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Ageing's all the rage: The science behind growing old

In a wide ranging discussion on ageing, Professor Dame Linda Partridge delves into the research findings on longevity in humans and animals, and ponders evolutionary perspectives on the ageing process. Presented by Dr Shane Huntington.

"If we can somehow slow down the ageing process - which is probably what these mutations are doing - then we can capture a very broad range of things that go wrong simultaneously rather than having to treat them piecemeal." -- Prof Dame Linda Partridge




Prof. Dame Linda Partridge
Prof. Dame Linda Partridge

Professor Dame Linda Partridge works on the biology of ageing. Her research is directed to understanding both how the rate of ageing evolves in nature and the mechanisms by which healthy lifespan can be extended in laboratory model organisms. Her work has focussed in particular on the role of nutrient-sensing pathways, such as the insulin/insulin-like growth factor signalling pathway, and on dietary restriction. Her current work is directed to developing pharmacological treatments that ameliorate the human ageing process to produce a broad-spectrum improvement in health during ageing.

She is the recipient of numerous awards, including giving the Royal Society Croonian Lecture in 2009 and a DBE for services to science. She is a Fellow of the Royal Society, the Academy of Medical Sciences, the European Academy of Sciences and the American Academy of Arts and Sciences. She is the Director of the UCL Institute of Healthy Ageing, as well as founding director of the new Max Planck Institute for Biology of Ageing in Cologne.

Further reading: "The New Science of Ageing" -- article by Linda PartridgeJanet Thorntonand Gillian Bates, 2011

Recent publications

Partridge Lab at UCL Institute of Healthy Ageing

UCL

 

Credits

Host: Dr Shane Huntington
Producers: Eric van Bemmel, Kelvin Param
Associate Producer: Dr Dyani Lewis
Audio Engineer: Gavin Nebauer
Voiceover: Nerissa Hannink
Series Creators: Kelvin Param & Eric van Bemmel

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VOICEOVER
Welcome to Up Close, the research talk show from the University of Melbourne, Australia.

SHANE HUNTINGTON
I'm Shane Huntington. Thanks for joining us. Thanks to a combination of modern medicine and hygiene more of us are reaching a ripe and riper old age; but with greater longevity new problems emerge and become prevalent. Ultimately, the gradual decay of our bodies leads to dementia, cancer and a raft of other debilitating conditions. Research into ageing considers not only the goal of, ultimately, extending our life span, but also the possibility that our later years will be fruitful and enjoyable. To discuss the science of ageing we are joined on Up Close today by Professor Dame Linda Partridge, director of the University College London Institute of Healthy Ageing, and founding director of the New Planck Institute for Biology of Ageing, in Cologne, Germany.  Professor Dame Partridge is in Melbourne to deliver the 2012 Graeme Clark Oration. Welcome to Up Close, Linda.

LINDA PARTRIDGE
Thank you very much indeed. It's a pleasure to be here.

SHANE HUNTINGTON
Linda, I would like to start by talking about your work and how it focuses on the genetics of ageing. What exactly do we mean by ageing and why are we taking this genetics perspective?

LINDA PARTRIDGE
Well, I think the ageing process is all too horribly familiar to many of us. It's a process of decline in function that, ultimately, increases the likelihood of the various ageing associated diseases that you've mentioned: cardiovascular disease, cancer, neurodegenerative disease and, of course, ultimately, death. Also very familiar in the animal world where it's very strongly characterised as well by a loss of fecundity as the animal gets older. Really, what the genetics of ageing is doing is giving us information about the basic biology of the process. It's always been a very powerful way in to biological mechanisms. So if you want to understand how the expression of a gene is controlled, how genes are transmitted between generations, how metabolism works, then you try and do the equivalent of messing up the engine of the car by throwing a spanner in. You make a mutation in the genetic material and try and isolate interesting mutants that affect the trait that you're interested in, in order to see how it works. That approach to ageing was started a little under 20 years ago, with a chemical mutagenesis in a nematode worm, one of the laboratory model organisms. Somebody called Michael Klass just fed these worms a chemical mutagen and isolated strains that were harbouring mutations in single genes and said do any of them extend life span. Somewhat to his and everybody else's surprise, actually, he found that they did. He could isolate strains of worms that were long lived. And it wasn't just an extension of the moribund period at the end of the life of the worm. These mutant long lived strains were wriggling and healthy long after all the controls were dead. So it seemed to be an extension of healthy life span, which made it particularly interesting.

