Coral reefs are crucial to the ocean's ecosystem, providing sustenance to a quarter of marine life. Today, more than one third of the world's reefs are deteriorating. What's causing coral reef destruction and possible new remedies to address it.
Each day around the world 150,000 people die; two-thirds from age-related diseases like cancer and heart disease. Many of these conditions lead to lengthy hospital stays and costly medical treatments. An aging world population is driving some countries to fund biological research aimed at preventing the development of life-shortening diseases. Recently, scientists have discovered that removing old, harmful cells delays the onset of age-related conditions in laboratory animals. The latest developments in aging research and what they could mean for human health.
- David Walker assistant professor of integrative biology and physiology at UCLA
- Felipe Sierra director, division of aging biology, National Institute on Aging at NIH
- Jan van Deursen professor, biochemistry/molecular biology, The Mayo Clinic
By age 65, most people will be diagnosed with two age-related diseases. Scientists at The Mayo Clinic recently found that removing old cells in mice prevented them from developing cataracts and muscle loss. At UCLA, researchers activated a gene in the stomach of a fruit fly that extended its life by 50 percent. But can these and other methods really prevent the onset of age-related illnesses and extend life?
Eventually, Cells Stop Dividing
“Senescence” is the term describing what happens when a cell loses its ability to divide. The phenomenon was discovered about 50 years ago, but until very recently, scientists couldn’t directly connect it to the aging process. Now, researchers have found that once a cell experiences senescence, it can begin to secrete harmful substances, releasing them in to the body. Dr. Jan Van Deursen of the Mayo Clinic said that in mice, senescent cells have been definitively linked to a loss of muscle mass and functional fat – two hallmarks of the onset of many age-related illnesses.
Delaying the Onset of Disease
Van Deursen and his colleagues found out that by removing senescent cells from mice, they were actually able to delay the onset of diseases in their tissues. The researchers also found no overt negative side effects from the removal of the cells. But Van Deursen is careful to point out that his research is not a fountain of youth-like solution. “I would like to stress that we did not see a reversal of aging,” he said. “It’s not like we turned an old mouse in to a young mouse.”
Genes With the Keys to Lifespan
David Walker, assistant professor of integrative biology and physiology at UCLA, is part of a team that has identified a gene in fruit flies that seems to control life span. When the gene’s activity is boosted, fruit flies can live up to 50 percent longer. A normal fruit fly lifespan is about two months. Walker’s team has figured out that the intestine, and the function of the digestive system, seem to be very important in aging. “The intestine is a vital organ for nutrient uptake…but it’s also a very important barrier that protects us from pathogens and toxins in the environment,” Walker said.
The Benefits of Calorie Restriction
Both the role of mitochondria and calorie restriction were the inspiration behind Walker’s study. It’s known that mitochondria decay is a function of age, and also that dietary restriction can extend lifespan. Although scientists don’t yet know the exact mechanism, dietary restriction is actually shown to boost mitochondrial activity. The gene that Walker and his team identified in fruit flies performs the exact same function.
You can read the full transcript here
MS. DIANE REHMThanks for joining us. I'm Diane Rehm. By age 65, most people will be diagnosed with two age-related diseases. Scientists at The Mayo Clinic recently found that removing old cells in mice prevented them from developing cataracts and muscle loss. And at UCLA, researchers activated a gene in the stomach of a fruit fly that extended its life by 50 percent.
MS. DIANE REHMJoining me here in the studio to talk about how new developments in aging research might apply to humans, Felipe Sierra of the National Institutes of Health. Joining us from a studio in Rochester, Minnesota, Jan van Deursen of The Mayo Clinic. This is such exciting research. I hope you'll join us with your questions, comments 800-433-8850. Send us your email to email@example.com. Join us on Facebook or Twitter. And good morning to you, Felipe Sierra.
MR. FELIPE SIERRAGood morning, Diane.
REHMAnd good morning to you, Jan van Deursen.
MR. JAN VAN DEURSENGood morning.
REHMFelipe Sierra, this is not brand new research, is it?
SIERRAThe research that was done at The Mayo Clinic is, of course, brand new, just published, but the field of senescence has been around with us for 50 years.
