December 14, 2019
Zombie Cells (David Sinclair Book LIFESPAN – Part 8)

Zombie Cells (David Sinclair Book LIFESPAN – Part 8)

You thought zombie cells would be in a
bad movie or an overly popular zombie apocalypse TV show, right? It sounds
like that, but actually zombie cells have been
around since the 60s. They’d been around forever. They’re a major part of aging. We
just didn’t know about it until the 60s. They’re not that new. They’re also called
senescence cells or senescent cells. So I will talk about those in just a minute,
where they are, what are they, who’s doing work on them, guys that may have been
doing a lot of work on them. They’ve actually got a medication for them, but
it’s not quite ready for primetime at least in terms of prevention. And we’ll
talk about why in just a minute. But before we do, just a brief
introduction to the series. This is part 8 of a series on “Lifespan” by David
Sinclair. David Sinclair is a PhD researcher at Harvard in aging. He’s been
into aging for a very very long time, and he covers a lot of the things in his
book, his new book “Lifespan” that I cover in my channel. So I’ve been having a
blast doing this series, and I hope you’ve enjoyed it as well. He goes into a
lot of the basics and talks about his own theory of aging – the information
theory – where basically we begin to lose our epigenetic functions, our ability
to access information that’s still within our DNA, the same DNA that we
had in our 20s. But for some reason, we just can’t access it as well. He also
talks in the book this image right here is from his book. It’s the hallmarks of
aging. And again we mentioned many of these things in the channel. He discusses
them in the book; for example deregulated nutrient sensing, altered intercellular
communications, loss of proteostasis, stem cell exhaustion, mitochondrial
dysfunction, epigenetic alteration. Again, that’s really deep in terms. That’s
probably the most popular theory right now, and it’s a very much related to his
information theory, genomic instability, and of course cellular senescence. We’re
going to talk about cellular senescence now in this video. This
prescription drug bottle that you see called Sprycel is dasatinib. It’s
was developed by folks in Mayo but I’m getting ahead of myself again. Let’s go
back and talk about the history and a little bit more about what they what we
know about it, what we’ve seen in terms of senescence cells. They were discovered
in 1961. Macrophages are more commonly noticed and dirtied asthma as senescence
cells but you can see it in tissue to multiple tissue types. The cell actually
shuts down its processes like epigenetics. Some people say it’s like a
grumpy retiree cell. Now what this cell does is it protects protects it from DNA
damage so therefore there is actually… some theorize purpose to these
senescence cells shutting down your epigenetics will protect yourself from
cancer. So that appears to be one of the functions of senescence cells. Another
function appears to have to do with healing. On the other hand though, this is
an inflammatory process. It sends out cytokines. And you may remember cytokines
are… “cyto” meaning cell, “kines” meaning attractants. So it attracts immune cells
to come to this area and start creating inflammation. That’s what immune cells do.
So it recruits other cells in terms of this grumpy retiree process as well. Now
Sinclair described the blue galactosidase stain in these zombie
cells. Mayo researchers remove these cells in
mice, and the mice lived 30% longer. And again, they removed them with a couple of
different methods. One of them dacatnib an immunoglobulin plus quercetin which
is a chemical from onions, wine, green tea. And that medication now is used for
leukemias. It’s again a more of a heavy-duty medication. And I think
anybody’s going to want to take it for or by prolonging life. Now do I supplement?
No, obviously, I don’t, clearly don’t try to supplement this myself. But I do a
couple of other things. I do fasting. I do extended water fasts in 2 days every
week. This is a Tuesday, by the way, when I’m recording this, so on my second day
of an extended water fasts. I also have… I would say maybe 3 to 5 glasses of
wine per week, have onions, garlic, green tea. So I do think I’d get my quercetins
naturally. I don’t take to get dacatnib, as I said. Now just back to one
overall statement. Remember, it’s cellular aging, not organ
related disease or “juventude” as Valter Longo put it in his book “The
Longevity Diet.” So again, medicines arranged wrong. We
don’t need to be folk spending years and years focusing on a heart, years and
years focusing on the brain, and ever look at the rest of the body. Because
these diseases don’t start from the heart or the brain. They start in the
cell. They start by in biochemistry. We need much more of a metabolic focus on
disease and prevention and longevity. Thank you very much for your interest.
This is Ford Brewer. I started off my career as an ER doc. And that can be frustrating
because most of the things bringing patients into the ER can and should be
prevented like heart attack and stroke. So I went to Johns Hopkins for training
in prevention, did well, ended up running the program, trained dozens of docs there
and have trained hundreds and even over a thousand doctors since then in
preventing disease. What’s even more important is I’ve helped thousands of
patients prevent heart attack and stroke rather than waiting for the devastation
and hoping for a cure.

9 thoughts on “Zombie Cells (David Sinclair Book LIFESPAN – Part 8)

  1. Excellent commentary regarding Dr. Sinclairs new book. Your summary helps tremendously to explain and expand upon very important new findings. It's much appreciated. There's so much new information in this field (and most every other science and technology) that I believe that the "palatable distribution" is a service that's both crucial and increasingly valuable.

  2. If your posts had a theme song I'd select Staying Alive by the BeeGees. I'm now doing my monthly 60-72 hour fast using electrolytes, boron and minerals, splash of salt water, coffee black sweetened with Monk fuit drops, berberine, desiccated offal powder, two 1 mile jogs followed by two HIT sprints. Started Sunday 1PM will have lunch tomorrow 10 oz Pacific cod 100 G protein, with 8oz bone broth flavored by chicken bullion, then reintroduce all my oil soluble vitamin regimen as I eat lunch.

    Since zombie cells seem to have a good purpose in the war against cancer, I winder if there is a hierarchy our immune systems challenge — which struggling sickly cell they recycle first or with priority when we're fasting for longevity— Thinking–maybe having SOME zombie cells is a good stressor.

  3. I recall reading about Quercetin back in 2007. I believe also in apple skin. There are only so many things you can do really. HIT a few times a week, Vitamin C liposimal if you make it yourself, K2, Keto. K2 & C will help keep your tissues, bones and vascular healthy, Keto keep inflammation under control, and HIT activates a bunch of protective processes. I did see a science program a few years back where old people doing regular HIT developed 'backside tissue quality' that was similar to those 30 years younger. It also seems that Vitamin C and also K2 have a whole bunch of functions more than we talk about. I note that they are now looking at IV C as an pain reliever as well now, which is certainly the better option to opiods.

  4. Would like to hear David Sinclair's take on fellow NAD coenzyme researcher Charles Brenner, who is a bit critical of supplementing with NAD precursors (NAM/NMN/NA) except for NR (Tru Niagen). Charles also mentions that pterostilbene is a more bio-available form of resveratrol, yet that appears to raise LDL in humans, so he is skeptical about these compounds.

    I'd also love to hear a discussion between evolutionary biologist Michael Rose and David.. Michael suggests it's hundreds of genes that become maladaptive as you age.. and doesn't believe the techniques to manipulate some pathway (ex. AMPK/MTOR/NAD via CR mimetics) will work on humans. Incidentally, Steven Austad , Keith Baar and Aubrey de Grey have also expressed reasons why Caloric-Restriction does not have much lifespan effect in humans.

    BTW, looking forward to David's friendly bet with Geoffrey Woo, that suggests changing gene expression of unhealthy cells, causes it mimic adjacent healthy cells.. while David I believe says that each cell has an original dna 'observer' copy that just needs to be activated.

Leave a Reply

Your email address will not be published. Required fields are marked *