March 11, 2025 • 13 mins
In this week's podcast on anti-aging strategies, I explore cellular senescence - what it is, how it's useful when we're young but promotes poor health when we age, and some things we can do to mitigate it.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:09):
Hey, everybody, welcome to another edition of Wisdom Wednesdays, and
welcome back to the Anti aging series. We are not
on number nine out of twelve and today we are
going to talk about cellular sinescence. So sinessnce is linked
to cell division, and there's very few sales in your
(00:30):
body that you're actually born with. And what we know
about ourselves is that they basically they commit suicide process
called apoptosis, but before they do that, they actually divide.
Speaker 2 (00:45):
And then it turns.
Speaker 1 (00:46):
Out that there is a limit to how often our
sales can actually divide. And this was first observed by
a guy called Leonard Hayflick in nineteen sixty five and
he showed that norman normal sorry human cells have a
limited capacity to proliferate or divide, and it was called
(01:07):
the Heyflick limit.
Speaker 2 (01:09):
So this is where your.
Speaker 1 (01:11):
Cells will stop dividing but actually remain metabolically active and
they kind of become a little bit.
Speaker 2 (01:19):
Like zombie cells. So there's some.
Speaker 1 (01:22):
Characteristics of sinescence cells. So the first is what we
call cell cycle arrest. This is where the sinescent cell
exit the sales cycle and they no longer divide, and
then you have something called sinescence associated secretory phenotype or SASP,
and that means that they secrete pro inflammatory cider kinds,
(01:46):
these messenger molecules that basically spread inflammation, and they secreate
growth factors and things called proteases that actually alter the
tissue macro environment and have a negative effect on surrounding cells.
And then there's this resistance to apoptosis that I talked about.
So that's where the sinescence cells resist program cell death,
(02:11):
leading to their accumulation over time, and that's when they
create a bit of molecular mayhem. So if you've ever
seen Game of Thrones, they're kind of like the White
Walkers in the body and we really don't want these.
So what happens, I'm how do we trigger this cellular sinescence. Well,
I've talked about teleomeres previously. Think of them like the
(02:34):
little caps on the end of your shoelases. And each
time the cell divides, that leads to progressive shortening of
the telomeres, these protective caps at the end of our chromosomes.
And when those telomeres become critically short, they trigger a
DNA damage response, which can often lead to sinescence. And
we talked about telomeres being one of the hallmarks of aging.
(02:58):
And then we have this DNA damage, so we know
exposure to things like oxidative stress, radiation, chemotherapy, they can
all cause DNA damage which can induce senescence. And we
get oxidive stress from lots of poor lifestyle choices as well.
And then we have something called oncle gene activation, so
(03:20):
you probably have heard of oncle genes, and the abnormal
activation of onco genes can induce senescence as a protective
mechanism against tumorogenesis or the creation of cancer. So it
can actually be protective when we're young, this senescence to
stop these uncle genes forming a big tumor. But as
(03:43):
we age, senescence and turns into a bad thing. So
it has this dual role. So as I said, the
beneficial affects tumor suppression by halting the proliferation of damage celles.
Senescence acts as a barrier against cancer development. And it's
also important in wound healing, So sinessin cells can promote
(04:04):
tissue repair by secreting factors that modulate the immune response
and facilitate regeneration. So that's the good part of senessen
So it's a natural process in the body. But the
detrimental aspects of sinessens are when we age and we
have this tissue dysfunction, and this accumulation of sinescence cells
(04:26):
contributes to this tissue dysfunction, chronic inflammation, and progression of
age related diseases. And then it can when we get older,
promote tumorogenesis. So these SASP cells I talked about them
a little bit earlier on those sinescence associated secretory phenotype.
Speaker 2 (04:48):
As we get older, they.
Speaker 1 (04:50):
Can create a pro inflammatory environment that supports the growth of.
Speaker 2 (04:55):
These pre malignant cancer cells.
Speaker 1 (04:58):
So, in summary, sestin can be a good thing when
we're young. It stops cancer developing, it helps with wound
healing as well, but as we age it can create
dysfunction and can then promote the growth of cancer.
Speaker 2 (05:11):
So what do we actually do about it?
Speaker 1 (05:13):
Well, it turns out there are quite a few things
that we can do to mitigate the impact.
