Dr. Paul Robbins of the University of Minnesota joins us to examine the science of healthy aging and the practical choices that support a longer health span, including regular physical activity, nutritious food, restorative sleep, and maintaining social connection.
Transcript:
Jeffrey Snyder, Broadcast Retirement Network
Well, Paul, it’s great to see you. Thanks for popping by the program this morning.
Dr. Paul Robbins, University of Minnesota
Yeah, thanks, Jeff. I’m very pleased to be here.
Jeffrey Snyder, Broadcast Retirement Network
And we’re going to talk about aging and all the research that you and the team are doing at the University of Minnesota. Before we get into that, let’s talk about, you know, we’re coming to the end of September, but September, I think, is aging month or better aging month. What does that mean to you as a professional, as somebody who is conducting research?
That must be an important month in your calendar.
Dr. Paul Robbins, University of Minnesota
It is, although I think about aging every month. And, you know, it just means we have to, you know, take time to stop to think about what we could do differently in our lives that might help us age a little bit better, kind of extend that period of healthy aging, delay the onset of the next comorbidity. And at this point, you know, we’re talking about exercise, diet, sleep, just simple things that we can all do a little bit better at.
Jeffrey Snyder, Broadcast Retirement Network
So go ahead and finish your thought, doctor.
Dr. Paul Robbins, University of Minnesota
No. Although, you know, for some of us, exercise is difficult. For some of us, diet is hard to manage.
So we are working towards developing ways that we might be able to actually develop drugs or biologics that can extend the period of healthy aging. So you don’t necessarily have to rely on diet, exercise, and sleep as the only effective treatments for extending health span.
Jeffrey Snyder, Broadcast Retirement Network
And my apologies for interrupting you, Paul. As a follow-up to that, it seems like just based on, you know, obviously folks in your industry, not only within the team at University of Minnesota, but across the spectrum, you’re doing a lot of research in this area, but it seems like, and I don’t want to get ahead of you, that there’s a lot that we can control outside of the biologics and the medicines that you were just talking about.
Dr. Paul Robbins, University of Minnesota
Absolutely. As I’ve said, you know, I think there’s a lot of information suggesting reducing caloric intake a little bit, or at least eating healthier, reducing excessive amounts of protein and carbohydrates, exercising a certain amount of time every week. And what is always undervalued is sleep.
We really need a certain amount of sleep. Although Jeff, you may need eight hours. I might need 10 or somebody needs three, but sleep is valuable because it kind of allows us to reset our clock and kind of cleanse us of toxic things that have accumulated during the day.
So sleep, exercise, diet are currently the most effective ways of keeping us healthier for longer.
Jeffrey Snyder, Broadcast Retirement Network
So let’s talk about, I want to get into the research. And again, I’m not going to ask you these hardball questions because candidly, I’m not in the field that you’re in, but I’m more out of curiosity. What are, you know, I’ve seen in some of the pieces put out by University of Minnesota and your department and other places, there’s something called a zombie cell.
I’m wondering what a zombie, I know what a zombie is because I’m a big George Romero fan and I’ve watched The Walking Dead, but what is a zombie cell and how does that interrelate to aging?
Dr. Paul Robbins, University of Minnesota
So zombie cell is the term that the press picked up on. So a zombie cell is actually what we term a senescent cell. And cellular senescence is a process that happens to cells in our body if they acquire damage.
And what’s interesting, if they acquire too much damage, they stop dividing and they release all these inflammatory factors that tell the immune system, I’m damaged, come clear me. So when a healthy person like yourself, Jeff, your immune system’s clearing these damaged cells all the time, but as they accumulate with age, because we accumulate more damage, our immune system starts to fail. We don’t clear these cells as effectively.
And so they lead to chronic inflammation that can lead to destruction of tissues and contribute to aging. So they’re called zombie cells because they don’t die. They’re trying to attract things to come attack them.
But with age, that changes and they accumulate and actually can drive disease and aging.