SIERRAYes, so senescence is one of possible fates of cells when cells that normally can divide, when, for one reason or another, they cannot do so anymore. And usually this is considered -- this was described originally 50 years ago by Leonard Hayflick and it was suggested that it was related to human aging, but we have not known that as a fact until now.
SIERRANow, what has been pretty much agreed by scientific communities recently is that senescence is one of two mechanisms that we have at the cell level to fight cancer. When a cell tries to divide forever, as in a cancer, you either activate its own cell death mechanism, it gets killed or it turns into a senescent cell, which cannot divide anymore therefore it does not produce a cancer.
SIERRAHowever, recent research has also shown that these senescent cells do not just sit there, but they secrete a lot of bad things, basically, which could or could not be one of the causes of aging and that's where we were until the recent research.
REHMNow Jan van Deursen, tell us about your recent study on senescent cells in mice.
DEURSENYes. What we did is -- so we knew about senescent cells accumulating in tissues and organs of mice and humans with age and the question we asked is, are these cells just innocent bystanders or are they actually doing bad things, such as driving the dysfunction of these tissues and organs, dysfunction that's typically associated with age-associated disorders?
DEURSENAnd so we designed an animal model where we could induce the killing of senescent cells, the clearance, so to speak, and what we found was that age-related diseases that were occurring in our mouse model, such as sarcopenia which is a loss of muscle mass and muscle strength which is very common in the elderly and associated with their loss of independence, the formation of eye defects such as cataracts and the loss of functional fat.
DEURSENAnd so what we found was that the accumulation of senescent cells in skeletal muscle, fat and in the eye actually drives the age-related pathologies and that clearing these cells is not only delaying the onset of these disorders, but can actually -- or it's not preventing those, but it's delaying the onset of these diseases.
REHMOkay, so let me just recap here a little bit. What you're saying is that by virtue of the elimination of these senescent cells in mice, what you were able to do was to delay the onset of diseases in their tissues. Is that accurate?
DEURSENYes. And I think an important finding of this study is also that we found no overt negative side effects of clearing these cells. So one big question is always in this type of research, you know, these cells accumulate for a reason. Is that reason -- is there a benefit to their accumulation? And as far as we can tell, the removal of the cells seems to be safe in our animal models, so there are no negative consequences.
DEURSENThen only positive consequences were noticed. But I would like to stress that we did not see a reversal of aging. It's not like we turned an old mouse into a young mouse.
REHMSo we're not talking about the fountain of youth, at least, yet. Is that correct?
DEURSENI think that's correct. Aging is a very complex process and all cells in our body essentially, over time, experience wear and tear and on top of that they experience these senescent cells that make the neighborhood in which cells live not so livable. They make it more difficult to do well so just by taking away these senescent cells, you basically improve the neighborhood in which cells live, but you're not taking away the damage that these cells have encountered...
REHMBut Felipe Sierra, there's a question here. If these senescent cells are harmful, why haven't human beings evolved in a way to simply get rid of them?
SIERRAWell, there are two aspects to that. One possibility, of course, is that the importance of fighting cancer for a multi-cellular organism like ourselves, the way we can grow to a size that we have and we can live for so long is precisely given by the ability of some of our cells to divide forever and that has the risk of cancer. So we evolved these mechanisms to get rid of the cancer and maybe that's a priority. Evolution cannot prevent us from developing a mechanism that keeps us healthy when we're young, even if it has a deleterious effect when we're old because evolution doesn't care about us when we're old.
REHMSo -- but when we are young, do these senescent cells behave differently from what happens as we age?
SIERRANot that we know. As far as we know, they behave the same, but they don't accumulate much because there's a system to get rid of them. They don't die like the other cells, the other mechanisms for fighting cancer. They do not die. However, the immune system clears them. So the senescent cells secrete several compounds that call the immune system to tell them, hey, I need to be removed.
SIERRAOkay, now what happens with age is that our immune system starts failing, too, so the cells are not removed as efficiently as when we were young and that's when the problems start accumulating.
REHMSo from these kinds of experiments with mice, can we extrapolate and begin to think that the same process could be at work in human beings?
SIERRAWell, the mechanism, as Jan probably could -- might be able to explain, because it's quite fancy genetics that they did, to be able to do this in mice so a similar way in humans will not be possible. However, the finding that the cells in these have the effects that they have makes us think that it's something that we should focus on. We should try to get rid of the cells. Before these results, we weren't sure that the senescent cells were indeed bad, now we know that they are bad and therefore there's a reason to focus either on eliminating the cells, at least eliminating their secretions, or at least neutralizing them one way or another.