SHANE HUNTINGTON
Now, in your laboratory you use the fruit fly, as many researchers in genetics do: Drosophila melanogaster. What is specific about this fruit fly that makes it so useful for these studies?

LINDA PARTRIDGE
Well, the fly is very dear to my heart. I've worked on it for quite a number of years now. It's useful for ageing research in a number of ways. So one of the most important ones is that by comparison with the worm, or even the single-celled yeast - which, surprisingly enough, is used for research into ageing - we can use the fly to ask whether the process that’s been identified in the simpler organisms is evolutionarily conserved, because the evolutionary distances between these little invertebrates are huge. And if two or three of them are showing an effect of the same kinds of genes on ageing then, very likely, that effect's going to turn up in mammals. So, for instance, the original mutants that were isolated in the worm that extended life span turned out to be in a - signalling that work that senses nutrients, and much as the costly activities of the animal - so its growth, its reproduction, its immune response, wound healing - anything that uses nutrients - to nutritional status. So we're talking about the very familiar insulin pathway. There's another thing that’s very like insulin called insulin-like growth factor. There's another bit of that whole network that senses amino acids and cellular energy levels. It was mutations in the genes involved in that whole nexus that turned out to extend worm life span. And one of the very important early contributions from the fly was to show that that effect was evolutionarily conserved. So the exact fly equivalence of the genes that were mutated extended the worm life span turned out to do it in the fly. One works with worms first, partly because it's easier to do mutagenesis experiments for other, dull technical reasons that I won't go into. Also worms are short lived. They only live about three weeks; whereas flies, it takes longer to do the experiments because they live a couple of months. But they're very well worth it because they're much more mammal like, so they have tissues that aren’t present in worms at all. They have a complex nervous system. They have a kidney. They have a heart; all of which are completely missing in the worm. So they're also a better indication, really, of things that are going to work in mammals. And it has actually turned out in very recent years that lesions in the same nutrient-sensing network extend life span in the mouse. So it seems that we're looking at a very fundamental aspect of the biology of ageing with these mutations.

SHANE HUNTINGTON
Are you able to extract directly from the file to humans? Or are there a number of intermediate steps, like the mouse and the rat and so forth, before you can make those determinations?

LINDA PARTRIDGE
For genetics we'd nearly always go through the mouse. The reason being, obviously, it's a mammal - so much closer to humans than these little invertebrates - but also it has a particularly well developed system for making mutations in genes for over-expressing genes; for doing all the kind of genetic manipulations that we'd want to do, knocking genes out. That’s why we'd go to the mouse on the way. And its genome and the contents of its genome are much more like our own than others of the invertebrates. But one can never extrapolate to humans from a mouse. I mean anyone involved in drug development will tell you that drugs may do marvellous things in mice, but it doesn't necessarily mean that they’ll have the same effects in humans. So, in the end, we have to turn our attention to humans; that, eventually, the only effective study of humans is humans themselves. And the way that people are tackling that at the moment is to look in humans that - again, the equivalent genes to the ones that were mutated extend life span and improve health during ageing in the animal models - and say well, if we can look at groups of humans that, clearly, have undergone healthy ageing - they’ve made it to 90 or 100, often with several siblings who have done so as well - then are there genetic peculiarities of those long survivors in these equivalent genes? Can we find natural genetic variants in the human population that seem to associate with the survival to great ages? And that seems to be getting the answer yes for this insulin, insulin-like growth factor signalling pathway. So genetic variants - particularly in something called a transcription factor - it's a molecule that alters the expression of other genes, and it's one of the main players in mediating the effects of insulin signalling. I think now, in seven independent human populations, it's turned out that variants in that molecule are associated with survival to advanced ages. So it's early days yet. Well one shouldn’t leap to conclusions here. It's far too soon to be sure. But it's at least looking quite promising that this work in the animal models is going to apply to humans.

