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 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.

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 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.

And then it turns.

And then it turns.

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 the Heyflick limit.

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 the Heyflick limit.

So this is where your.

So this is where your.

Cells will stop dividing but actually remain metabolically active and they kind of become a little bit.

Cells will stop dividing but actually remain metabolically active and they kind of become a little bit.

Like zombie cells. So there's some.

Like zombie cells. So there's some.

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, 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, 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 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. 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 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 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 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 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.

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, 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, 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 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. 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 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 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 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 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.

As we get older, they.

As we get older, they.

Can create a pro inflammatory environment that supports the growth of.

Can create a pro inflammatory environment that supports the growth of.

These pre malignant cancer cells.

These pre malignant cancer cells.

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.

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.

So what do we actually do about it?

So what do we actually do about it?

Well, it turns out there are quite a few things that we can do to mitigate the impact.

Well, it turns out there are quite a few things that we can do to mitigate the impact.

Of cellular senescence.

Of cellular senescence.

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 activates the enzyme telomerase, which can actually help to preserve our telomeres, and that means.

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 activates the enzyme telomerase, which can actually help to preserve our telomeres, and that means.

That you reduce your cellular aging.

That you reduce your cellular aging.

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 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.

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 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.

So the second way.

So the second way.

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 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.

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 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.

In humans, just to be a war.

In humans, just to be a war.

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 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 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, 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 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 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 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 and molecules that are designed to selectively eliminate senescence cells and therefore mitigating their detrimental effects on the surrounding tissues and minimizing aging.

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 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 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, 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 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 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 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 and molecules that are designed to selectively eliminate senescence cells and therefore mitigating their detrimental effects on the surrounding tissues and minimizing aging.

And there's a.

And there's a.

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 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 pulmonary fibrosis.

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 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 pulmonary fibrosis.

Right.

Right.

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 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, 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 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. 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 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?

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 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, 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 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. 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 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?

So I think it's going to be a number of years before we know.

So I think it's going to be a number of years before we know.

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.

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.

Sales start to accumulate.

Sales start to accumulate.

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.

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.