Pages

Saturday, 16 October 2010

The End of Age by Tom Kirkwood - Reith Lectures 2001 - Lecture 1

my highlights from the Reith Lectures 2001 by Prof. Tom Kirkwood. Lecture 1 - Brave Old World. Listen to the 30 minute lecture plus 15 minutes of questions. Printable version.

Never in human history has a population so wilfully and deliberately defied nature as has the present generation. How have we defied it? We have survived. Our unprecedented survival has produced a revolution in longevity which is shaking the foundations of societies around the world and profoundly altering our attitudes to life and death.


At the same time, science has made hitherto undreamed-of advances in human biology. The explosive force of these two revolutions coming together lies at the heart of my series of Reith Lectures, as it has been at the heart of my work. Science has new things to tell us about the process of ageing. 


We know now that ageing is neither inevitable nor necessary.


Life expectancy at the start of the 19th century was scarcely forty years. Some of course lived to a good old age but they were a distinct minority.


Life expectancy in the United Kingdom today is around 75 years for a man and nearly 80 years for a woman, and it is still getting longer. 


Over the course of the last half-century, life expectancy has continued to increase steadily by two years each decade. It is almost as if for every decade we have lived, we have gained an extra 20% free.


The real calculations are more complicated than this because the figures I have given are for life expectancy at birth. Working out how our individual expectation of life has changed must take account not only of changes in death rates but also how long we have lived already. Nevertheless, it is striking that it is the death rates of the older age groups that are presently showing the greatest declines. 


It is these older age groups - those over 85 years - who now constitute the fastest growing segment of the population.


A phrase often used to describe what is happening is "demographic change". This dry expression masks the greatest triumph that our species has achieved. I emphasise the word triumph because there are far too many people who like to dwell on the dangers inherent in the longevity revolution without celebrating the progress that has opened these new horizons. 


The demographic change has two causes, both of which are reasons for joy. Firstly, people are living longer on the average than at any time in human history. Secondly, birth rates are tumbling across much of the planet. Because fewer children are dying, parents no longer need to raise large families as insurance against child mortality. These two factors - longer lives and smaller families - are shifting the balance of the generations. They are clear signals of our success in taming the age-old scourge of premature, preventable death. 


we cherish extraordinarily negative stereotypes of the ageing process. The stereotypes have, if anything, grown more negative as life expectancy has increased. Survival to old age is less of an achievement and as life has become more secure, the inevitability of eventual ageing seems more of an affront. 


The technologies to enhance survival - vaccines, antibiotics, water purification systems, electricity, and so on - are at hand and require only effective implementation. 


Taking the human race as a whole, just 1% of the world's population was aged 65 and above a century ago. This figure has already risen seven-fold and will rise to around 20% by the middle of the 21st century. Already in the UK today, 85% of newborns can expect to celebrate their 65th birthday. And those now reaching 65 can expect to survive 16 more years if they are a man, or 19 years if they are a woman. 


The starkest feature of ageing - its hallmark, in fact - is that the risk of falling ill and dying increases inexorably as we get older. This unwelcome principle was first cast into mathematical form in 1825 by Benjamin Gompertz, a pioneer of actuarial science. What Gompertz found was that, like compound interest, adult mortality rates increase exponentially with age. In effect, your risk of dying doubles with every eight additional years that you live.


The medical term to describe the change from a pattern of mortality dominated by acute infectious disease to a pattern in which the chronic degenerative diseases play the major role is the 'epidemiological transition'. Linked to this is the idea of 'mortality substitution'.

Put bluntly, mortality substitution means that you have to die of something. 



If you are spared early death from infections like tuberculosis and typhoid, you fall prey instead to conditions like heart disease, cancer or stroke. Not only does ageing make each of these diseases more likely individually, but you are also more likely to experience a multiplicity of conditions. Many diseases, disabilities or just plain causes of frailty, like thinning bones, weakening muscles, and diminishment of the senses, are intimately linked to the ageing process. 


