been trying that,
• 1:02:33
  and they've got very promising results.
• 1:02:35
  So that's a very live topic that Jeff Bezos put $3 billion into a
• 1:02:38
  company that was mostly focused on that.
• 1:02:40
  Yeah, it's interesting. Obviously one of the side
• 1:02:42
  effects of growth hormone is acromeglia, so I don't know if
• 1:02:45
  that's one of the side effects you were talking about.
• 1:02:47
  People talk about Neanderthalism when you use too much.
• 1:02:50
  And of course hormone replacement for the anti aging
• 1:02:53
  clinics, that's part of the obviously the regimen that they
• 1:02:57
  put you on. They do a bunch of blood screens
• 1:02:59
  and the rest of it. And then some people think it's
• 1:03:01
  because of inflammation that obviously your hormone levels
• 1:03:04
  and of course aging in your body determines that you don't need
• 1:03:07
  as many hormones and fight or flight response is different as
• 1:03:10
  you get older. So it's a lot more complicated
• 1:03:12
  than that. So first of all, both hormone
• 1:03:15
  itself, it's pretty clear that you don't want to have high
• 1:03:19
  levels of growth hormone when you're growing during
• 1:03:22
  development. It's good to have low levels
• 1:03:24
  when you're growing, either low levels of growth hormone itself
• 1:03:27
  or of other molecules that are important for the activity of
• 1:03:31
  growth hormone. However, after you're growing,
• 1:03:34
  when you're when, when you're an adult, the situation is very
• 1:03:38
  different. Secondly, it's very important to
• 1:03:41
  recognise that we're not talking about the normal use of growth
• 1:03:46
  hormone that made growth hormone famous, namely improving muscle,
• 1:03:51
  because it turns out it's not very good with muscle.
• 1:03:54
  There are other things you can do.
• 1:03:55
  For example, there's a very interesting project called
• 1:03:57
  follistatin which is good and muscle, but growth horn yes, you
• 1:04:02
  get more let. Me ask, you tell me filostatin
• 1:04:04
  was used for myostatin inhibition, wasn't wasn't that
• 1:04:07
  kind of the idea? That you actually statin is yes,
• 1:04:09
  yeah for myostatin, for myo is Greek for muscle.
• 1:04:14
  Again, statin is Greek for inhibition.
• 1:04:16
  So basically the more myostatin you have, the less muscle you
• 1:04:19
  have. Folostatin antagonizers inhibits
• 1:04:22
  myostatin. So you're acting kind of one
• 1:04:24
  step removed, but you're actually causing more muscle to
• 1:04:27
  happen. If you have more folostatin, and
• 1:04:29
  it often works in biology, that being one step removed is more
• 1:04:34
  is a good way of avoiding side effects a better way than if you
• 1:04:37
  do things in the more route one approach for various reasons.
• 1:04:42
  Hold it there for a second Doc. Hey George, look up myostatin
• 1:04:44
  inhibition on the the Google. You'll find some dogs, some
• 1:04:49
  greyhound looking dogs. You'll also find some bulls that
• 1:04:52
  are missing the actual gene that is out there.
• 1:04:55
  Now, some people have said they can use CRISPR technology and
• 1:04:58
  that obviously that would allow you to develop muscle really
• 1:05:01
  with absolutely no action, not even going to the gym.
• 1:05:04
  Is there any truth in that that some people are using CRISPR
• 1:05:06
  technology to modify their genome?
• 1:05:09
  Yes, it's certainly, well, actually not CRISPR per SE.
• 1:05:12
  You don't use CRISPR to insert a new gene, not these days anyway.
• 1:05:16
  You do CRISPR to modify genes that are already there.
• 1:05:19
  But you can certainly use gene therapy to insert a new copy of
• 1:05:24
  an extra copy of forestatin. And various people, including my
• 1:05:28
  great friend Liz Parrish have done that.
• 1:05:32
  So, you know, it's it's an exciting possibility.
• 1:05:35
  And as I say, it seems to work better for muscle with growth
• 1:05:37
  hormone. But when we come back to the
• 1:05:39
  thymus, which is what I was talking about earlier, the
• 1:05:42
  immune system there, it seems that growth hormone itself has
• 1:05:45
  genuine benefits and as I say, side effects.
• 1:05:50
  So the people who were working on this and giving this to
• 1:05:52
  people were not just giving growth hormone itself, they were
• 1:05:56
  also giving a couple of other things, DHEA and metformin to to
• 1:06:01
  to limit those side effects. You know, there's been a lot of
• 1:06:05
  discussions about different peptides and peptide
• 1:06:07
  technologies changed. What do you see?