SHANE HUNTINGTON
Linda, when you look at some of the genes involved in ageing are there any patterns - groups of genes - that you find in all organisms that seem to lead towards some of the negative effects of ageing?

LINDA PARTRIDGE
Well, really, they're the ones that I've mentioned that are involved in this nutrient sensing. So one of the most fundamentally evolutionarily conserved things about ageing is the effect of nutrition itself. This has been known about much longer than these kinds of genetic effects. So if you take a mouse and force it to eat less than it wants to eat - so if you just leave the mouse in the cage with the food, you can measure how much it eats - and you can take an experimental group of mice and give them half that. You can do the same thing with rats. This was actually discovered, originally, in the 1930s. Then what you get is a long lived animal, often very long lived, and they show an extraordinarily broad spectrum improvement in health during ageing. So they get less cancer, less cardiovascular disease. Their cognitive performance is maintained better. They maintain their agility, their neuromuscular performance, immune profile. I could go on. Almost everything that goes wrong during ageing does so less in these dietarily restricted animals; to the point where, quite often, it's difficult to say what they died of; whereas the normal fully fed controls have usually got some obvious pathology that killed them. it's much harder to say what a dietarily restricted animal has died of. It just died. So that’s very interesting. Really, what we would like to do is to capture the mechanisms that mediate those effects and elicit them pharmacologically because it certainly looks as though the effects of diet itself will apply in humans. So it's recently been shown, in the last couple of years, that dietarily restricted rhesus monkeys, now, behave very like dietarily restricted rodents; that they live longer and, again, show this very broad spectrum improvement in health. So that’s getting much closer to humans. The reason we will probably never know for sure, experimentally, with humans whether dietary restriction can extend their life span is that very few people actually have the willpower to adhere to the kind of diet that's necessary. I mean it involves a reduction of 20 to 30 per cent in food intake, and most people just can't stick to that. A few heroic individuals do manage it. Interestingly, most of them are men.  I think nobody quite understands why. It's possible, of course, in a non-invasive way to look at whether they're showing similar health improvements to the ones that are seen in the monkeys and the mice; and they are. So, for instance, almost any marker that you can have of risk for atherosclerosis is improved in these self-restricting humans. So, really, what we want to do is to capture the benefits of that, pharmacologically. Understanding just what genes and molecules mediate the effects of dietary restriction is the realm of genetics. That’s the information that it's giving us, is what are going to be the good pharmacological targets for achieving the health benefits of dietary restriction without having to go on a diet. 

SHANE HUNTINGTON
This is Up Close, coming to you from the University of Melbourne, Australia. I'm Shane Huntington. In this episode we're talking about the genetics of ageing with Dame Linda Partridge. Linda, there are, really, two distinct issues we're talking about here today. One is how long we actually live, and the second is how well we live into those later years. Are you, in your laboratory, working on both of these issues?

LINDA PARTRIDGE
I think what almost everybody working on biology of ageing wants to achieve is improved health during ageing. I mean the major burden of ill health is now falling on the older section of the population; is causing them great unhappiness. It's causing their carers great unhappiness as well, and their families and friends, and economics costs to society are huge. In fact, for many countries, the cost of ageing related disease has been rated as rapidly becoming unaffordable as older people in the population increase. So what we're about is health during ageing. I mean life span's increasing anyway, with people like me intervening. It's been doing so since the middle of the 19th century. What we're having to deal with is the health consequences of that life span increase that’s happening anyway.