When we speak loosely of a person dying of 'old age' we have in mind the notion of multiple system failure. The actual cause of death may be quite specific but if it had not been this particular cause today, it would have been something else tomorrow. It is the idea that this intrinsic deterioration is something fixed or immutable - to be revealed more clearly as we peel away one preventable cause of death after another - that has come to be seen in a new and questioning light. 


The new realisation is that science no longer dictates that our bodies have to wear themselves out and die according to some preordained plan.



The commonest misconceptions about the ageing process are that we age because in some fundamental sense we cannot survive for longer, or that we are programmed to die because this is necessary to make way for the next generation. Neither of these ideas is correct. 

The glum fatalism that says that we cannot hold ourselves together for longer is contradicted by the existence of organisms that manage the amazing feat of living indefinitely without intrinsic deterioration. Sea anemones and freshwater hydra are examples of species that show no signs of ageing. There are also several species of fish and giant tortoise that live considerably longer than us, and which age much more slowly. 



The second misconception - that we are programmed to die - is remarkably tenacious. We seem to be psychologically tuned to seek a purpose in the biology of ageing, but this tuning leads us astray.


We now understand that our bodies are not programmed with some unavoidable sell-by date; we are not programmed to die. 


the more we learn about how we age, the more we come to realise that we are programmed for survival. It is by understanding why this programming falls short of allowing us to survive indefinitely that we may learn deep lessons that we can turn to our advantage. 


The lie to the suggestion that we must limit our survival in order to make way for the next generation is that it is only in the last few human generations that survival into old age has been anything other than a rarity.


Once we relinquish the idea of a programmed death, we can begin to make better sense of our ageing. We do this by taking a fresh look at the fact that our ancestors lived short lives and by asking ourselves, in those circumstances, how much effort should their bodies have directed at maintenance and repair. 


The human body is astonishingly well programmed to cope with a huge variety of challenges to its integrity on a daily basis. Many of these challenges are at the sub-microscopic level and the body's defences involves an extensive repertoire of cellular and molecular protection systems. 


The price we pay for these protection systems is that they require energy, and this is often in limited supply. When survival is uncertain because of the many hazards of the environment it is better not to squander effort on a greater level of bodily maintenance than is needed, but to attend instead to the all-important biological imperative of begetting and raising offspring. 


If, to a rough approximation, the average life span of our ancestors was around 35 years and only a tiny percentage survived to 70 years, then a body which held itself together for three score years and ten would do just fine. 


When we understand that we age because our ancestral genes placed limited priority on long-term maintenance and repair, we get some rather clear insights into the processes that lead to the frailty and diseases of old age. 


The first and most encouraging message is that as soon as we recognise that we are programmed not to die, but to survive, we can see that the ageing process is malleable. Ageing comes about through the gradual build-up of unrepaired faults in the cells and tissues of our bodies as we live our lives, not as a result of some active mechanism for death and destruction. If we can discover the nature of these faults, we can hope to slow their accumulation. 


There is good reason to believe that the improved health and survival of older people today at least partly reflects the fact that the kinder conditions of present-day living have alleviated some of the burden of faults. If we can understand the protection systems with which we are already endowed, and enhance their performance, we may be able to do much better. 


 we should guard against unrealistic expectations of a 'quick fix'. Ageing is a complicated process with multiple causes affecting every organ of the body.


We have seen already how frustratingly slow and difficult it has been to take the sting from heart disease, cancer and stroke. To get excited about potential 'fountains of youth' and life spans of 200 years and more is not only to indulge in fanciful and unrealistic speculation, it also shows what a long way we have still to go to get the challenges of the longevity revolution into proper perspective. 


The paradox about the longevity revolution, and its greatest inherent danger, is that we find ourselves in the present situation without having thought very much, until recently, about the kind of world we are creating. It is easy to win support for saving lives. Davy's safety lamp, Jenner's triumph of inoculation against smallpox, Fleming's discovery of penicillin - these are unquestionable gains. It is easy to win support for the fight against a killing or disabling disease, as can be seen from the generous public support for so many disease-focussed medical research charities.