• 1:06:10
  Do you see anything on the horizon on that that seems to be
• 1:06:12
  maybe working on some of the things that you because you
• 1:06:15
  always talk about engineering solutions versus versus medical
• 1:06:19
  solutions. So I don't know if that falls
• 1:06:21
  into that when you start using peptides or is that really a
• 1:06:23
  medical solution? First of all, let me correct
• 1:06:29
  your terminology there. And I don't really say that
• 1:06:32
  engineering solutions are not medical solutions.
• 1:06:35
  You know, your, your audience may, may get the impression that
• 1:06:40
  I'm thinking there's medicine and then there's like
• 1:06:41
  cybernetics. I'm not talking about that kind
• 1:06:43
  of. So there's definitely, I think
• 1:06:47
  engineering means just thinking like an engineer.
• 1:06:49
  You know, I came up with this whole idea of damage repair,
• 1:06:52
  this divide and conquer approach and it was, it took me 6 or 8
• 1:06:57
  years really to get my colleagues in the community who
• 1:07:01
  are very, very knowledgeable, of course, to understand that what
• 1:07:05
  I was saying with even scientific, let alone plausible.
• 1:07:08
  You know, it was, it was tough because it was such a paradigm
• 1:07:11
  share just because I was thinking like an engineer.
• 1:07:14
  So it's definitely medical. But yeah, I mean peptides, OK,
• 1:07:20
  peptides have that. They're a controversial area and
• 1:07:24
  they're controversial for a good reason, namely that the main
• 1:07:28
  groups that were promoting and, you know, reporting really
• 1:07:33
  promising results with with these peptides were from Russia
• 1:07:38
  and were, well, the Soviet Union as it was back then, and were
• 1:07:43
  not reporting things in what Westerners would consider
• 1:07:47
  rigorous ways. And there was a a conspicuous
• 1:07:53
  lack of corroboration of their results by other scientists from
• 1:07:57
  other labs. So there is still a lot of
• 1:08:01
  skepticism around the efficacy of peptides.
• 1:08:06
  Interesting. Hey George, I threw one of the
• 1:08:08
  dogs in Notion. I just wanted the audience to
• 1:08:10
  see because obviously what happens when you inhibit
• 1:08:13
  myostatin, you actually end up, it seems like with almost double
• 1:08:16
  muscle. There's bulls that actually are
• 1:08:19
  missing that gene and others. I don't know if it's been
• 1:08:21
  scientifically, you know, if that's what they did, if it was
• 1:08:24
  science, or if the animals were born that way.
• 1:08:26
  It seems like most of the stuff I've read, the animals were born
• 1:08:28
  that way. Have people successfully removed
• 1:08:30
  the myostatin inhibition from their body?
• 1:08:33
  So first of all, you're right, the the gene was a spontaneous
• 1:08:37
  mutation that knocks out myostatic.
• 1:08:40
  As far as I'm aware, nobody has tried doing that or even, you
• 1:08:45
  know, reducing the expression of myostatin simply because
• 1:08:49
  increasing the expression of filostatin is appears to be a
• 1:08:53
  safer way to go about things. Essentially what you're doing
• 1:08:57
  with these, you know, interventions that are one step
• 1:09:02
  removed. If you're giving the body more
• 1:09:05
  of a chance to figure out how to minimize side effects, even side
• 1:09:09
  effects that you don't know about yet, You're essentially,
• 1:09:12
  you know, you're, you're, you're giving, you're, you're letting
• 1:09:16
  the body's inherent self protection machinery be more
• 1:09:20
  influential in, you know, optimizing the situation.
• 1:09:24
  That's the way I look at it. I got you.
• 1:09:27
  Well, obviously we've seen lots of crazy sports technology
• 1:09:30
  coming out of the Eastern Bloc nations that everybody's always
• 1:09:33
  trying to obviously improve their life performance, trying
• 1:09:36
  to find something that can't be tested for.
• 1:09:38
  So and and some of that falls over into anti aging because
• 1:09:40
  they're obviously trying to extend their longevity in
• 1:09:43
  sports. It's a lot of it.
• 1:09:45
  You know, you, we mentioned a little while ago we were talking
• 1:09:48
  about that maybe the, there's, there's an issue on one side of
• 1:09:51
  this where people, you know, may have a moral issue with it or
• 1:09:55
  may have a, you know, obviously population issue.
• 1:09:59
  You know, do you feel like you've dealt with a lot of that
• 1:10:02
  where obviously some people don't want to extend the
• 1:10:05
  lifespan? Because obviously there's a lot
• 1:10:06
  of discussions about all these different, you know, World
• 1:10:11
  Economic Forum type agencies are obviously globalists, that a lot
• 1:10:15
  of people have this belief that they want to reduce the global
• 1:10:17
  population, they want to increase.