SHANE HUNTINGTON
Do you think that we'll actually get to the point where we find the maximum life span for humans, no matter how healthy we are up until that point?

LINDA PARTRIDGE
Interesting. At the moment what the demographers say is they can't see it. So the increase in life expectancy has been going at about two and a half years per decade since about 1850; so, pretty much, a linear increase. It varies a bit between different countries. When the demographers analyse the data, by now, of course, the increases in survival are happening mainly in 80, 90 year olds, the older section of the population; but there's no signature of an approaching wall of death. It's not clear at all what the intrinsic limit on human life span is going to turn out to be; although, of course, the practical limit may be about to be reached with the epidemic of metabolic disease and diabetes in young people. 

SHANE HUNTINGTON
Why is it that some animals live so long and others don't? I mean we have scenarios where you have some of the giant tortoises living for over 100 years, humans living for a similar amount, but then smaller mammals having significantly shorter life spans. What, genetically, is different that gives us these different life spans?

LINDA PARTRIDGE
That is a really fascinating question and it's one to which we categorically don't have an answer yet; but people would really like to know. I mean, obviously, the natural variation in life span is much greater than anything anyone's managed to produce in the lab - you know, 200 years in the bowhead whale, for instance. And people have looked at these animals and measured things about them that are - candidate processes that might make them live a long time - do they have less oxidative stress - all kinds of things. The problem is that there are so many other differences between these different kinds of animals - they're different sizes and shapes and they have different mating systems - there are all kinds of other traits that differ. And pinning particular genetic differences to the life span difference, where it occurs, is practically impossible. So people have often looked at rather more local differences that ought to be easier to analyse. So what I mean here is cases where the same genome gives rise to very different life spans. Honey bees, for example - the worker bees and the queen be - the single queen bee in the colony - have the same genome, but due to differences during rearing one of them becomes a queen and the rest become workers. And the queen can live for a decade or more, whereas the workers go for a few weeks or months. So that's a case where you've got the same genome giving rise to big differences in life span and, probably, I think, there's going to be better hope of figuring out what's going on there; although, at the moment, nobody knows what the answer is. 


SHANE HUNTINGTON
As we start to live longer and we end up with a variety of these new problems you mentioned earlier that require significant resources to manage as a society, are some of these issues - like osteoporosis, dementia and various forms of blindness - are these actually coupled to ageing? Or are we going to find that they are just a consequence of us living longer; not necessarily coupled to the ageing process itself?

LINDA PARTRIDGE
I think one of the really heartening findings that's come out of the study with animals is that you can make single gene lesions in a mouse - and, yes, it lives a long time, but more importantly, it shows this broad spectrum improvement in health. So, recently, a mouse has been produced. It's just got one gene missing. It has fewer cataracts. It gets less osteoporosis. It maintains its glucose handling better as it gets older. It's less diabetic, if you like. It's got a better immune profile. Its motor co-ordination remains at youthful levels for longer and it has fewer skin problems. Now, those are things that you would think have got nothing to do with each other in terms of the mechanics that actually produce the different - either disabilities or diseases that happen during ageing. Yet here's this one underlying process that, evidently, controls ageing because it's affecting life span, and it's doing it by affecting all these different things that go wrong at once. So it looks as though ageing really is a causal risk factor for the diseases of ageing. If we can somehow slow down the ageing process - which is probably what these mutations are doing - then we can capture a very broad range of things that go wrong simultaneously rather than having to treat them piecemeal. And I think that's why these findings are important.

SHANE HUNTINGTON
What about cancer, Linda? Does that fall into the same category? We seem to have had a huge rise in the number of - or the percentage of our population that is affected by cancer in recent years. 