 The declines in mortality rates of older people are forcing the forecasts of future life expectancy to be revised upwards. Should we be pleased or depressed? Surely we should be pleased, but it is astonishing how poorly this news is sometimes received. 


Just last summer, an article presenting new forecasts of even longer life spans in the most affluent countries was published in one of the world's leading science journals. A brief editorial trailer for this report announced glumly that the situation was "even worse than expected". I wonder just how old was the member of the editorial team who penned that piece? 


One cannot pretend for a moment that there is not a lot that is disagreeable about getting older. This is all the more reason why we should direct unprecedented attention to ensuring that all reasonable effort be directed at removing the obstacles to enjoyment of the later years of life. This is not mere altruism nor a pat on the back for our older fellow citizens, put, like the old donkey, out to grass. 


First and foremost it is a recognition of that most fundamental of human rights, respect for all individuals as equals. 


It is absolutely staggering not only how much prejudice exists against age but also how unaware of it we remain. On a regular basis we read, hear or ourselves make flippant, jokey or negative remarks about the state of being old. 'Grumpy old', 'silly old', 'boring old', 'dirty old' - the linkages are so familiar that we fail to notice what we are doing. 


If we were suddenly to acquire the same sensitivity to ageism that we have to racism and sexism, we would be in for a shock. But do we not realise that we will all grow old? Can we not celebrate the fact that this privilege has been won for us by our collective ingenuity? Do we not realise that the best prospect for our own well-being in old age is to build a world in which equality, independence and active participation of all generations are positively encouraged? 


New scientific understanding means that we can never think of ageing in the same way again. Our longer lives are carrying us into new territory for which we need to plan and prepare. We cannot afford to be complacent. If we ignore the implications of the longevity revolution …. 


If we fail to plan for the radically different world that will soon surround us, then crisis will be upon us and our bright dreams of a brave old world will surely fade and die. 

Thursday, 14 October 2010

Why dietary restriction substantially increases longevity in animal models but won’t in humans

reposted from: sciencedirect via http://ageaction.ncl.ac.uk/AgeAction_book.pdf



 by John P. Phelan and Michael R. Rose
Abstract
Caloric restriction (CR) extends maximum longevity and slows aging in mice, rats, and numerous non-mammalian taxa. The apparent generality of the longevity-increasing effects of CR has prompted speculation that similar results could be obtained in humans. Longevity, however, is not a trait that exists in a vacuum; it evolves as part of a life history and the physiological mechanisms that determine longevity are undoubtedly complex. Longevity is intertwined with reproduction and there is a cost to reproduction. The impact of this cost on longevity can be age-independent or age-dependent. Given the complexity of the physiology underlying reproductive costs and other mechanisms affecting life history, it is difficult to construct a simple model for the relationship between the particulars of the physiology involved and patterns of mortality. Consequently, we develop a hypothesis-neutral model describing the relationship between diet and longevity. Applying this general model to the special case of human longevity and diet indicates that the benefits of caloric restriction in humans would be quantitatively small.

Processed carbohydrates may increase health risks more than saturated fat does

reposted from: Scientific American, May 2010 (download full article) - Original Source (subscription required)

Carbs against Cardio 
More data that refined carbohydrates, not fats, threaten the heart
BY MELINDA WENNER MOYER

Processed carbohydrates, which many Americans eat today in place of saturated fat, may increase the risk of obesity, diabetes and heart disease more than fat does.

In March 2010 the American Journal of Clinical Nutrition published a meta-analysis—combines data from several studies—compared the reported daily food intake of nearly 350,000 people against their risk of de-veloping cardiovascular disease over a period of five to 23 years. The analysis, overseen by Ronald M. Krauss, director of atherosclerosis research at the Children’s Hospital Oakland Research Institute, found no association between the amount of saturated fat consumed and the risk of heart disease.

Although saturated fat boosts blood levels of “bad” LDL cholesterol, it also increases “good” HDL cholesterol.