• 1:10:19
  And of course, if you were successful in in increasing
• 1:10:22
  people's lifespan three to four, 5-6 hundred years, that
• 1:10:25
  obviously goes against what it seems like people just right
• 1:10:28
  now, people think that the plan is overpopulated.
• 1:10:31
  What are your thoughts on that? Have you had a lot of
• 1:10:32
  interaction with people that have said that to you?
• 1:10:35
  So I haven't had it when people are asking me questions of
• 1:10:38
  counting the number of times that they say the word
• 1:10:40
  obviously, and you say it five times.
• 1:10:42
  That's not counting the time that you said, of course.
• 1:10:43
  And the reason I, the reason I do that is because it's a, it's
• 1:10:49
  a pretty, it's a pretty reliable red flag for things that are
• 1:10:53
  remotely obvious. So first of all, the the idea
• 1:11:01
  that there would be some kind of overpopulation consequence of
• 1:11:05
  aging under control is probably the single most common concern
• 1:11:10
  that people raise. But it is one of many concerns
• 1:11:14
  that people just like, you know, it's just an embarrassment that
• 1:11:19
  people raise them because they are so trivial to rebut.
• 1:11:23
  And, yeah, people don't want to listen to the rebuttal.
• 1:11:27
  They want to believe that aging is some kind of blessing in
• 1:11:30
  disguise. You know, in particular for
• 1:11:32
  overpopulation. You just have to do the numbers.
• 1:11:34
  You just have to say, well, OK, look, how many people do we
• 1:11:37
  have? We have 8 billion people, right?
• 1:11:39
  How many acres do we have on the planet of land?
• 1:11:41
  Do we have on the planet? It's well over 8 billion, You
• 1:11:44
  know, even if you don't count the places that are unpleasant
• 1:11:47
  to live. So, so, you know, there's not a
• 1:11:50
  shortage of space. The only problem is pollution.
• 1:11:53
  Obviously we are making far too much carbon.
• 1:11:54
  We're making far too much, you know, plastics that don't
• 1:11:58
  degrade and so on. But hello, in case anybody had
• 1:12:01
  forgotten, we are working on on technologies to fix that, which
• 1:12:04
  will be completely out there way before there's any demographic
• 1:12:08
  consequence of dealing with aging.
• 1:12:10
  Even if we take a completely worst case scenario in terms of
• 1:12:16
  women continue to have kids as the same rate as they are today,
• 1:12:19
  which obviously we know from past history is not going to
• 1:12:21
  happen anyway. So.
• 1:12:23
  So that's nonsense. But yeah, I mean, you know,
• 1:12:27
  there's all many of other things here that are nonsense.
• 1:12:31
  The first one is this whole idea that the powers that be want us
• 1:12:35
  to have fewer people on the planet.
• 1:12:36
  Why would they want that? You know, I mean, perhaps
• 1:12:39
  because they haven't realized, they've forgotten that we are
• 1:12:42
  getting rid of, you know, there's a carbon capture
• 1:12:45
  technology coming and so on. You know, the fact is at the
• 1:12:50
  moment the issue is the global economy.
• 1:12:52
  That's the actual issue. The people who are actually in
• 1:12:54
  charge are, you know, the people who governments and heads of
• 1:12:59
  state of the major economies and what they want is prosperity.
• 1:13:03
  How are they going to get prosperity by no longer spending
• 1:13:07
  all this an unbelievable amount of money keeping sick people
• 1:13:10
  alive? How we do that we stop them
• 1:13:13
  getting sick in the 1st place. Even in the early stages when
• 1:13:18
  these first generation interventions are going to be
• 1:13:23
  probably fairly expensive to administer.
• 1:13:26
  So what? Because they'll still pay for
• 1:13:28
  themselves. Why many made times over really
• 1:13:31
  quickly right now I want to also point out since obviously from
• 1:13:36
  my accent, everybody can tell that I am from that far off
• 1:13:38
  place called the rest of the world where we don't, where we
• 1:13:41
  pay for our health care in a different way.
• 1:13:44
  You know, you know, it doesn't matter how you pay for it.
• 1:13:48
  It doesn't matter. The point is, you know, whether
• 1:13:51
  it's through subsidies or taxation or whatever, it's
• 1:13:54
  trivial to distribute the increased prosperity prosperity
• 1:13:59
  equitably, right? So that everybody who's old
• 1:14:01
  enough to need such therapies gets them.
• 1:14:04
  Everybody who's entitled to make money out of the therapies
• 1:14:06
  because they've got the intellectual property gets it.