LINDA PARTRIDGE
Yes. That is best documented for the effects of diet itself rather than of these mutations at the moment. This is very young science. Some of these findings have really just been published in the last couple of years; so huge amounts of work going on, looking at different diseases, exactly what's improved, are there any down sides and so on. One of the clearest things about dietary restriction itself is that it almost abolishes cancer in rodents. That's in animals that tend to die of cancer. It's the commonest cause of death. Putting them on a diet can almost stop it in its track.

SHANE HUNTINGTON
Linda, you're an evolutionary biologist by training. How has this influenced your particular approach to studies in ageing?

LINDA PARTRIDGE
I think ageing is a trait that is quite hard to think about unless you understand how it's evolved because it's a very, very old trait. It's a change in what the animal's like as it goes through time. So you could imagine that it's just like development: it's a program process with a nice, well oiled machinery of genes that make the right thing happen in the right place at the right time. What the evolutionary approach tells us about ageing is that it's not like that. It's a much more haphazard process because no genes have evolved to cause damage, decline and death. Rather, it's happening as a side effect of other things. Actually, what it's a side effect of is the inability of natural selection to control what happens in later life. So, in brief, even if you're dealing with an animal that's potentially immortal, it is, nonetheless, going to die because of the impact of extrinsic hazard: disease, predation, accidents and so on. So as the cohort goes through life, depending how hazardous the environment is, its numbers will go down. And if you have mutations that affect the late part of that life span - I mean more individuals will live to be young than will live to be old. So natural selection will be much more effective in controlling the kinds of things that happen to young animals than the kinds of things that happen to old ones. And given that nasty mutations that affect the late part of the life span could creep into the population because natural selection is relatively powerless to do anything about them. I think knowing that haphazard nature of ageing and the fact that it's a side effect of other things is quite useful when thinking about its mechanisms.

SHANE HUNTINGTON
So, in that sense, ageing isn't an advantage in some species for population control or anything of that effect. It is, as you say, just a side effect. 

LINDA PARTRIDGE
Early ideas about ageing were very much of the kind that you described; that it was somehow good for the species; maybe having turnover enables natural selection to act more quickly. One suggestion was that it rids the species of older, worn out individuals - which is, of course, a circular argument, but there were a number of arguments of that kind.  Perhaps it's good for the group in some way. Working through the proper population genetics of that compared with the selection on individuals for reproductive success, these are very weak evolutionary forces. We do see ageing in nature. It's not an artefact of captivity or westernised human societies. And definitely, the overwhelming selective force is for individuals to survive and reproduce. So it really is something of an evolutionary paradox that ageing takes such different rates and can evolve by natural selection, until you understand that it's evolving just as a side effect, not because it's of any benefit, either to individuals or to the groups that they live in.

SHANE HUNTINGTON
I'm Shane Huntington. My guest today is Dame Linda Partridge. We're talking about the science of ageing here on Up Close, coming to you from the University of Melbourne, Australia. When you look at some of the nastier aspects of ageing, such as Alzheimer's and dementia, how do you go about using the investigations of the fruit fly in your laboratory to look at these particular problems?

LINDA PARTRIDGE
Because interventions like improved diet or single gene mutations can produce this very broad spectrum improvement just in natural ageing related health people have become very interested in examining the way in which they interact with specific genetic models of ageing related disease. And I think, probably, most of the work - and, certainly, the most informative work there has been done on neurodegenerative disease. So what people usually do is to express in their animal model a toxic protein that's associated with a particular form of human neurodegeneration. So, in our case, that's actually Alzheimer's disease. And we've looked, particularly, at two proteins called abeta and tau, which are heavily implicated in the development of Alzheimer's disease. We've looked at how the clearance is affected by the ageing process itself, because Alzheimer's is, predominantly, a disease of ageing. It's a sporadic disease that comes on with age. We've looked at how these mutants in insulin signalling affect the production in the clearance of these toxic proteins. It turns out that there are quite strong interactions. We're by no means the only people to have found this. It's also been found for the kinds of proteins that cause Parkinson's and Huntington's disease. The ability of the nerve cells to clear these proteins gets worse with age. Somehow, what these ageing pathways are doing is keeping the cells able to keep clear of these proteins for longer. Part of it seems to be that they produce less of them by mechanisms that aren't really understood. But also the various cellular clearance mechanisms - just the mechanisms that the cell normally uses to get rid of toxic rubbish - seem to be increased in intensity by the presence of the mutations that extend life span. So, of course, there's a lot of interest in understanding the exact mechanisms of that at the moment and, potentially, manipulating it, pharmacologically, to prevent neurodegeneration. 