Jeffrey Snyder, Broadcast Retirement Network
Well, thank you for that explanation, Paul. Let me just follow up on that. You mentioned some of the damage.
How do we, at a cellular level, again, I’m outside of my, I’m over my skis here, but how do we receive damage that would create these cells? Is it from the sun? Is it from the food that we eat?
From the air that we breathe?
Dr. Paul Robbins, University of Minnesota
Yes, yes, yes, and yes. So there are a variety of things that can damage a cell. And we think that the predominant type of damage that drives senescence, drives these zombie cells is damage to your DNA, to actually the chromosomes and encode the genes that control the composition of our cells and body.
So that damage that occurs leads to this induction of a pathway that then tells the cells to stop growing. The type of things that can induce that damage, obviously UV, cigarette smoke, exposure to x-rays, but also our cells are not perfect metabolic machines. And we generate reactive oxygen species due to problems that are mitochondria or other parts of the cell.
And that can contribute to driving DNA damage. So it’s not just extrinsic factors, they’re actually intrinsic factors that contribute to this. And what we know is that individuals that may have changes that allow them in their body, allow them to repair that damage more effectively seems to stay healthier for longer.
So we really think repairing the damage, preventing senescence, preventing this inflammation would be beneficial.
Jeffrey Snyder, Broadcast Retirement Network
And you mentioned inflammation. What I know of inflammation, when I bang my knee and I have a bruise, I get some kind of evidence that I’m inflamed or I get plantar fasciitis or something like that. It’s very evident to me.
If I have this cellular inflammation, would it present where I would know and say, hey, I’m being very basic here, but my cells are inflamed. Would I know that?
Dr. Paul Robbins, University of Minnesota
No, you wouldn’t. This isn’t like you’re having a massive infection or you’re having a toothache because you said you damaged your knee. This is more kind of lower levels of inflammation, but from cells that are in tissues.
So the way I describe this to the lay public, it’s like a bushel of apples where one rotten apple releases factors that cause all the other apples in the bushel to begin to rot. And that’s how we envision this. So if you have 1%, 5% of cells in your liver, your kidney, your brain that become damaged, they become inflammatory, they accumulate, they can cause damage to basically normal cells that are adjacent to it or near it.
So you see the spread of cellular senescence, spread of inflammation, spread of damage, and that contributes to disease and it contributes to aging. And can I- There’s nothing that you would be able to know, yes, I have a high senescent cell burden at this point. There’s no way of you to determine that.
Jeffrey Snyder, Broadcast Retirement Network
But is there like a lab test or test that, so let’s just say if someone out there watching and they want to reach out to their primary care physician, their interest is piqued. Hey, do I have inflammation? Can you actually measure that at a blood level?
Can the average person go to their PCP and ask about that?
Dr. Paul Robbins, University of Minnesota
So there are markers of inflammation, but they haven’t necessarily been tied back to senescent cells. So an important question that my lab, our institute, and people around the country, around the world are working on is trying to develop a simple blood test so we really can predict your senescent cell burden. And we have hints of what we have to look at.
And there are factors that are measured when you go to the doctor that we think are linked back to senescence, but we need maybe a slightly better biomarker profile. So these assays are coming so that you could in the future, whether that’s two years, five years, 10 years, you can have a blood test or a urine test, or maybe a saliva test that would really identify if you have a high senescent cell burden. Because we don’t all age the same way.
So I may have a higher senescent cell burden, whereas it may be your mitochondria aren’t aging as well, or your stem cells aren’t aging as well, or there’s another, what we call hallmarks of aging that’s affected than you as compared to others. So we need to identify those individuals. And so, yes, we are working on these sorts of blood tests.
I can’t say where they’re quite there yet.
Jeffrey Snyder, Broadcast Retirement Network
Okay. Well, fingers crossed. And hopefully before my time runs out, I’m hoping that we could figure that out.
Dr. Paul Robbins, University of Minnesota
So am I.