Speaker 2 (05:18):
Of cellular senescence.
Speaker 1 (05:20):
And the first thing no prizes for guessing this is
regular physical activity and it has been shown to reduce
markers of cellular senescence and promote healthy aging. One of
the ways that it does this is by teleomere preservation.
Regular physical activities associated with longer telomeres, and it actually
(05:41):
activates the enzyme telomerase, which can actually help to preserve
our telomeres, and that means.
Speaker 2 (05:49):
That you reduce your cellular aging.
Speaker 1 (05:51):
And then the second way by which exercise is useful
is reduction of sinescence cells. So it's been shown that
exercise can decrease the accumulation of sinescence cells, thereby improving
tissue function. And this can actually be improved by exercising
in the fasted state increases a tophogy and that clean
(06:15):
up within muscle sales and it can remove those sinescence cells.
And there's a study published in Preventative Medicine that found
that individuals who engage in regular running had longer telomeres
that equated to approximately nine years of reduced biological aging
compared to sedentary counterparts.
Speaker 2 (06:35):
So the second way.
Speaker 1 (06:36):
That we can do it is around diet, because diet
plays a critical role in modulating cellular senescence. And we
know that calorie restriction either long term calorie restriction. I've
talked about the pros and cons of that before, or
intermittent fasting, and that's actually been linked to the delayed
(06:57):
onset of cellular senescence, and it's been owned in various
different organisms that it can extend their lifespan, but that
hasn't been replicated.
Speaker 2 (07:05):
In humans, just to be a war.
Speaker 1 (07:06):
But then eating anti inflammatory foods. We know that foods
such as amiga three fatty acids are highly anti inflammatory,
and also foods that are rich in antioxidants and things
like extra virgin olive oil. They can all mitigate oxidative
stress and therefore reduce senescence. And there was a study
(07:29):
that showed that individuals who consumed a diet that was
anti inflammatory with lots of amiga three fatty acids, fruits, vegetables,
these sorts of things had reduced risk of chronic diseases
that were associated with sinescence. Then the third thing is
around stress management. And so I've talked before about the
(07:51):
impact of stress at a cellular level, and it's been
shown that elevated stress levels are associated with accelerated TeleMe
tell me or sorry shortening, leading to increased cellular senescence
and inflammation. So stress causes inflammation at a cellular level,
(08:11):
and that promotes the onset of sinessence in various cell types.
So making sure that you are using effective stress management techniques,
trying to avoid things that are highly stressful, and then
using things like exercise, meditation, and those sorts of things,
having hobbies, those can actually then slow telling me are
(08:36):
shortening and reduce hallmarks of aging. And what I mean
by that is overall stress management techniques have been shown
to do that. And then the fourth thing you'll not
be surprised to hear is about quality sleep. Because when
you're asleep, your DNA repair mechanisms kicking right, and that
reduces the likelihood of damage induced sinescence. As so, if
(08:59):
we're having poor sleep, we're not repairing our DNA and
therefore you're more likely to get senescence. And sleep is
also important for hormone regulation, things like melatonin and other hormones,
and melatonin actually has antioxidant properties that actually protects against
cellular damage. So making sure that we have quality sleep
(09:20):
because the studies have shown that individuals with poor sleep
quality or shorter sleep exhibit shorter telomeres and have higher
levels of cellular senescence markers. Now there's one other thing
that is emerging at the minute, and that is these
therapeutics called senalytics. So snalytics are a class of drugs
(09:44):
and molecules that are designed to selectively eliminate senescence cells
and therefore mitigating their detrimental effects on the surrounding tissues
and minimizing aging.
Speaker 2 (09:58):
And there's a.
Speaker 1 (09:58):
Number of and potential senalytic e agents that are actually
being looked at at the minute. One is cursed curstin
q u e r c E t i n and
dasatinib d A s A t I n i B.
That's a bit of a mouthful to try saying that
(10:20):
after a few drinks, dacatinib and cursotin. Now that combination
has actually been shown to clear sinescent cells in pre
clinical studies and actually improve physical function in aged mice
and humans, and early human trials suggest that there are
potential benefits for individuals with things like osteoarthritis and idiopathic
(10:45):
pulmonary fibrosis.
Speaker 2 (10:46):
Right.