SIERRAIt's worth doing now and I think that's where their research will go in the near future.
REHMAnd I would certainly think, Jan van Deursen, that drug companies would be awfully interested in your work?
DEURSENYeah, that's the case and so we have received interest from several companies. And I'm actually quite optimistic that -- we used a genetic trick to kill cells and now the next step is to find a way to clear them in humans or in mice.
REHMAll right, and we're going to take a short break here. You're listening to Jan van Deursen at The Mayo Clinic and Felipe Sierra at NIH.
REHMAnd we're talking about some very exciting new research going on currently in mice and elsewhere. With me here in the studio is Felipe Sierra. He's director of the Division of Aging Biology at the National Institute on Aging at NIH. Joining us from a studio at the Mayo Clinic in Rochester, Minn. is Jan Van Deursen. He's professor of molecular biology and biochemistry at the Mayo Clinic. They are both extremely excited about their work. Now joining us from a studio at UCLA is David Walker. He's assistant professor of integrative biology and physiology at the University of California Los Angeles. Good morning, Dr. Walker. Thanks for joining us.
MR. DAVID WALKERGood morning. I'm very happy to be here.
REHMThank you. Tell me about your fruit fly study.
WALKERSo we're interested in some of the same basic questions. We're very interested to try and understand the basic biology of aging. And in this recent study what we did was we identified a gene. The gene's called PGC1. And we made a discovery which is that if we up regulate, if we boost the activity of that gene in the intestine of the fly that's able to make the whole animal live significantly longer, as much as 50 percent in certain cases.
WALKERAnd really at the same time we see that this, as well as extending the lifespan of the animal, we actually slow many of the hallmarks of aging within the fly intestines. So we're really...
REHMHow long does the normal fruit fly live?
WALKERNormal healthy flies live between six and eight weeks or, you know, just under two months.
REHMSo I gather that would make them a good subject for your study.
REHMAnd when do they begin showing signs of aging?
WALKERWell, just like people, the major features of aging are recapitulated in the fly when they reach around middle age. So after about four weeks or a month the flies begin to -- their reproductive capacity declines. They become much less active. They lose the ability to fly and climb. And they even lose cognitive abilities. They don't remember quite so well as when they're young.
REHMSo it sounds as though you're saying that there's something very, very important about the digestive tract as it relates to aging. Do you believe that that also applies to human beings?
WALKERWell, that's one of the major findings of our study with respect to the fly. But yes, that we find that we can slow aging at the organismal level by slowing aging of the intestine. And the study was, you know, exclusively done in the fly. But it does raise questions about intestinal aging in other species, mammals, including people, of course.
WALKERThe intestine is, you know, a vital organ of course for nutrient uptake for, you know, getting energy from food. But it's also a very important barrier that protects us from pathogens and toxins in the environment. So, you know, we can -- in some ways it makes a lot of sense that maintaining healthy intestinal function as we age is very important for our health.
SIERRAYeah, I would like to add that the intestine in the fly has one particular characteristic that is unique in the fly but it's not unique in us. The intestine is the only organ in the fly that has stem cells that can actually proliferate. So maybe in us -- and I don't disagree with David on the importance of the intestine in terms of absorption and being a barrier to chemicals -- but in humans we have other tissues that share this thing with the intestine of the fly, which is we have stem cells. We have a regenerate capacity. And maybe what he's observing in the intestine being unique to him testing, in mammals it could be unique to all regenerative tissues including those that eventually could show cell senescence and things like that.
REHMInteresting. And Jan Van Deursen, what's your reaction to the fruit fly study by Professor Walker? Could it be tried with mice?
DEURSENActually it has been done in mice. There's a study by the -- where one researcher I know involved named Bruce Spiegelman (sp?) where they over expressed this gene, the PGC1 alpha in skeletal muscle. And that study shows that the mice lived longer as well. So I think that this concern that there might be some specific thing about flies that would make this gene work with regard to longevity I think has already been kind of shown in mice that it works even when expressed in a different tissue. And, Dr. Walker, correct me if I'm wrong on this mouse study.