• 1:14:08
  You know, it's just like it's, it's like it's completely
• 1:14:13
  obvious. And, you know, so the question
• 1:14:16
  we have to ask ourselves is why do people cling to the idea that
• 1:14:20
  there are all these problems and that, you know, that aging is
• 1:14:23
  some kind of blessing in disguise?
• 1:14:25
  And the answer is very, very, very obvious.
• 1:14:28
  It's simply that people are terrified of getting their hopes
• 1:14:30
  up. People have been doing what I'm
• 1:14:32
  doing today since the beginning of civilization.
• 1:14:35
  They've been saying we are, we have the way to bring aging
• 1:14:38
  under control, to have the fountain of you, right?
• 1:14:42
  I'm not saying we have it yet. I'm saying, but I am saying
• 1:14:44
  we're going to have it fairly soon with high probability,
• 1:14:46
  right? So the point is, everyone before
• 1:14:51
  me has been wrong, right? So why should people, you know,
• 1:14:55
  not? I mean, I think it's justifiable
• 1:14:56
  to hesitate to be, to be a little skeptical until there's
• 1:14:59
  more evidence that I'm actually not wrong, right?
• 1:15:02
  Yeah. I don't have a problem with
• 1:15:04
  that. But the point is it does
• 1:15:06
  underpin this unbelievably deep seated irrationality which comes
• 1:15:10
  out everywhere. Look at the look at the science
• 1:15:13
  fiction that's written. Look at all the movies.
• 1:15:14
  This. Yeah, it's.
• 1:15:15
  Incredible. This, this, this constant stream
• 1:15:17
  of movies about a post aging world, right?
• 1:15:20
  And that's all dystopic. They're all dystopic in one way
• 1:15:23
  or another. And the reason is that sells.
• 1:15:26
  And the reason it sells is because people want their, what
• 1:15:29
  I often call the pro aging trance, to be entrenched.
• 1:15:35
  Yeah, I get you. Well, let me ask you this.
• 1:15:37
  What do you think? What scientific advancements do
• 1:15:39
  you believe are the most urgent that they were going to be
• 1:15:42
  prioritized? Is there a list of them that you
• 1:15:43
  would say to achieve that meaningful life extension in the
• 1:15:47
  next few decades? What has to happen now for that
• 1:15:49
  to move forward? Though I have a rather perhaps
• 1:15:53
  counterintuitive answer to that, I don't think that we need big
• 1:15:59
  progress in human beings. We do need it, of course, as
• 1:16:02
  soon as possible, but I don't think that's what we could be
• 1:16:05
  looking at as our priority. Well, I think we should be
• 1:16:07
  looking at rather counter intuitively, is big progress in
• 1:16:11
  mice. Why the hell would I say that?
• 1:16:14
  The answer is that that's what acknowledged experts care about.
• 1:16:20
  So I'm an acknowledged expert, but I'm only one, OK?
• 1:16:24
  And I am the only one who has the luxury of being able to to
• 1:16:27
  tell it like it is because I lead a nonprofit that's funded
• 1:16:31
  independently by philanthropy. Everybody else, either they work
• 1:16:34
  in industry or they work in academia and they have to, you
• 1:16:37
  know, kiss us all the time. So they can't say things that
• 1:16:44
  can be characterized by others as irresponsible, right, However
• 1:16:50
  much they're not irresponsible. So therefore, what has to happen
• 1:16:54
  is enough progress in the laboratories around the world,
• 1:16:57
  whether it's my laboratory or somebody else's, that the rest
• 1:17:02
  of the expert community feel they have permission to say
• 1:17:06
  publicly the kind of thing that I've been saying for 20 years,
• 1:17:09
  That we're in striking distance of bringing aging under true
• 1:17:12
  medical control. And thus that the time is now
• 1:17:16
  when the world should be putting proper money, proper effort into
• 1:17:21
  hastening that point and saving the most astronomical number of
• 1:17:25
  lives. Literally, we're talking about
• 1:17:26
  40 million lives a year, right? And of course, all the attendant
• 1:17:32
  suffering that's that's associated with, you know,
• 1:17:35
  getting old before you die. Now, how is that going to
• 1:17:39
  happen? Answer is what at the moment we,
• 1:17:43
  if we take mice of the thought that I was talking about
• 1:17:45
  earlier, mice are in middle age, right?
• 1:17:48
  What we do at Mice Foundation and we try to extend their
• 1:17:52
  lives, which is extended by about 30 or 40%.
• 1:17:58
  All right. Now, what does that mean?
• 1:18:00
  What does that mean in actual numbers?
• 1:18:02
  These mice on average live about 2 1/2 years.
• 1:18:05
  And so we start when they're 1 1/2 years old, and the amount
• 1:18:09
  that we can add to that is about four months, All right?