Speaker 1 (10:47):
Then, another molecule called phisotin. This is a flavonoid that's
found in things like strawberries, apples, onions, and it has
actually got demonstrated s analytic activity in lots of animal
studies and improves the health span and reduces markers of sinescence.
And then there's a drug called navital clax and that
(11:12):
was originally developed as a cancer drug, but it's actually
been shown to induce apoptosis or program cell death in
sinescence cells. But there are a number of side effects
that actually remain their concerned. So there's actually quite a
few human trials that are going on right now. I
wouldn't be dashing out and buying dasatinib and curstin or fystin,
(11:35):
although I do have my eye on these things. But
the Male Clinic is actually doing some synolytic trials and
looking at dacatinib and cursotin in older adults to evaluate
its effects on physical function and inflammatory markers and chronic diseases.
And then Unity Biotechnology is actually conducting some clinical trials
(12:00):
on senalytic drugs for osteoarthritis, age related macular degeneration, and
neurodegenerative diseases. And then there's there's there's quite a big
study going on called the Team Study, and that is
targeting aging with met form and t a m UH
and a low met form. It is not a senalytic.
(12:22):
This big study is investigating whether met forming, which is
an anti diabetic drugs some people may have heard of,
whether or not it can slow the aging process, and
one of the things that they're looking at is its
impact on cellular senescence. So, although I actually think that
some of these snalytics hold great promise, more research is
(12:44):
needed before I part with my hard earned cash on
those and I do want to see the studies showing
their long term safety and their effectiveness, and then critically,
what doos do we actually need in humans?
Speaker 2 (12:57):
So I think it's going to be a number of
years before we know.
Speaker 1 (13:00):
The answers to all those questions. But in summing up,
cellular sinessence is a double edged sword. It protects against
cancer and use, but it also contributes to inflammation, tissue dysfunction,
and aging as those sinescence.
Speaker 2 (13:16):
Sales start to accumulate.
Speaker 1 (13:18):
But fortunately we know that regular exercise and nutrient rich
anti inflammatory diet, stress management and quality sleep, and potentially
synolytic therapies can all help to mitigate the negative effects
of cellular sinessence and promote healthy aging. That's it for
this week, folks, Catch you next time.
Hey, everybody, welcome to another edition of Wisdom Wednesdays, and
welcome back to the Anti aging series. We are not
on number nine out of twelve and today we are
going to talk about cellular sinescence. So sinessnce is linked
to cell division, and there's very few sales in your
(00:30):
body that you're actually born with. And what we know
about ourselves is that they basically they commit suicide process
called apoptosis, but before they do that, they actually divide.
Speaker 2 (00:45):
And then it turns.
Speaker 1 (00:46):
Out that there is a limit to how often our
sales can actually divide. And this was first observed by
a guy called Leonard Hayflick in nineteen sixty five and
he showed that norman normal sorry human cells have a
limited capacity to proliferate or divide, and it was called
(01:07):
the Heyflick limit.
Speaker 2 (01:09):
So this is where your.
Speaker 1 (01:11):
Cells will stop dividing but actually remain metabolically active and
they kind of become a little bit.
Speaker 2 (01:19):
Like zombie cells. So there's some.
Speaker 1 (01:22):
Characteristics of sinescence cells. So the first is what we
call cell cycle arrest. This is where the sinescent cell
exit the sales cycle and they no longer divide, and
then you have something called sinescence associated secretory phenotype or SASP,
and that means that they secrete pro inflammatory cider kinds,
(01:46):
these messenger molecules that basically spread inflammation, and they secreate
growth factors and things called proteases that actually alter the
tissue macro environment and have a negative effect on surrounding cells.
And then there's this resistance to apoptosis that I talked about.
So that's where the sinescence cells resist program cell death,
(02:11):
leading to their accumulation over time, and that's when they
create a bit of molecular mayhem. So if you've ever
seen Game of Thrones, they're kind of like the White
Walkers in the body and we really don't want these.
So what happens, I'm how do we trigger this cellular sinescence. Well,
I've talked about teleomeres previously. Think of them like the
(02:34):
little caps on the end of your shoelases. And each
time the cell divides, that leads to progressive shortening of
the telomeres, these protective caps at the end of our chromosomes.