WALKERYeah, we're -- I'm aware of that study from Dr. Spiegelman's lab, yeah. They also showed, I believe, that it delayed the onset of sarcopenia in those animals. And the same gene has (unintelligible) ...
REHMWhat is sarcopenia?
WALKERSarcopenia is the loss of muscle tissue as a function of age. So this gene has also been implicated in a number of other age related neurodegenerative diseases such as Parkinson's disease and even Huntington's disease. So it does seem to be, you know, a potential target to intervene in aging.
REHMDr. Sierra, I've read that you refer to this study of cell senescence as the holy grail of the aging field.
SIERRANot the holy grail of the aging field. The holy grail of the senescence cell field.
REHMAll right. I'll take that.
SIERRABasically there are several lines of research, as Dr. Van Deursen said. Removing the senescence cells did not abolish aging. We're not going to become immortal.
SIERRAThere are many aspects to aging and cell senescence is one of them. Now when I talk about the holy grail in that sense, it's because the cells have been known for 50 years. And what has been at the center of everybody's attention is, are they really important. There's not many of them. They don't accumulate to large numbers. So the question of whether they have a physiological role in the decay of tissue function has always been in the back of people's mind. Yes, they are there. Okay, fine. Are they bad? Or maybe they are good. We don't know.
SIERRAAs you asked me earlier, why do we still have them? Maybe they're good. And that question actually has not been answered and will not be answered for a while. Maybe there are some circumstances that we have not tested yet in which the senescence cells will be important. For example, because they secrete these things that call the immune system into action, maybe that's -- they play a role in those circumstances. We just don't know.
SIERRABut the holy grail comment was because it was so important to determine what happens if we get rid of them or if we increase them. And that's what has been done with this study.
REHMWe have a question from Elizabeth in Boston. "To what extent is research on mitochondrial mechanisms related to this research?" She says, "I have two sons with mitochondrial disease."
SIERRAOkay. Mitochondrion has been one of the other big fields that we have been studying in aging. The free radical hypothesis which is the one that everybody says free radicals are bad for you, okay. Well, it's -- there's a lot of questions there, but the research of mitochondria has been very, very important. And things like PGC1F, for example, has been shown to be activated by resveratrol, which is another compound that people know about that helps with aging physiology.
SIERRASo there's a lot to be said about how important mitochondria are. After all, they are the ones that produce all the energy that we use or most of the energy that we use. So defects in mitochondria can have very severe consequences, as unfortunately happens in these mitochondrial diseases. With aging, the effects are not as dramatic, but nevertheless there's a decay in their functioning and that plays a role.
REHMDr. Walker, what about calorie restriction? How do you think it plays a role in the aging process?
WALKERWell, that's a very interesting question, very appropriate to our study. So both the role of mitochondria and also dietary or caloric restriction were one -- were an inspiration behind our study. So as Felipe mentioned, it's known that mitochondria decay is a function of age. And it's also been known for a long time that dietary restriction can extend lifespan. We don't really know the mechanism, but one of the physiological (sounds like) carlets of dietary restriction is actually boosting mitochondrial activity. And that's exactly the same physiological function that PGC1 exerts.
WALKERSo we -- one of the things we were interested to do was to see what if we boost mitochondrial activity via PGC1 without changing the diet of the flies. Would that have the same life extending effect as diet restriction? And as we published it does indeed when we target PGC1 to the digestive tract of the fly. So these things are -- mitochondria and diet restriction, they're all related.
REHMAnd to you, Jan Van Deursen, are senescence cells related to the causes of Alzheimer's Disease?
DEURSENIt isn't clear right now. Our model that we used -- our mouse model that we used did not have Alzheimer-like defects. One of the studies that is currently ongoing in the lab performed by Dr. Dan Baker is to specifically look at the effect of senescence all clearance on Alzheimer's disease. There is a mouse model for Alzheimer's disease and we are setting up the clearance of senescence cells. It's known that there is an inflammatory component to Alzheimer's disease which might be caused by -- or influenced by senescence cells.
DEURSENSo that's a very good question. Can the clearance of senescence cells also improve the function of the brain and the central nervous system? And unfortunately our model did not -- we were unable to draw any conclusions on the existing model. But that's currently ongoing.