Saturated fats are not so bad; they indicate that carbohydrates could be worse.

A 1997 study Krauss co-authored in the Journal of the American Medical Association evaluated 65,000 women and found that the quintile of women who ate the most easily digestible and readily absorbed carbohydrates—that is, those with the highest glycemic index—were 47 percent more likely to acquire type 2 diabetes than those in the quintile with the lowest average glycemic-index score. (The amount of fat the women ate did not affect diabetes risk.) And a 2007 Dutch study of 15,000 women published in the Journal of the American College of Cardiology found that women who were overweight and in the quartile that consumed meals with the highest average glycemic load, a metric that incorporates portion size, were 79 percent more likely to develop coronary vascular disease than overweight women in the lowest quartile.

These trends may be explained in part by the yo-yo effects that high glycemic-index carbohydrates have on blood glucose, which can stimulate fat production and inflammation, increase overall caloric intake and lower insulin sensitivity, says David Ludwig, director of the obesity program at Children’s Hospital Boston.

Right now, Post explains, the agency’s main message to Americans is to limit overall calorie intake, irrespective of the source.

“We’re finding that messages to consumers need to be short and simple and to the point,” he says. 

Nobody is advocating that people start gorging themselves on saturated fats, tempting as that may sound. Some monounsaturated and polyunsaturated fats, such as those found in fish and olive oil, can protect against heart disease. What is more, some high-fiber carbohydrates are unquestionably good for the body. But saturated fats may ultimately be neutral compared with processed carbs and sugars such as those found in cereals, breads, pasta and cookies.

“If you reduce saturated fat and replace it with high glycemic-index carbohydrates, you may not only not get benefits—you might actually produce harm,” Ludwig argues. The next time you eat a piece of buttered toast, he says, consider that “butter is actually the more healthful component.”

Tuesday, 12 October 2010

The truth about diet pills

reposted from:

We all want a quick fix for our weight problems. But are slimming pills really the answer?
Dr Porter’s verdict: Alli has proved disappointing; Capsiplex: the four clinical studies on this diet aid are too small, and too short, to be taken seriously; Slimweight patch: pseudoscience at its best
An effective slimming pill has been the holy grail of the pharmaceutical industry for decades, but despite spending billions of pounds on the quest, it has proved elusive. Most of the drugs developed over the past 40 years have been withdrawn, and few doctors rate the only licensed version still available in the UK (orlistat, which works by impairing absorption of fat). So why are pharmacists, health-food shops and online retailers doing such a brisk trade in over-the-counter slimming aids?
I wish I could report that the nutriceutical industry had pipped the pharma giants to the post, but the truth is far more mundane and the fact that people in the UK spend an estimated £75 million a year on this type of slimming pill simply reflects a triumph of marketing over common sense. The wilder the claim, the more popular the product seems to be. Capsiplex — available online and from high street chemists and health-food shops — is a case in point. It uses a “proprietary patented matrix of excipients and coatings” to deliver capsicum extract, which the manufacturers claim will boost your energy levels and help you to “burn 12 times more calories”. All for the sum of £29.99 for a month’s supply, although price wouldn’t seem to be an issue as suppliers were reported to have sold out within three days of the UK launch earlier this year.
Or how about the Slimweight patch (available online) that uses “transdermal technology ... previously found only in science fiction” to deliver a mix of ingredients, including seaweed and guarana, to help you to effortlessly lose up to 4lb a week? Yours for only £19.86 a month.
What nutriceutical slimming aids such as Capsiplex and Slimweight have in common is that they are based on some real science. Capsicum extract — the natural ingredient that gives chillies and peppers their kick — has been shown by researchers to boost the body’s metabolism temporarily, but that doesn’t necessarily translate into useful benefits in the real world, or in the longer term.
The four clinical studies trumpeted on Capsiplex are too small, and too short, to be taken seriously. The largest to be listed on the website monitored 14 volunteers over two weeks, the smallest followed only six subjects over eight days.
Suffice to say that I could not find any quality research suggesting that Capsiplex has anywhere near the potential to meet the promise on the website that “now you can lose all the weight you want and keep it off”. And I will happily eat my words if such evidence does exist, along with the entire Saturday edition of The Times in which it appears.
The Slimweight patch stretches its scientific credentials even farther. By bombarding prospective purchasers with references to cutting-edge patch technology that results in “no side-effects due to transdermal admission methods”, the manufacturers seem to be hoping that they will be so impressed that they won’t notice the dearth of decent data to back up the slimming claims. Pseudoscience at its best.
It seems unfair to mention orlistat (Alli), the only fully licensed slimming aid, in the same breath as nutriceuticals, but it is flawed too. It may have taken more than a decade of research and development to bring to market, and gained the blessing of the National Institute for Health and Clinical Excellence, but my experiences suggest that it’s not all it’s been cracked up to be.
Orlistat works by blocking the action of enzymes in the bowel — lipases — that break down fats into their constituent components so that they can be more easily absorbed. The net result is a significant reduction in fat absorption with about 25 per cent to 35 per cent of the fat content of a meal that would otherwise have been absorbed passing straight through the bowel, significantly reducing a person’s calorie intake.
Not surprisingly, when combined with a sensible diet and exercise programme, there is good evidence that orlistat speeds up weight loss. Overweight volunteers taking the prescription-only dose (120mg versus the 60mg in over-the-counter Alli) have been shown to lose 2-5kg (4-11 lb) more over a 12-month period than those given dummy versions of the drug.
But, away from the controlled environment of clinical trials, orlistat has proved a disappointment. While it may accelerate short-term weight loss, it doesn’t work in the longer term — most of my patients using it have failed to get anywhere near their target weight, or ended up even heavier after stopping the drug. And there is now a dawning realisation among doctors that surgery (such as gastric banding) is the only truly effective medical intervention for tackling obesity — which is a sad indictment of the profession, the individual and society.
Even if the pharmaceutical industry does find its holy grail — and there are contenders in the pipeline with modes of action ranging from tricking the brain into thinking that the stomach is full, to making eating less enjoyable by impairing smell and taste — slimming drugs are only ever likely to be a useful tool for getting people down to a healthy weight in the short term. The difficult part is keeping them there, and that requires a profound and sustainable change in their diet and lifestyle (the reason, of course, why they were fat in the first place).
Pills are all very well, but unless you take them for ever they strike me as part of the problem rather than the solution.
How can taking a short-term slimming aid help unless it is accompanied by long-term dietary and lifestyle change? Or, to put it another way, could slimming pills make matters worse by encouraging overweight people to have their cake and eat it

Sunday, 10 October 2010

Is science on the brink of creating the elixir of life?

reposted from: Daily Mail

Is science on the brink of creating the elixir of life?

By MICHAEL HANLON Last updated at 5:00 AM on 9th October 2010

Once I had a very odd dinner with an elderly and distinguished scientist who told me how he planned to live for ever - or at least for a very long time indeed. We ate in his beautiful house by the sea in California. Our meal consisted of one bowl of rice each and a glass of water. With this extreme diet, my host said - limiting himself to 800-1,000 calories a day (the average male is recommended to consume 2,500) - he hoped to stave off death for many more decades.

Such a regime was based on the well-established theory that by reducing calorie intake, people can dramatically increase their lifespans. This had been shown, after numerous scientific investigations, to work in animals from fruit flies to mice. Professor Roy Walford, a biologist at UCLA, was 74 years of age when I met him. He had no doubt that extreme calorie restriction would work in people, too. However, despite his punishing diet, he was to die five years later from the auto-immune disorder Lou Gehrig’s disease. Seventy-nine years was a little better than the three score years and ten which have been approximated as the human lot since Biblical times - but his innings only matched the average lifespan for an educated, middle-class white California male of his generation. It is tempting, then, in the light of this story, to write off the theory that by eating the bare minimum we can slow the ageing process. But it seems Professor Walford was probably on to something, even if the fates conspired to ensure that he personally did not benefit from his diet thesis.