And when those telomeres become critically short, they trigger a
DNA damage response, which can often lead to sinescence. And
we talked about telomeres being one of the hallmarks of aging.
(02:58):
And then we have this DNA damage, so we know
exposure to things like oxidative stress, radiation, chemotherapy, they can
all cause DNA damage which can induce senescence. And we
get oxidive stress from lots of poor lifestyle choices as well.
And then we have something called oncle gene activation, so
(03:20):
you probably have heard of oncle genes, and the abnormal
activation of onco genes can induce senescence as a protective
mechanism against tumorogenesis or the creation of cancer. So it
can actually be protective when we're young, this senescence to
stop these uncle genes forming a big tumor. But as
(03:43):
we age, senescence and turns into a bad thing. So
it has this dual role. So as I said, the
beneficial affects tumor suppression by halting the proliferation of damage celles.
Senescence acts as a barrier against cancer development. And it's
also important in wound healing, So sinessin cells can promote
(04:04):
tissue repair by secreting factors that modulate the immune response
and facilitate regeneration. So that's the good part of senessen
So it's a natural process in the body. But the
detrimental aspects of sinessens are when we age and we
have this tissue dysfunction, and this accumulation of sinescence cells
(04:26):
contributes to this tissue dysfunction, chronic inflammation, and progression of
age related diseases. And then it can when we get older,
promote tumorogenesis. So these SASP cells I talked about them
a little bit earlier on those sinescence associated secretory phenotype.
Speaker 2 (04:48):
As we get older, they.
Speaker 1 (04:50):
Can create a pro inflammatory environment that supports the growth of.
Speaker 2 (04:55):
These pre malignant cancer cells.
Speaker 1 (04:58):
So, in summary, sestin can be a good thing when
we're young. It stops cancer developing, it helps with wound
healing as well, but as we age it can create
dysfunction and can then promote the growth of cancer.
Speaker 2 (05:11):
So what do we actually do about it?
Speaker 1 (05:13):
Well, it turns out there are quite a few things
that we can do to mitigate the impact.
Speaker 2 (05:18):
Of cellular senescence.
Speaker 1 (05:20):
And the first thing no prizes for guessing this is
regular physical activity and it has been shown to reduce
markers of cellular senescence and promote healthy aging. One of
the ways that it does this is by teleomere preservation.
Regular physical activities associated with longer telomeres, and it actually
(05:41):
activates the enzyme telomerase, which can actually help to preserve
our telomeres, and that means.
Speaker 2 (05:49):
That you reduce your cellular aging.
Speaker 1 (05:51):
And then the second way by which exercise is useful
is reduction of sinescence cells. So it's been shown that
exercise can decrease the accumulation of sinescence cells, thereby improving
tissue function. And this can actually be improved by exercising
in the fasted state increases a tophogy and that clean
(06:15):
up within muscle sales and it can remove those sinescence cells.
And there's a study published in Preventative Medicine that found
that individuals who engage in regular running had longer telomeres
that equated to approximately nine years of reduced biological aging
compared to sedentary counterparts.
Speaker 2 (06:35):
So the second way.
Speaker 1 (06:36):
That we can do it is around diet, because diet
plays a critical role in modulating cellular senescence. And we
know that calorie restriction either long term calorie restriction. I've
talked about the pros and cons of that before, or
intermittent fasting, and that's actually been linked to the delayed
(06:57):
onset of cellular senescence, and it's been owned in various
different organisms that it can extend their lifespan, but that
hasn't been replicated.
Speaker 2 (07:05):
In humans, just to be a war.
Speaker 1 (07:06):
But then eating anti inflammatory foods. We know that foods
such as amiga three fatty acids are highly anti inflammatory,
and also foods that are rich in antioxidants and things
like extra virgin olive oil. They can all mitigate oxidative
stress and therefore reduce senescence. And there was a study
(07:29):
that showed that individuals who consumed a diet that was
anti inflammatory with lots of amiga three fatty acids, fruits, vegetables,
these sorts of things had reduced risk of chronic diseases
that were associated with sinescence. Then the third thing is
around stress management. And so I've talked before about the
(07:51):
impact of stress at a cellular level, and it's been
shown that elevated stress levels are associated with accelerated TeleMe
tell me or sorry shortening, leading to increased cellular senescence
and inflammation. So stress causes inflammation at a cellular level,
(08:11):
and that promotes the onset of sinessence in various cell types.