• 1:18:14
  Now, if you ask what could we do 100 years ago, the answer was we
• 1:18:20
  could already get four months. Is that fucking crazy or what
• 1:18:25
  You know? Yeah, that is kind of crazy
• 1:18:27
  actually. You could do it back then.
• 1:18:29
  Right. And that underpins why we, my
• 1:18:34
  colleagues are so hesitant to say, yeah, in the relatively
• 1:18:38
  near future we're going to be able to do a lot better.
• 1:18:41
  I believe we can do a lot better where the divide and conquer,
• 1:18:44
  you know, combinatorial approach, throwing lots of
• 1:18:46
  different damage repair treatments at Meister already
• 1:18:50
  middle-aged before we do anything right.
• 1:18:52
  And that's what we're doing at my foundation.
• 1:18:55
  And I believe that when we get it right, which which I believe
• 1:18:58
  won't take more than another couple of attempts, we will get
• 1:19:03
  a full year of life extension. Now, that means three times the
• 1:19:08
  effect size of what we can do so well, what we can do today,
• 1:19:12
  right? That is the kind of dramatic
• 1:19:15
  transcending of what people have done in the past that will give
• 1:19:19
  my colleagues permission to stand alongside me and say,
• 1:19:23
  listen, Mr. Trump, listen, all the.
• 1:19:26
  Yeah, Mr. Mr. She and everyone around the world, you know, get
• 1:19:31
  the fuck on with it. And it won't be just us saying
• 1:19:34
  that. So the following day Oprah
• 1:19:36
  Winfrey's going to be saying it, and then DeGeneres and all those
• 1:19:38
  people, and the day after that, it will be impossible to get
• 1:19:42
  elected, whoever you are, without having a manifesto
• 1:19:45
  commitment to do it. So that is my focus.
• 1:19:50
  So do you think, I mean, how close do you think you are to
• 1:19:52
  reaching longevity escape velocity for a human that's a
• 1:19:55
  mouse? When do you think it'll actually
• 1:19:57
  be a reality for the human race? Are we on a 10 year timeline?
• 1:20:00
  A 20 year timeline? What do you think?
• 1:20:02
  So that is across the right question, but it comes down to
• 1:20:05
  what I said about MICE. I think we have a 5050 chance of
• 1:20:09
  going to that threshold of one year extension in mice within
• 1:20:12
  three to four years from now, maybe even a couple of years if
• 1:20:15
  we're lucky right now. The question then is assuming
• 1:20:20
  that I'm right about the societal reaction to that, which
• 1:20:24
  is these steps, you know, first of all, the experts start saying
• 1:20:27
  different things, then Oprah Winfrey starts saying different
• 1:20:29
  things, then the government start doing different things,
• 1:20:31
  right? If that's all true, if that's
• 1:20:34
  all true, which I think it's with, I think it's nailed on,
• 1:20:37
  that's nailed on. Then I think we are looking at
• 1:20:43
  about a decade from that point. So in other words, three or four
• 1:20:46
  years from now to get to the mass and then another 10 years
• 1:20:49
  to get to the humans. Now, of course, again, I'm, I'm
• 1:20:52
  emphasizing as I always have to do, but this is all
• 1:20:54
  probabilistic. There's all manner of unforeseen
• 1:20:56
  obstacles that we might encounter because this is
• 1:20:58
  pioneering technology. But who the hell cares?
• 1:21:01
  I mean, I certainly think there's at least a 5% chance
• 1:21:03
  that we won't get to any to, to, to, to, you know, longevity to
• 1:21:07
  the theatre larity for 100 years.
• 1:21:10
  But who the hell cares about that?
• 1:21:12
  A 50% chance is quite enough to be worth fighting for.
• 1:21:16
  No doubt and I'm sure the market obviously would would be would
• 1:21:20
  be obviously their appetite would be voracious.
• 1:21:23
  They would obviously be super excited about the possibility
• 1:21:25
  that what do you think? Obviously AI is on everybody's
• 1:21:28
  mind. Every time I turn around
• 1:21:29
  somebody's asking about the impact of AI and this business
• 1:21:31
  that business or otherwise. What do you think a is role is
• 1:21:35
  in playing to achieve life extension?
• 1:21:36
  I mean, do you think it's in regards to the research and
• 1:21:39
  development and obviously potential therapies, do you
• 1:21:41
  think it's going to be a tool that maybe in the next two or
• 1:21:44
  three years actually can improve those numbers you just gave me
• 1:21:47
  as far as timelines? Yeah, so you always said
• 1:21:49
  obviously twice then. And sure enough, what, what what
• 1:21:52
  you said was much less nonsense. The roadway I is very, very
• 1:21:59
  large indeed. It already is.