Jeffrey Snyder, Broadcast Retirement Network
Yeah, I’m sure we all have a vested interest in this. Actually, you have more of a vested interest than anyone. Let me ask you, I was just reading a story about the Japanese culture.
I think Japan has over 100,000 people, if I’m not mistaken, that are triple digits. Should I move to Japan? So what makes that place, what makes Japan so unique relative to other cultures?
Or does American society have people that are centenarians or Chinese? Go ahead, I’m sorry.
Dr. Paul Robbins, University of Minnesota
Great question. So we actually have a large grant with people at Albert Einstein and Columbia University to understand the genetics of centenarians that might help guide drug development. And that’s because part of your longevity, and there’ve been recent reports that say 40, 50% of longevity is linked to your genes.
So centenarians have what we call rare variants. So these are changes in the DNA sequence that may alter expression of certain genes. So a centenarian, what’s interesting is they are healthy.
It’s not that they just live to 100. They’re healthy. They’re 90, 95, or 100.
And then the medical costs at end of their life is remarkably low because they’re healthy, and then they die in their sleep. I mean, not all, but that’s more what you’re seeing. So we think it’s the genetics.
So partially we think in Japan, there’s a genetic composition and their genes linked to longevity in the Japanese culture. But it may be diet. It may be exercise.
The Japanese walk a lot. I think they eat more fish. Don’t eat a lot of red meat.
So there’s obviously an environmental component too. But what we want to do is identify drugs that mimic the effects of these rare variants in centenarians to try to turn all of us into centenarians, or the ability to stay healthy to the very end of your life, which is kind of a goal to stay out of the nursing home.
Jeffrey Snyder, Broadcast Retirement Network
Let me ask you an oddball question. Are there limits to, and I know you’re not a MD, but you’re a clinician. You do a lot of the research.
Are there limits to how long the human body, and I’m thinking about the cardiovascular system, can last? So you’ve got these centenarians that are living into their 120s. I guess Abraham lived several hundred years.
That’s a whole different story. We’ll have to talk to the Bible about that. But in all seriousness, are there limits to how long the human body can last?
Dr. Paul Robbins, University of Minnesota
It’s a great question. A lot of debate going on. There’ve been numerous studies, including somebody at the University of Minnesota in their institute, that has done a study, historical study, looking at longevity in all cultures.
And they say the maximum human lifespan is 115 to 117. In fact, I don’t think there’s anybody over 120. I mean, right now, the longest lived person is, I don’t know, 112, 115.
So that we think is the maximal lifespan. But that’s with, you know, and that’s with diet, these rare variants that centenarians carry, et cetera. What we don’t know is if we develop drugs that kind of mimic what we’re seeing going on in centenarians, or can eliminate senescent cells, or can improve your stem cell function, et cetera, can we surpass that?
But our goal, and I keep saying this, is we’re not trying to keep people alive for longer. We’re trying to keep them healthier for longer. And if the side effect of being healthier for longer is you live longer, that’s great.
But we don’t want to also increase the time you spend in the nursing home. We want to keep you healthier, you know, to the very end of life. So we say kind of compressing that period of comorbidity that you have end of life, and you start to acquire all these different age-related diseases.
Jeffrey Snyder, Broadcast Retirement Network
Well, I for one, I’m hopeful that you continue, you and your colleagues, not only at University of Minnesota, but across the globe, continue the work. I think you guys are making great progress. And I think it’s going to be beneficial for not only Americans, but people all over the planet.
Now, there are probably economic challenges and things that governments will have to think about as people start to live longer. But hey, from my perspective, if someone is halfway through his life, that’s not a bad thing. Paul, we’re going to have to leave it there.
Thanks for making a few minutes with us. Great work at the University of Minnesota, and we look forward to having you back on the program again very soon.
Dr. Paul Robbins, University of Minnesota
Great. Thank you very much, Jeff. I enjoyed it.
Thank you.
