Can you imagine a tenured professor at a place like Harvard Medical running
around the world saying, I'm gonna sell you a pill that's a fountain of youth?
You'll grow young? I've been faculty at Hopkins Medical, and
I can tell you, it's extremely competitive. You need to be very very
strong in your science. So as you can see from the headlines in his own statements
Dr. Sinclair is clearly looking for a fountain of youth pill, as this headline
and subtitle says. He hasn't found it yet, but he's sure getting rich, famous, and
having a blast while doing it. And in fact, one of his failed companies and
even though the company failed netted him about 8 million bucks. So again,
he's doing well. And I admit, sure, I can get a little
cheeky. I got it from my grandmother Vera. She was the black sheep of the family,
but she saved lives in World War 2. The one ten years ago that we found which
got a lot of media attention was from red wine.
It's called resveratrol, and don't ask me to say that again. That's a hard word -
resveratrol. And so resveratrol as you probably you probably heard is in red
wine. Now the problem with that is that you'd need to drink about a hundred
glasses of red wine a day. Nope, I don't recommend that, don't do
that. He appeared on Joe Rogan recently, and he
made the statement there's a Jewish blessing "may you live until 120." That's
obsolete. Obviously, it's hyperbole, but I want to make that obsolete. Can we actually
make it an expectation to live to 120? Now let's start let's go back and look
at actually aging in and of itself. Talks about the term whack-a-mole medicine. When
you look at medicine today, you've got cardiologists to look at heart disease,
oncologists to look at cancer, neurologists to look at stroke. Its focus
on one disease at a time. But the reality is let's not take a specific disease and
try to delay that targeted disease. Let's look at the underlying aging process, and
there are aging processes that we can find that are very much associated with
creation of all of these diseases - heart disease, cancer, lung disease, things that
start helping in our 40s, 50s, 60s, and 70s. That's actually called juventude.
Juventude depending on how you want to pronounce it. Dr. Sinclair didn't come up
with that term. Valter Longo, a well- respected gerontology researcher came up
with that. Nir Barzilai, principal investigator of the TAME study (Targeting
Aging with Metformin). Let's deal with the underlying mechanisms of aging, and I use
the term mechanisms in plural because there are six or eight of them that are
very important. Telomeres - as our telomeres get shorter, we age. Stem cell
exhaustion, cellular senescence, that's kind of a technical word. Think of it as
zombie cells. Epigenetic are alterations, and of course, mitochondrial dysfunction
and genomic instability. He actually unseated the mitochondrial
theory of aging. What do you mean unseated? First seventy years, the mitochondrial
theory of aging, this thing, this concept that free radicals burns up the furnaces
of our cell the mitochondria and results in our slow starvation as we age of
their cells of energy, that's been the real key for our aging. Now
all of these mechanisms are active. But again, the mitochondrial
theory was by far the most important. It toasty. He started talking about a thing
called the information theory of aging, and he used the analogy of the demented
concert pianist where you go to a concert, the pianist starts off very well
and then occasionally starts missing a note and then more notes and then more
notes and then pretty soon, it's just chaos. On a cellular basis, that's what's
happening with us. But he's actually found a disease model, a group of people
with a genetic disease called the Werner mutants. Their DNA is just madly
unpacking like a vacuum-sealed bag of yarn that's been ripped open. In fact,
when you look at these kids, they have greatly accelerated premature aging. He
said, you know there's a lot of things we call junk DNA or non-coding. In fact, 69%
of our DNA we've known as non-coding that's where it came up with a term ERC
loop. The senescence cells are zombie cells. Since then, Mayo researchers
have removed these in mice, and the mice live already percent longer. The Mayo
folks have taken his discovery and developed a thing called Sprycel
simply from vegetables, onions, wine, green tea. You may remember the term
quercetin because in the COVID-19, it's become a big deal in terms of being an
for something that helps get zinc across the cell membrane with the
perception that's going to decrease infection from SARS-CoV-2 or the corona
virus. Rapamycin - it was discovered in Rapa Nui Easter islands. You know that
that's what the guys these statues which has created a lot of attention. In fact,
there's another fellow, his name is David Sabatini because of
his work with rapamycin, mTOR, autophaghy - auto meaning the self and phagy meaning to
eat. It's basically where our own cells are using a mechanism to
recycle. In this case in this diagram from the New England Journal, you see
this green damaged mitochondria which is being digested and used for materials
and energy. In fact, it turns out that if we don't have that autophagy going on
quite a bit, that causes us to die early. Now that's
not something that's totally new. Valter Longo has been doing work with that, are
getting a lot of acclaim with the longevity diet, and Prolon fasting
mimicking diet. And we've known for quite a while, fasting is a big deal in terms
of prolonging life. And two of the big guys studying the genetics of aging were
yes Valter Longo and David Sinclair. When you look at it, it's surprising the
overlap that we as humans have with our genetics of aging and a bunch of other
animals that you would think are totally unrelated, ranging from yeast to worms to
fly to rabbits and mice. In fact, there was a professor for a couple of decades
ago, and he created thousands of mutant yeasts. One of them was a yeast called
Saccharomyces cerevisiae. He changed that genetically to where there was a
significant change in aging. Dr. Sinclair, when he came to Boston from the
University of New South Wales, studied at Harvard and MIT. He got this yeast
from Dr. Mortimer and started doing a lot of research on it. It's a form of
Baker's yeast. If you starve that yeast, it doubles its lifespan. If you give a
lot of sugar to that yeast, it ages early and died. It activates genes in there in
the RAS area and PKA, and it inactivates
antioxidant functions. So again, that's where a lot of that basic work was
discovered for these ERC loops. We've gotten more information from studying a
disease model - Werner mutants. There's a lot of other things to learn and think
about, a lot of other science that Sinclair contributed to. For example, he's
brought back mice from blindness to being able to see using epigenetics.
Here's the question: how can somebody that's a tenured Harvard faculty run
around the world saying, I want to sell you a fountain of the youth pill, make
eight million dollars on failed companies, and still stay there at
Harvard? Well, maybe it's because he's tenured, maybe they can't fire him. I don't
think so. I think it's because he's creating really, really good science. So
it's good science. He's just got sort of a snake oil of presentation, and I'm okay
with that. A lot of other people are too. Thank you
for your interest.