• 1:22:01
  You know, I mean, it's no accident that the Nobel Prizes
• 1:22:03
  for physics and chemistry both got awarded to breakthroughs in
• 1:22:07
  AI this year. The breakthrough in chemistry,
• 1:22:11
  the the price in chemistry was given mainly to well, one part
• 1:22:15
  of it was given to Dennis Hassabis, the seminar that we've
• 1:22:18
  been friends with since he was an undergrad.
• 1:22:19
  You know, one of the, you know, probably the single smartest
• 1:22:22
  person I've ever met. And that's a huge statement
• 1:22:24
  because I've met an awful lot of very smart people.
• 1:22:29
  The main thing it was given for was the creation of a program
• 1:22:33
  called Alpha Fold, which is all about predicting the
• 1:22:39
  three-dimensional shape of a protein by from its amino acid
• 1:22:44
  sequence. It's the sequence of these
• 1:22:48
  little units called amino acids that it's built from.
• 1:22:51
  This is a classic problem in biology and nobody had got
• 1:22:56
  anywhere with it for decades and now it's more or less completely
• 1:23:00
  solved. Now, the reason that's so
• 1:23:02
  important is because it means that you can, you can skip a
• 1:23:08
  huge, big step in the development of drugs.
• 1:23:11
  For example, if you want to know how to develop a drug, you want
• 1:23:13
  to know that it fits correctly against a protein.
• 1:23:16
  You know when it interacts with the protein in a particular way.
• 1:23:20
  And the way to do that is to figure out what the shape of the
• 1:23:22
  protein is first and then, you know, design your drug
• 1:23:27
  appropriately. Now you can do that without
• 1:23:29
  figuring out the type of the protein in the test tube.
• 1:23:32
  You can just do it in silica, that it makes an enormous
• 1:23:36
  difference to how rapidly you can develop drugs.
• 1:23:39
  So, you know, you think about when the human genome was
• 1:23:42
  sequenced 20 years ago, what was the utility of that same deal?
• 1:23:46
  Anyone could sequence things before that, but they had to.
• 1:23:50
  It was a very, very laborious process.
• 1:23:52
  Suddenly they didn't need to because they already had the
• 1:23:54
  sequence before they started. And so it's speed up a whole
• 1:23:58
  bunch of biology all over the place.
• 1:24:00
  So this applies to the whole of medical research, not just to
• 1:24:04
  aging. That's fine.
• 1:24:05
  It applies to aging. So, so the rest of medical
• 1:24:09
  research can have it. And we're going to get more and
• 1:24:11
  more of this AI is applicable to many other areas of medical
• 1:24:17
  research. And if it gets better and
• 1:24:20
  better, which it's doing obviously at an insane rate
• 1:24:22
  right now, you know, we will see that over and over again very
• 1:24:25
  quickly. Here's my last question for you,
• 1:24:28
  doc. I'm just wondering, you know,
• 1:24:29
  what are your thoughts on aging as far as an evolutionary
• 1:24:31
  process? Do you think there's a chance
• 1:24:33
  that by extending life we might disrupt biological balances that
• 1:24:37
  we don't necessarily understand as of yet?
• 1:24:39
  Is there anything like that that might have an impact?
• 1:24:43
  So I I think I explained earlier that the reason we age is
• 1:24:46
  because, well, I didn't really explain this properly, so let me
• 1:24:48
  do it from scratch. The reason we age is because
• 1:24:52
  evolution doesn't care enough about old individual.
• 1:24:56
  Evolution cares about the perpetuation of genetic
• 1:24:58
  information. So that means that after an
• 1:25:02
  individual has reached the delta and sexual maturity and has has
• 1:25:05
  had offspring, then evolution doesn't care anymore.
• 1:25:08
  Evolution let's suck individuals age.
• 1:25:11
  This has been known for, you know, many many decades.
• 1:25:14
  It's not controversial at all. This is not me saying this is
• 1:25:17
  just known, right? OK, so then the question is
• 1:25:22
  supposedly we suddenly didn't have aging in humans.
• 1:25:25
  What difference would that make? You can ask that at 2 levels.
• 1:25:28
  You can say, well, OK, what difference would it make to the
• 1:25:32
  global ecology? Well, honestly, we're making
• 1:25:36
  enough impact on the global ecology already.
• 1:25:38
  I don't think that's kind of a thing.
• 1:25:40
  You know it. Might be a quality of life
• 1:25:42
  question right where you might be worried about their quality
• 1:25:44
  of life physically and mentally. So that's what I was going to
• 1:25:47
  come to next. The question is, is evolution in
• 1:25:49
  any sense going to fight back? Is the body going to try and
• 1:25:52
  make us be miserable because we were born a long time ago?