For there is a growing scientific consensus that ageing - against which humanity has been battling for millennia - might not be inevitable.


Of course, the quest for eternal youth has been led by charlatans, frauds and snake-oil salesmen through the ages. There is money to be made by promising the Holy Grail - as the questionable claims on the labels of countless anti-ageing beauty products will attest. For centuries, lotions and potions have been touted as elixirs of longevity. These have ranged from products containing monkey glands to injections of minced dog testicles. Unsurprisingly, all have failed. Still, the search continues.

We have been told that exercise, red wine, chocolate, Vitamin C and various cocktails of antioxidants are the answers. The latest elixir claim comes from scientists in Italy, who announced this week that mice given dietary supplements rich in three amino acids (similar to the concoctions favoured by human bodybuilders) lived on average 12 per cent longer than mice fed on ordinary food (see: ScienceLongLife). For humans, this would mean about an extra ten years of life. And yet the world still awaits its first 125-year-old. The record stands at 122 years - achieved by Frenchwoman Jeanne Calment, who died in 1997. But the truth is, charlatans apart, the ageing process may be more amenable to change than was thought.

For a start, life expectancy (the number of years a newborn is predicted to live) is increasing by five hours a day in Britain. This means a baby born in five years’ time should live a year longer than a baby born today. This is, for the most part, simply a result of better healthcare. For evidence we need only look at the first big jump in life expectancy, which took place in the 19th century when infant mortality rates dropped because of improved diets, better medicine and proper sanitation. We haven’t conquered age, it’s just that more and more of us are living to our full potential. But we may now be nearing a surprising breakthrough.

According to a new book, The Youth Pill, by health journalist David Stipp (Amazon.co.uk) with a selection of reviews on his book at DavidStipp.com, in a few decades a number of pills may be available, which will help delay the onset of most serious illnesses by up to ten years. This would give us at least five extra years of healthy old age and allow the 122-year barrier to be breached.

Until recently, those scientists working on increasing the longevity of fruit flies or mice have shied away from making claims that humans could benefit from their work on genetics. But now, as Stipp points out, this attitude seems to be changing; more and more experts now say that human lifespan can be increased - and what’s more, they agree that it would be a good idea.

How we grew old, and why, was a mystery until recently. It was commonly supposed that our bodies simply wore out, like machines. But this wasn’t a good analogy. Unlike most machines, our bodies are equipped with efficient repair systems that keep our cells healthy for decades. In fact, we do not really start to ‘age’ at all until we are into our 20s. So, discovering why these mechanisms stop working as we enter middle and old-age is the key to understanding the ageing process. Ageing is, after all, not entirely inevitable. Several organisms appear to hardly age at all and live for centuries.

Humans are among the longest-lived of all species, but our longevity is exceeded by some giant tortoises which can live for nearly 200 years. Bowhead whales have recently been found, alive and well, with antique harpoons embedded in their skulls which can be dated back to the 1790s. Some of these animals may be more than 300 years old. There is a pattern in all this. Big creatures tend to live longer than small ones. Anything that can fly or swim tends to live longer than animals stuck on the ground. Understanding these differences gives us our first clue as to how ageing works - and to what might be done to delay it.

The evolutionary theory of ageing states that animals age at a rate commensurate to their likely survival time in the wild. Mice age quickly because - being small and feeble - they are likely to be eaten, starve or perish due to cold before too long. Evolution has given the mouse a body that literally lives fast and dies young. It’s full of sex hormones turbocharging its chances of reproducing before it is eaten by predators. It makes little sense for a mouse to be equipped with, say, anti-cancer mechanisms, if the chances are that it will be an owl or cat’s dinner within a year or two.

On the other hand, elephants age slowly because, being big, they are hard to kill. It takes a long time for them to die of starvation and they cope well when times get tough. So elephant bodies have evolved complex DNA repair systems which can keep them going for half a century or more.