SHANE HUNTINGTON
When you look at the fruit fly how do you determine if it has some sort of mental disorder?

LINDA PARTRIDGE
How do you know if your fly is demented? Good question. In various ways - behaviourally: simply exploiting the natural behaviour of the animal. Flies like to go upwards. If you accidentally take the bung out of the tube they're living in they will end up on the ceiling, and you can test their ability to climb fairly easily by bunging them down to the bottom of a climbing apparatus and seeing how long it takes them to get to the top. We can show the toxic proteins affect that. we can do electrophysiology. And we can actually measure, functionally, how long a neuronal circuit takes to transmit a nerve impulse through it; for instance, from the eyes to the muscles for the escape response. And again, we can show that these toxic proteins impair that. Sometimes we can show that nerve cells are actually lost, that they die as a consequence of the presence of the protein. So there are a number of different readouts that we can use. 

SHANE HUNTINGTON
Now, with all this information is it likely, in the near future, we'll be able to develop a drug that allows us to age more healthily and in a more, I guess, enjoyable way? Or are we all just going to have to deal with caloric restriction in some fashion?

LINDA PARTRIDGE
Obviously, that's one of the main preoccupations of the whole research field at the moment. And there's been one interesting proof of principle, at least, which is a drug called rapamycin, which is already licensed for human use as a cancer/chemo therapeutic to prevent restenosis after surgery for arterial disease and also is an immunosuppressant. Those are its licensed uses. What it actually does is to tamp down the activity of one of the molecules in this nutrient sensing network - not surprisingly, called target of rapamycin, or TOR. It's involved in sensing amino acids and energy status. It turns out that if you feed mice rapamycin it makes them live longer. Rapamycin is turning out to have a much broader therapeutic range than anyone supposed. So, for instance, it's effective in some of these animal models of neurodegeneration that I mentioned - the toxic protein models - and it also seems to tickle up the immune system of older animals so that they become more responsive, for instance, to vaccination against influenza. So I think some of this progress is going to happen in that kind of way, by broadening the therapeutic range of existing drugs. But we're probably also going to need some new ones.

SHANE HUNTINGTON
Do you see a significant set of side effects for such a longevity pill, if you will?

LINDA PARTRIDGE
Well, rapamycin, for instance, I wouldn't recommend anybody to rush off to their doctor and start taking because it is an immunosuppressant; although we don't know what the relative doses that are required for immunosuppression and extension of life span at this point, and it also impairs wound healing. So although it's used to prevent rejection after transplant, it's recommended for use only after the wound has healed because, otherwise, it will impair healing. So, obviously, one doesn't want those side effects. And part of the research effort at the moment is trying to understand exactly how we can modulate the activity of the signalling network to maximise the health benefits and to minimise the side effects. And certainly, there are some potential targets at the moment, so to speak, downstream of TOR in [signalling cascade] that might be more promising; that might shed some of these undesirable side effects but maintain the benefits. I think that's just a matter for research at the moment. We don't know.

SHANE HUNTINGTON
We all know our chronological age, but if we were to head into a doctor's surgery and ask what our biological age is what sort of thing would they be measuring and what would that actually mean to us?