• 1:25:56
  And the answer is absolutely no, because the body is a machine,
• 1:26:00
  just like the car. It's a machine that is
• 1:26:02
  functioned both mental and physical, is determined by its
• 1:26:07
  structure. And what we're doing here is
• 1:26:09
  we're restoring the structure, we're eliminating damage.
• 1:26:13
  Damage is changes to the structure and composition right
• 1:26:16
  at the molecular and cellular level.
• 1:26:17
  So we're restoring the structure and thus we are restoring the
• 1:26:21
  function as well. That's all it's about.
• 1:26:25
  But, you know, it's, it's, it's really important to understand
• 1:26:27
  this. And of course, one can see
• 1:26:29
  things where we have had, you know, complicated interactions
• 1:26:35
  between technology and evolution.
• 1:26:37
  Probably the best one is the immune system.
• 1:26:39
  People have a weaker immune system now than what they did
• 1:26:41
  100 years ago or 200 years ago now.
• 1:26:44
  Why? Because we can, because we've
• 1:26:47
  got medicine now. And so people who had a weak
• 1:26:51
  immune system genetically, you know, used to die before they
• 1:26:55
  could reproduce. Now they don't, so they can
• 1:26:58
  reproduce. And so on average, we have
• 1:27:01
  people with a weaker immune system.
• 1:27:02
  Actually, it's even stronger than that because it turns out
• 1:27:04
  that women with a weaker immune system are more fertile on
• 1:27:07
  account of like, basically they have less risk of rejecting the
• 1:27:10
  fetus. So it's been insanely rapid over
• 1:27:12
  half a dozen generations. We've got a big reduction in
• 1:27:15
  the, but who cares because we do have modern medicine that's not
• 1:27:18
  going to just randomly disappear.
• 1:27:19
  If it did, then we'd be screwed, but it's not going to.
• 1:27:23
  Got you. That's a great answer.
• 1:27:24
  It actually makes a lot of sense.
• 1:27:26
  All right, for the audience. Listen, Doctor Aubrey de Grey,
• 1:27:28
  we really appreciate you joining the show tonight.
• 1:27:30
  Thank you for the information. It's great.
• 1:27:32
  We'll obviously stay on top of it.
• 1:27:33
  Why don't you share with the audience if they would like to
• 1:27:35
  get involved with the Longevity Escape Velocity Project, your
• 1:27:39
  social media or anything else you've got upcoming books or
• 1:27:41
  maybe appearances around the country.
• 1:27:43
  Sure, totally. So first of all, you have kindly
• 1:27:45
  put my foundation's website under my name.
• 1:27:50
  I I assume that the audience can see that the same icon.
• 1:27:52
  Absolutely. In the chat also.
• 1:27:54
  Right, so that's the place to go.
• 1:27:55
  Of course we have links to all our social media on there.
• 1:27:59
  I'm on all the obvious places, LinkedIn, Twitter and so on.
• 1:28:02
  So it's easy to find me. I do a lot of public speaking.
• 1:28:07
  I don't know whether we have yet got a calendar up on on our
• 1:28:13
  website of where in the world Aubrey Degray is going to be.
• 1:28:16
  But honestly, you know, seeing me in podcasts like this, it's
• 1:28:20
  just as good as seeing me in person.
• 1:28:22
  And if for most people, so, you know, looking me up on YouTube
• 1:28:26
  works as well. And I, you know, I thank you for
• 1:28:30
  having me on the show and for giving me exposure to a new
• 1:28:34
  audience that I hope has learnt a bit about where we are in all
• 1:28:39
  of this, why it's so important and how you can help, namely by
• 1:28:44
  supporting this work. I do want to talk a little bit
• 1:28:46
  about support. It's just in my last comment,
• 1:28:49
  please, because you know, a lot of people will say to
• 1:28:52
  themselves, okay, I can't do this.
• 1:28:53
  I'm not well, okay, some of you are biologists.
• 1:28:56
  Hello, you know, choose the right field to go into.
• 1:28:59
  Then there's of course, people are in the media, people like
• 1:29:01
  you. You know, you've done a good,
• 1:29:02
  you've done a good thing here. You've saved a bunch of lives in
• 1:29:05
  the future by just interviewing me a bunch of lives, you know,
• 1:29:10
  Because every day that we bring forward the defeat of aging is
• 1:29:13
  110,000 lives. I mean, that's 30 fucking World
• 1:29:16
  Trade Centres, right? Yeah, there was no doubt, right?
• 1:29:21
  I think our plan always and George and I try to do that as
• 1:29:23
  much as possible as educate and unify the country.
• 1:29:25
  Division and chaos is obviously a tool on the left.