Birds also live a long time because, although small, they can fly and thus avoid predators. Bats live longer than mice for the same reason, and porcupines and tortoises are long-lived simply because they make a difficult meal. In each case, their bodies age slowly to make the most of their potential life spans. Still, knowing why we age tells us little about how we age - and even less about what we might be able to do about it. There is growing evidence, however, that the very hormones that enable us to reproduce - those which produce eggs and sperm - may in themselves contribute to the ageing process. ‘Death,’ said one biologist, ‘is the price we pay for sex.’

Advances in DNA analysis - reading the entire genetic codes of organisms - have opened up exciting new areas in ageing research, allowing scientists to pinpoint individual genes which may be be responsible for the breakdown in our bodies over time. Yet the reality is that many of the resulting ‘breakthroughs’ have proved to be dead ends. For decades, ‘free radicals’ (waste chemicals produced by our bodies as by-products of respiration, digestion and the action of muscles) have been suggested as possible drivers of the ageing process.

Big creatures tend to live longer than small ones. Anything that can fly or swim tends to live longer than animals on the ground.

Some scientists have claimed that we should take large quantities of free-radical neutralisers called antioxidants (which include Vitamin C and are best found in fruit and vegetables). Yet Vitamin C, it turns out, may actually increase free-radical damage and very large doses can interfere with the body’s natural repair mechanisms.

It is such contradictions that have led researchers to focus, instead, on calorific restriction. Mice placed on near-starvation diets have seen their life expectancies increase 20-35 per cent. If such results were achievable in humans, the average Briton’s life expectancy would rise to almost 100 - with the potential to carry on to 150. This is precisely what Professor Roy Walford was trying to achieve with his grimly tedious rice and water diet in California. And the truth is that research into whether calorie restriction will greatly extend our lifespans would take decades to reach firm conclusions - simply because we are so much larger than mice.

Even so, research on rodents has uncovered how extreme calorie restriction appears to switch on a genetic mechanism called a stress response. This has evolved to allow animals to survive tough conditions (such as a very hard winter when little food is available). It seems the bodies of mice - and possibly those of humans, too - react to starvation by boosting their repair mechanisms, triggering anti-inflammatory responses which slow the damage done to vital organs as they age.

The problem for humans is that near-starvation is unlikely to catch on. What people are much more likely to turn to are drugs which mimic the effects of extreme calorie restriction, without having to live on lettuce. And such drugs may soon be available. One could be based on the chemical resveratrol which is a plant compound found in red wine. In 2006, Harvard scientist David Sinclair found that this could activate a stress-response gene called Sir2 in mice which extended their lives.

Vast fortunes are being spent by the big drug firms on anti-ageing drugs

The happy fact that the elixir of youth is found in wine was suggested as the possible reason why the French, who eat a lot of supposedly unhealthy meat and cheese, smoke too much and drink a lot of alcohol, have one of the world’s highest life expectancies.

Then, last year, three teams of researchers in the U.S. reported that another chemical which mimics the effects of starvation, called rapamycin, makes mice live longer by suppressing the onset of cancer. The chemical was isolated from a fungus found on Easter Island in the Pacific. Unsurprisingly, the big drug firms are trying to exploit these discoveries. Vast fortunes are being spent on anti-ageing drugs which mimic calorie restriction. The problem, sceptics point out, is that the ageing mechanism in rodents may be quite different to the one in humans.

Therefore, resveratrol and similar chemicals may not prove to be the answer (the same may be true of the Mr Universe protein supplements trumpeted this week). But the likelihood is that, in a few years, pills will be developed that will be able chemically to copy the effects of a near-starvation diet and that may well increase lifespan in humans.

If this happens, what would a world of 130-year-olds be like? Of course, there is a big difference between being a healthy 130-year-old and someone who has spent the last 40 years of their life suffering from dementia. So what about the anti-ageing pioneer Roy Walford? Ironically, his death was caused by a rare disease that is exacerbated, not ameliorated, by a low-calorie diet. But if he was right, then by helping publicise what was once an obscure field of scientific research, his last, hungry years by the Pacific may not have been in vain.