LINDA PARTRIDGE
It's a very interesting question. Can we make a battery of measurements that will tell us how long we've got? Certainly, there are some overall predictors, but there's a very wide range of variation on all of them. They're not particularly strong predictors. They're just an average difference between people. I mean the sorts of things that doctors look at are pretty good. If one looks at blood - looking at inflammatory markers, cholesterol, any indication of diabetes - these are very important health indices generally. I think a number of them are just being used already in treatment of patients. We don't have the list of 10 that we can measure and tell you if you've got exactly 15 years to go. We're not at that stage yet.

SHANE HUNTINGTON
Linda, when we're talking about dietary restriction what are the actual mechanisms involved that lead from that point to us ageing better and longer?

LINDA PARTRIDGE
We don't have a complete answer to that question, although we know some things. I mean one obvious possibility - because if your dietarily restrict an animal it loses fat - is that somehow the presence of fat itself is bad for health. And fat isn't just a storage tissue, it's extremely metabolically active. It sends out all kinds of chemical messengers, some of which are to do with signalling to the appetite regulating system; but some of them may be harmful. So part of it may be simply having less fat. It's not clear whether or not that's a really important player or not at the moment, but it may be. The other thing is that it seems to alert systems that, basically, defend cells against toxins. So the whole cellular stress resistance, toxin defence machinery seems to be out-regulated. It may be that that's partly protective against ageing. And also, just having few nutrients around may stop the stimulation of processes that are otherwise harmful; so the kinds of cell growth and proliferation that could eventually, for instance, go over into atherosclerosis, which is, basically, an overgrowth disease - as is cancer. So it may well not just be one single mechanism. It could be quite a lot of different things. We're beginning to understand what, at least, some of them are.

SHANE HUNTINGTON
Linda, if we can take out a single gene or a couple of genes and get such incredible biological advantage why hasn't the evolutionary process just eliminated these over the various centuries we've been in existence?

LINDA PARTRIDGE
I think that's a really interesting question. It was one of the reasons why, at first, I found it really very surprising that removing a gene can improve an animal's health during ageing. I think it goes like this: over evolutionary history humans and other animals have, mainly, faced the prospect of starvation, not of having to maintain health in the presence of a rich food supply and at relatively low levels of exercise. I think what we're looking at, in both laboratory animals and westernised humans, is a situation that hasn't been seen before in evolution. We're, largely, protected against infectious diseases. We have an abundant and very high quality food supply. We don't have to fight or run around much to get what we need or to find mates or anything else. Essentially, it's a very highly protected environment with an almost zero risk of food shortage or starvation - at least in westernised societies, of course, which is what we're talking about. So I think the animal models are there for a good model for humans in this situation; which is something that evolution hasn't seen before, and it is throwing up the kinds of health problems that wouldn't have occurred in animals in their natural environment. I think that's why taking out genes that were there, predominantly, to do with avoiding starvation in the past can be beneficial in the presence of a high level of nutrition and not very many ways of burning it off.

SHANE HUNTINGTON
Professor Dame Linda Partridge, Director of the University College London Institute of Healthy Ageing, and Founding Director of the new Max Planck Institute for Biology of Ageing in Cologne.  Thank you for being our guest on Up Close today and talking about the science of ageing.

LINDA PARTRIDGE
It's been a great pleasure. Thank you very much for inviting me.

SHANE HUNTINGTON
Relevant links, a full transcript and more info on this episode can be found at our website at www.upclose.unimelb.edu.au. Up Close is a production of the University of Melbourne, Australia. This episode was recorded on 17 July 2012. Our producers for this episode were Kelvin Param and Eric van Bemmel. Associate Producer, Dyani Lewis; Audio Engineer Gavin Nebauer. Up Close is created by Eric van Bemmel and Kelvin Param. I'm Shane Huntington. Until next time, goodbye. 

VOICEOVER
You've been listening to Up Close. We're also on Twitter and Facebook. For more info visit www.upclose.unimelb.edu.au. Copyright 2012, the University of Melbourne. 


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