Aging, the inevitable process that we all experience, has intrigued scientists for generations. What exactly is aging, and how can we define it on different levels, from the systemic to the cellular? In this blog, we'll explore the various facets of aging, its theories, and one crucial aspect: cellular senescence.

Aging: More Than Just Numbers

When we think about aging, we often consider our chronological age – the number of years since our birth. But deep down, most of us yearn to defy our chronological age, to feel and perform at a level that belies the passing years. This quest introduces us to the concept of biological age, which delves into the health and vitality of our cells. This is measured through DNA methylation tests and similar assessments. Then there's functional age, where we gauge how well our bodies perform compared to our age-matched peers. Are you stronger, faster, with a firmer grip than others your age?

Additionally, there's the concept of felt age, which is all about how old we perceive ourselves to be. Chances are, most of us feel younger than our chronological age. On the flip side, there's perceived age – how old others would guess us to be. The ultimate goal is to have all these ages be younger than our biological age. This not only adds years to our lives but life to our years.

Theories of Aging: Damage vs. Programmed

Scientists have two main camps when it comes to explaining why we age. The first camp believes in damage accumulation as the primary cause. It posits that aging occurs due to the cumulative damage that our cells and mitochondria sustain over time. In essence, aging is the result of this accumulated wear and tear. The solution, according to this theory, is to either eliminate or repair this damage.

The second camp, on the other hand, leans towards programmed aging. This theory views aging as a programmed process, akin to software running on a computer. The program's goal is to get us past our reproductive years, and once that goal is achieved, the program shifts, causing our bodies to deteriorate. Interestingly, there's significant overlap between these two theories, as we'll see in the context of cellular senescence.

Understanding Cellular Senescence

Cellular senescence is a critical concept in the study of aging. To put it simply, think of a cell's life as a journey from birth to death. Just as we experience stress in our lives, cells can also encounter stressors in their environment. Cells respond and adapt to stress on a continuum.

At lower stress levels, cells upregulate their defenses, such as antioxidant systems, to combat oxidative stress. But when stress surpasses a certain threshold, akin to taking damage in a battle, cells shift their focus to repair. Autophagy, the recycling of damaged components within cells, is one way they try to mend the damage.

However, if the stress becomes too overwhelming, a cell enters a state of senescence. This means that the damage has exceeded the point of repair, and the cell is marked for apoptosis, or programmed cell death. Importantly, senescent cells are not allowed to reproduce, preventing the propagation of damaged cells.

The Accumulation of Senescent Cells

As we age, senescent cells accumulate in our tissues and organs. This discovery is relatively recent, with most research emerging in the past decade. The implications of this accumulation are profound. Imagine a plant with healthy green leaves. Over time, due to various stressors like nutrient deficiency or pests, some leaves turn yellow and fall off. This natural process of shedding damaged parts is akin to apoptosis.

However, as we age, senescent cells in our bodies are like those yellowing leaves that refuse to fall off. They continue to consume resources, attract problems, and contribute to a cascade of damage that accelerates aging. Senescent cells, in essence, are the culprits behind the gradual decline in tissue and organ function as we grow older.

What Can We Do?

Understanding cellular senescence offers hope in the quest to age gracefully. While the debate between damage and programmed aging continues, the damage control camp suggests that we can do more to address the accumulation of cellular damage. By promoting healthy lifestyles, managing stress, and potentially harnessing emerging therapies, we can slow down the accumulation of senescent cells and, in turn, extend our healthspan.

In conclusion, aging is a multifaceted process, and cellular senescence is a vital piece of the puzzle. While we may not have all the answers about aging just yet, our growing understanding of senescence paves the way for innovative approaches to healthier aging. In future blog posts, we'll explore practical strategies to promote longevity and vitality by addressing cellular senescence head-on. Stay tuned for more insights into the fascinating world of health and wellness!

In this episode, you'll discover:

• Aging is a complex process with various dimensions, including chronological, biological, functional, felt, and perceived age, each offering insights into how we age.
• Two main theories of aging exist: damage accumulation, where aging results from cumulative cellular damage, and programmed aging, which views aging as a biological program shifting over time.
• Cellular senescence, the state where cells can no longer repair themselves but haven't undergone programmed cell death, plays a crucial role in aging by accumulating in our tissues and organs, contributing to declining health with age. Addressing senescence offers hope for healthier aging.

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Transcription

Dr. Latt Mansor:

What is aging? What's the definition from a systemic level, cellular level, what are the main theories?

Dr. Gregory Kelly

Well, so I think when we think about aging, you know, sometimes you'll see things like, well, like our birth age, right? Chronological age. And I think for all of us, me included, but probably most of the listeners, we want to be younger than that in a sense, right?