REHMAnd you're listening to "The Diane Rehm Show." We have a great many callers. I do want to open the phones. First let's go to Phoenix, Ariz. and Phyllis. Good morning, you're on the air.
PHYLLISThis is a fascinating program for me because I am extremely elderly and a stroke survivor. And I'm wondering if they are doing any research into the brain cell that has been killed by strokes. If there is any hope for regenerating brain cells.
SIERRAWell, once a neuron is killed, unfortunately there is no way of regenerating that neuron that we know of. Maybe in the future we will find, but right now, no. There is a lot of research on stroke. There's an institute in INDS which funds most of the research on stroke. But like all these age related diseases, we feel that there is a commonality to all of them that the aging processes are what's behind all of this. So in terms of treatments or cures, we don't have much in hand now. And to tell you the truth, I'm not that familiar with what the INDS funds. So I don't know if anything is on the way for that.
REHMBut let me ask David Walker. This notion of growing older but growing older in a healthier way is really what all this research is about. Am I correct there?
WALKERYeah, that's correct. I guess the approach is instead of targeting the individual diseases of old age one by one, what we try and do is focus on the underlying aging process itself, because as we're all saying that's the number one risk factor for all these disorders. And if we could find a way to slow that underlying aging process then we would improve the overall health of the aging population, rather than target the individual diseases. And I think that would have a huge impact on stroke, but also on Alzheimer's disease, cancers, cardiovascular diseases, all these diseases.
REHMAnd what about other countries? Are they doing similar research? Are they ahead of us? What about that, Dr. Sierra?
SIERRAOther countries are doing similar research. I was recently at the meeting in the Netherlands. Actually Dr. Van Deursen was there too. They are doing very similar type of research. Different countries of course have different capability in terms of money. Some countries are going up, some are going down in terms of their funding for research in general. So the United States of course has been a workforce in research for many, many years and we continue to be.
REHMDo you think given the importance of what we're seeing both here in the digestive tract with fruit flies and senescence cells that perhaps we're focusing too much on the heart and the brain in the research that is being done here in this country, Sr. Sierra?
SIERRAWell, I agree with what was said that aging is the major risk factor for all of (word?) . And I think funding for that is a priority. But I'm not going to comment on how funding is distributed.
REHMI understand that. I'm just wondering about people's focus, though, and whether you'll see in the coming months and years greater focus in this direction?
SIERRAYes. We are seeing a greater focus on aging in general. However, researchers, being what they are, they tend to go wherever they think it's most interesting. And many of them have reason to go to cardiovascular and to Alzheimer's or whatever.
REHMFelipe Sierra of the National Institute on Aging at NIH. Short break and more of your calls when we come back.
REHMWelcome back as we talk about new research that looks into preventing disease from developing as we age. Let's go right back to the phones to Deep Gap, N.C. Good morning, Lee.
LEEGood morning. How are you?
WALKERI'm -- this is my first time. I really appreciate the opportunity and I really enjoy your show. I've listened for years.
REHMI'm so glad. Thank you.
REHMAnyway, my comment is that -- no, I've been aware of ways of cleaning out senescent cells, you know, from your body, you know, for many years. And I mean, you know, there have been methods, you know, for clearing the body out, you know, for thousands of years. You know, various kinds, you know, fasting, various kinds of diets. So there are many different ways of doing this already and I'm just kind of curious as to -- now, I think the genetic research is extremely interesting, but I would also be interested to see how that would work, you know, along with these other more traditional ways of clearing out the body.
WALKERWell, this question may be -- Jan, could perhaps answer this better than I since it comments on his study, but yeah, the comment on the diet, yes. We've known for a long time that restricting dietary intake without malnutrition can extend our lifespan, but the mechanism underlying that we don't know. And I think that's what a lot of us in the basic biology of aging are trying to figure out.
DEURSENSo Felipe mentioned that one way of getting rid of senescent cells is by the immune system. So, in essence, perhaps activities that boost the immune system could help keep your senescent cell levels down. For instance, there is one interesting study that has linked the clearance of senescent cells or at least the prevention of accumulation to exercise.
REHMTo exercise, healthy eating, I would think probably not smoking.