So making sure that you are using effective stress management techniques,
trying to avoid things that are highly stressful, and then
using things like exercise, meditation, and those sorts of things,
having hobbies, those can actually then slow telling me are
(08:36):
shortening and reduce hallmarks of aging. And what I mean
by that is overall stress management techniques have been shown
to do that. And then the fourth thing you'll not
be surprised to hear is about quality sleep. Because when
you're asleep, your DNA repair mechanisms kicking right, and that
reduces the likelihood of damage induced sinescence. As so, if
(08:59):
we're having poor sleep, we're not repairing our DNA and
therefore you're more likely to get senescence. And sleep is
also important for hormone regulation, things like melatonin and other hormones,
and melatonin actually has antioxidant properties that actually protects against
cellular damage. So making sure that we have quality sleep
(09:20):
because the studies have shown that individuals with poor sleep
quality or shorter sleep exhibit shorter telomeres and have higher
levels of cellular senescence markers. Now there's one other thing
that is emerging at the minute, and that is these
therapeutics called senalytics. So snalytics are a class of drugs
(09:44):
and molecules that are designed to selectively eliminate senescence cells
and therefore mitigating their detrimental effects on the surrounding tissues
and minimizing aging.
Speaker 2 (09:58):
And there's a.
Speaker 1 (09:58):
Number of and potential senalytic e agents that are actually
being looked at at the minute. One is cursed curstin
q u e r c E t i n and
dasatinib d A s A t I n i B.
That's a bit of a mouthful to try saying that
(10:20):
after a few drinks, dacatinib and cursotin. Now that combination
has actually been shown to clear sinescent cells in pre
clinical studies and actually improve physical function in aged mice
and humans, and early human trials suggest that there are
potential benefits for individuals with things like osteoarthritis and idiopathic
(10:45):
pulmonary fibrosis.
Speaker 2 (10:46):
Right.
Speaker 1 (10:47):
Then, another molecule called phisotin. This is a flavonoid that's
found in things like strawberries, apples, onions, and it has
actually got demonstrated s analytic activity in lots of animal
studies and improves the health span and reduces markers of sinescence.
And then there's a drug called navital clax and that
(11:12):
was originally developed as a cancer drug, but it's actually
been shown to induce apoptosis or program cell death in
sinescence cells. But there are a number of side effects
that actually remain their concerned. So there's actually quite a
few human trials that are going on right now. I
wouldn't be dashing out and buying dasatinib and curstin or fystin,
(11:35):
although I do have my eye on these things. But
the Male Clinic is actually doing some synolytic trials and
looking at dacatinib and cursotin in older adults to evaluate
its effects on physical function and inflammatory markers and chronic diseases.
And then Unity Biotechnology is actually conducting some clinical trials
(12:00):
on senalytic drugs for osteoarthritis, age related macular degeneration, and
neurodegenerative diseases. And then there's there's there's quite a big
study going on called the Team Study, and that is
targeting aging with met form and t a m UH
and a low met form. It is not a senalytic.
(12:22):
This big study is investigating whether met forming, which is
an anti diabetic drugs some people may have heard of,
whether or not it can slow the aging process, and
one of the things that they're looking at is its
impact on cellular senescence. So, although I actually think that
some of these snalytics hold great promise, more research is
(12:44):
needed before I part with my hard earned cash on
those and I do want to see the studies showing
their long term safety and their effectiveness, and then critically,
what doos do we actually need in humans?
Speaker 2 (12:57):
So I think it's going to be a number of
years before we know.
Speaker 1 (13:00):
The answers to all those questions. But in summing up,
cellular sinessence is a double edged sword. It protects against
cancer and use, but it also contributes to inflammation, tissue dysfunction,
and aging as those sinescence.
Speaker 2 (13:16):
Sales start to accumulate.
Speaker 1 (13:18):
But fortunately we know that regular exercise and nutrient rich
anti inflammatory diet, stress management and quality sleep, and potentially
synolytic therapies can all help to mitigate the negative effects
of cellular sinessence and promote healthy aging. That's it for
this week, folks, Catch you next time.
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