We want to perform at a better level. So that's things like now your biological age, which, you know, those would be like the DNA methylation test or other things like that. You'd have functional age, which now you get into, like, you know, how are you function or, you know, like, are you faster, stronger, better grip strength, you name it, than your age dictates.

Perceived age, right? So that's, you know, how old do you feel? And most of us are going to say, oh, younger than our chronological age. Or that's, I'm sorry, that's felt age. And then perceived age would be how old someone, like really a group of people looking at us would guess we are. And, and so the goal for me always is we want all those ideally to be.

You know younger than our biological age and in terms of how then science understands it. There's almost then two camps of like why we age One would be damage accumulation. So everything's lumped into what we age because Damage occurs in ourselves mitochondria and that accumulates and that accumulated damage over time Function and that's what aging is, right?

It's just an accumulation of damage and spinning out of that is the solution is let's, you know, get rid of or repair that damage. The other camp is more about what's called programmed aging and think of it almost like software, like it's designed to get us. Past a certain point so we can reproduce and after that, the things that were advantageous for that are actually programmed to kind of fall apart because we don't need to do that anymore so that the software runs differently as we get older and there's while there's these two camps, there's definitely overlap.

So we're going to talk about cellular senescence. You could make a strong argument. It's Damage control, but it also looks like we build more senescent cells like almost as a program as we get older as well. So it's probably not black and white, no matter what the theory is. It just explains part of it.

And I'm always most attractive. Well, is there something we can do? And the damage control camp seems like there's more we can do currently than trying to change the programming. And

let's explain what is senescence, you know, to, to those who are not familiar with

that term. Senescence has to do with, so think of a cell as just like we, like being born, living its life, and then passing away.

Scientific terms that get tagged with that and the passing away would be apoptosis cellular death and more specifically like a planned cellular death and unplanned one from trauma that would be necrosis, right? So, but what happens in a cell's life or life cycle is that cells can be stressed just like we can be stressed.

And they'll try to respond and adapt to that stress. And I tend to put that on a continuum. So, at a low level of stress, something they can adapt to, you'll see them upregulate things like antioxidant defenses, right? They'll make more glutathione, as an example. But, you know, enzymes like SOD and catalase that help them deal with that oxidative stress.

And no matter what the stress is, oxidative stress is almost invariably a side effect. So bottom line is with the, that modest amount of stress, they'll try to toughen up and defend themselves. And if stress is beyond that, I go back again to like when I was in the Navy, right? You're going to take some damage, like you're, you're hit with something and you're going to try to clean up the damage, right?

So in the Navy we would have Like a damage control party, right? That was their job. Like, go to wherever the damage is and repair. And something like autophagy would be in that, right? Which is, autophagy is specifically recycling of damaged proteins, organelles, things inside a cell, to try to reuse those things and repair the damage.

But if stress is beyond that, then a cell can become a senescence. And what that means is, the damage is beyond where it can be repaired. And so the cell's kind of targeted to go through apoptosis. And once that happens, it's not allowed to make new copies of itself, because we don't want to reproduce damaged cells.

So senescence would be that middle ground between, okay, there's beyond what I can repair, but I haven't gone through apoptosis. I haven't passed away yet. And so a senescent cell, by definition, is that and why that's important is these senescent cells accumulate in our tissues and organs as we get older, which is relatively new ish science, meaning, you know, goes back 20 years or less, but then the contribution to how that I guess causes our tissues to perform poorly as we age.

That's really still exploding. Like, I would say most of the science on that's been within the last 8 to 10 years. So just in a simple thing, sense of, like, the analogy we'll often use at NeuroHacker is think of a plant. You know, young, healthy plant, all the leaves, green, plant is thriving. But, you know, maybe because of nutritional stress or not enough water or pests in the environment.

Some stressor, you know, now one or two of the leaves starts to turn yellow. Ideally, that leaf will just fall off, right? And apoptosis, that word we use, that comes from a Greek word that literally translates as falling off, right? It means the same thing. It's this idea of, oh, the cell's not healthy. It's done its job.

It falls off. What happens as we age is those yellow leaves, more and more of them pop out on the plant. And once a plant gets to a certain amount of yellow leaves, it will struggle to stay alive, right? To do its job because the yellow leaves are still sucking resources, right? They're still using nutrients.

They're attracting now pests and other things from the environment to cause almost an accelerating cascade of damage. So think of senescent cells as the equivalent. It's these yellowing leaves, equivalent in our tissues, that are just growing and spreading more and more as we age.

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