DEURSENYes. So I think we don't know -- or without having a drug that can clear these cells it seems like common sense that a healthy lifestyle will prevent the accumulation and perhaps promote the clearance of cells through natural ways. And I think the caller is absolutely right, but I don't think, apart from the study on exercise, I'm not aware of, you know, other lifestyles that -- or proof of other lifestyles that could help keep the senescent cell levels down.
REHMBut, Dr. Van Deursen, is that where this might be headed toward? For example, the development of some drug therapy that could rid the body of senescent cells?
DEURSENYeah, I think that's a very promising line of research. I think that all the research that has been done on the targeted killing of cancer cells, sort of targeted therapies, find a drug that kills specifically a kind or certain types of cancer cells and leave the normal cells, the healthy cells in our body unattached. That research has been going on for several years now. And I think the clearance of senescent cell approaches can really benefit from that research.
DEURSENAnd I think that clearance of senescent cells might actually be a lot easier than killing cancer cells because senescent cells cannot divide. And senescent cells cannot escape the drug as easy as cancer cells do. That's the major problem with the targeted drug therapies, is that the cancer cells mutate and find a way around a drug. And I think because senescent cells don't have the ability to proliferate, I think they will be easy targets. And personally, I'm very optimistic that there will be, maybe in addition to some lifestyle changes, that there might be specific drugs being developed over recent years that can actually attack these cells.
REHMHelp me to understand what happens during, for example, radiation as a cancer therapy and what that does to both senescent cells and cancer cells.
DEURSENSo the radiation and chemo basically introduces DNA and protein damage. And cancer cells are somewhat more sensitive to that and die more readily after experience chemo or radiation, but normal cells also will experience damage. And normal cells, as a result of that could go into senescence. Now that we know that senescent cells do bad things, that's maybe why chemo and your radiation treatments are associated with accelerated aging. And so perhaps in the future, if you find a way to get rid of senescent cells, maybe that would also benefit people that receive cancer treatment.
REHMInteresting. Dr. Walker, do you want to comment?
WALKERNo. I would agree with those statements and sentiments, yeah.
REHMAll right. And let's go to Louisville, Ky. Good morning, Annie.
ANNIEGood morning. Thanks for taking my call.
ANNIEMy question is, I've been sort of reading about the longevity diet, about calorie restriction, optimal nutrition and the whole idea is still sort of vague for me. So I don't know if you've already touched on this or not, but I'm just wondering if maybe you guys could talk about it just a little bit more. And, let's see, I had another question, what do you guys think about a vegan diet as a way to prolong life and as opposed to like eating meat or eating dairy, things like that?
REHMWell, you understand these are not dieticians, but Dr. Sierra, you might want to comment.
SIERRAYeah, so there so was this thing about dietary restriction, it increases lifespan and increases…
SIERRA…health. Those are studies, for the most part, done in animals. We don't know whether there's other effects in humans. There are some…
REHMAnd how severe are those dietary restrictions?
SIERRAQuite. Quite. Depend on the species and different conditions. They are from weaning of a mouse, in other words, from about 21 days of age until they die, a 40 percent restriction. So that's a quite -- it's not just your regular diet. That's a very -- and yet, with no malnutrition. Now, the thing that's not that clear is that your genetic background affects how dietary restriction will work. So we don't know in humans, which have a varied genetic background, they have their genius genetic background. Some of us might be helped by dietary restriction and some of us might not.
SIERRANow, if you have a heavy BMI of 27 or 28, there's no question that diet will help you. But this extreme diet that we subject the animals to, I see them primarily as a research tool to identify the mechanisms so that, like we have been doing with other things, once you identify the mechanism the idea is to develop mimetics of the diet restriction where you don't restrict yourself, but you take something that makes the body think that you are doing that.
REHMI see. I see. Jan van Deursen, I'd be interested in your work with centenarians.
DEURSENWell, we're not doing work with centenarians, but what we are learning from centenarians is that they typically have a very long health span, which is basically the period in one's time that a person is free of major chronic diseases. The health span in centenarians is very long. And one interesting goal, I think, or more recent goal is not to increase lifespan so much as health span, to improve the quality of life. We're trying to learn from centenarians why their health span is so good and try to mimic that so that ordinary folks, like my family, might be able to improve the quality of their health in later years.