• 1:29:28
  We try to keep it that everybody wants to unify and this
• 1:29:31
  information you're providing when it comes to health, and of
• 1:29:33
  course all of us are aging, it's a big concern.
• 1:29:36
  You know, my wife is actually a competitor.
• 1:29:37
  She's competes in the IFBB Pro. So that aging topic, skin
• 1:29:41
  elasticity, you know, loss of muscle atrophy, those are
• 1:29:45
  discussions that she's regularly engaged in.
• 1:29:47
  She's obviously much more knowledgeable than I am.
• 1:29:49
  But I think the audience is really because we've had a
• 1:29:52
  reaction to the other shows that were like this, that were health
• 1:29:54
  oriented and the reaction's always been over the top, lots
• 1:29:57
  of details. They wanted to get more
• 1:29:58
  information, they wanted to understand more about it.
• 1:30:00
  So I think it's always great. George, you got anything in the
• 1:30:02
  chat? Anything else you want to share
• 1:30:04
  or you good? No, we're good and.
• 1:30:06
  While George is looking, let me just say, you know, it's all
• 1:30:09
  about money. At the end of the day, these
• 1:30:11
  experiments are expensive. Every single experiment that we
• 1:30:13
  do cost 3 or $3,000,000 or more because the the 1000 mice giving
• 1:30:18
  them a lot of different interventions.
• 1:30:21
  So you know, anyone who feels able to contribute, even, you
• 1:30:24
  know, every dollar counts. It's like it's, it makes all the
• 1:30:28
  difference. It really, you know, it's, it's
• 1:30:30
  essential to get these experiments done to figure out
• 1:30:33
  what's going to work and kick off what the, the, the, the
• 1:30:36
  cascade of events that I mentioned earlier, you know, at
• 1:30:39
  the end of the year, people who want to get a tax write off,
• 1:30:41
  obviously we're A5O1C3. So that's an issue.
• 1:30:45
  And we actually currently have a matching campaign going.
• 1:30:50
  One of our donors has given a few $100,000 which will with
• 1:30:55
  which he will double anything that people give so.
• 1:31:00
  That's great. What I'll do Doctor, We'll share
• 1:31:03
  that with our audience. I'll put I'll post it up for
• 1:31:05
  you. I actually saw that matching,
• 1:31:07
  you know, endowment. I didn't know if it was still
• 1:31:09
  going on, but I'll make sure I put that up on my social media.
• 1:31:11
  I want to thank you again, Sir, for joining us.
• 1:31:12
  We really appreciate it. Now tomorrow night we have Josie
• 1:31:14
  Glavich, the red headed Libertarian coming on you guys
• 1:31:17
  like that. She's got a lot to say.
• 1:31:19
  You've seen her over on Tim Poole's show.
• 1:31:20
  She'll be great at the end of the week.
• 1:31:22
  That's it for interviews for this week.
• 1:31:23
  So of course we've got, we've got the Global Finance Forum on
• 1:31:26
  Friday and we should, George, you think 2 weeks away on the
• 1:31:29
  Crypto Power Hour, you think that show will be up?
• 1:31:31
  No 3 weeks. Probably more you.
• 1:31:35
  Think so. OK.
• 1:31:36
  All right, well, I appreciate listening.
• 1:31:37
  Doctor Aubrey. Great.
• 1:31:38
  We really appreciate you joining us tonight.
• 1:31:40
  Thank you so very much for being here and keep up the good work.
• 1:31:43
  God country family, we're out of here.
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• 1:31:53
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  They would run up to the bamboo fence and they would be shooting
• 1:33:58
  between the bamboo at the buildings, you know, just
• 1:34:01
  shooting inside. The Wanted man is Joseph Kony,
• 1:34:05
  charged with abducting huge numbers of children, forcing
• 1:34:08
  them to kill and mutilate innocent victims.
• 1:34:12
  Somebody had to pay the price. Sam did that.
• 1:34:15
  Sam Childers never stopped, because the bad things never
• 1:34:18
  stop. There is only one Sam Childer.
• 1:34:20
  There is no one else like him in the world.
• 1:34:23
  And I said to him, I said. Would you go?
• 1:34:26
  Now to get Kony in the Congo, he says, without a doubt in a
• 1:34:29
  second. Now it's the DRC.
• 1:34:31
  Tell us what's happening to children in the DRC.
• 1:34:33
  Do you have ISIS there? You have Islamic State and you
• 1:34:37
  have ADF? Hey, Sandy.
• 1:34:38
  Joseph Kony's still alive. He's in the Congo, and now God
• 1:34:41
  has me in the Congo, you know, So hopefully we'll meet up one
• 1:34:45
  day, but maybe I can lead him to the Lord or send him there.
• 1:34:50
  One or the other, huh?