DEURSENAnd that also has of course an important socioeconomic advantage. If you can compress the period in one's life that one is dependent on doctors, hospitals and maybe nursing homes, that would decrease the healthcare costs quite dramatically. And we all know that this is very important.
REHMBut is there something different that you've seen about centenarians? Do they live differently? Do they eat differently? Do they sleep differently?
DEURSENWell, this is not my area of expertise, but what we're always joking about at meetings is that these people do not particularly live healthy lifestyles. They don't necessarily watch their diet. Some of them even smoke. They -- it seems like their genetic composition is such that they're resistant to a lot of age-related disease or deterioration. And we say genetic -- I say genetic because usually siblings have also -- of these centenarians -- have a long life expectancy. So there is definitely a genetic component to all this.
REHMAnd that brings me full circle. I mean, if Dr. Sierra, you're born with a genetic makeup, that is no matter what you do, if you drink, if you smoke, if you don't exercise, if you overeat and you're gonna live beyond 100 then how does that affect your thinking about all this research?
SIERRAWell, certainly that is true. If I knew that I had the genetic…
SIERRAOkay. I would misbehave, however, I don't know. I don't know. So the bottom line is that these centenarians are really extreme cases. There are very few of them. So the chances that my genetic components are so that I would become a centenarian are extremely, extremely -- I have low chance.
SIERRASo I'd rather take care of myself, exercise, eat good and so on because I can't count on being like these ones that have been studied. Now, one thing that I would like to add, when we talk about centenarians and Jan talked on the -- touched a little bit on the cost to society. So I recently heard -- and I have not seen the data, but I was told by somebody who works with centenarians. One thing that we do know is that most of the cost of healthcare occurs in the last five years of your life, but it takes a third of the cost when you die at 100 than it takes when you die at 80.
SIERRAWhen you die at 80, you have a slow decay that requires a lot of health services and it's very expensive. When you die at 100, indeed your health span has been increased to a point that you don't even go to the doctor when you're 80. You start going about a year before you die. And then you die very fast. So the cost of the last five years is only a third of what would be otherwise.
REHMFascinating. And you're listening to "The Diane Rehm Show." Let's go to Salt Lake City, Utah. Good morning, Tom.
TOMHi. I have two questions. So I was wondering what the difference is between health and lifespan, but I guess that was partially answered.
TOMBut also what point in a human life cycle these problems seem to really develop? And I guess, you know, to be frank, like, you know, if I'm in my 20's now, you know, and what's kind of the time frame that we're looking at in terms of like an actual treatment to, you know, remove these senescent cells so that, you know, practically speaking we might be able to actually, you know, enjoy this extended health span?
REHMThat's an interesting question, Dr. Sierra.
SIERRAWell, for one thing we cannot remove the senescent cells yet so you don't have to worry yourself about that. But in terms of when you can start a treatment to prevent aging, it's unlikely that people will -- even that the FDA will approve or that people will start a treatment when you're healthy to make you live longer if you are only 20. This becomes more relevant when you are getting old. So you start thinking about it. And it starts bothering you. And in that sense, for example, the NIA funded a study that showed that rapamycin extends the lifespan and the health span, as far as we can tell.
REHMWhat is that?
SIERRAIt's a compound that was found in the island of Rapa Nui. And that's why it is called rapamycin. Rapa Nui is what in here is called Easter Island. Okay. So this compound has been used as an immunosuppressant for transplant patients.
SIERRABut it acts -- the molecular way in which it works at the cell level is very well known. And studies in flies and worms had shown that modifying the activity of that pathway did lead to longer life. So it was tried in mice and it did. It made the mice live longer. Okay. Now, the interesting thing is that for several reasons the treatment of the mice started when the mice were almost two years old, which has been extrapolated -- I don't know how correct this is, but would be equivalent to a 60-year-old person.
SIERRAThen we're talking about something that as a 60-year-old you start thinking about what I'm gonna do when I get old.
REHMFelipe Sierra, he's at the National Institute on Aging, Jan van Deursen, professor of molecular biology and biochemistry at The Mayo Clinic and David Walker, he's assistant professor of integrative biology and physiology at the University of California, Los Angeles. Fascinating work gentleman. I will be interested as I grow older hearing all about it. Thank you all so much.
SIERRAThank you, Diane.
REHMAnd thanks for listening all. I'm Diane Rehm.
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