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Hang on for the good old days

A longer life is now a reality. To make it worth living, on the other hand, is the real challenge. Alok Jha reports. BY THE time you finish reading this newspaper, your life expectancy will have gone up by roughly six minutes. This time tomorrow, it will have increased by almost five hours.

A longer life is now a reality. To make it worth living, on the other hand, is the real challenge. Alok Jha reports.

BY THE time you finish reading this newspaper, your life expectancy will have gone up by roughly six minutes. This time tomorrow, it will have increased by almost five hours.

The reason is clear: rapid advances in medicine and biology have been among the biggest achievements of the past century and we are all living longer. Where anyone reaching the age of 60 was considered to be near death’s door at the start of the 20th century, 60 is barely old enough for retirement at the start of the 21st century.

And scientists are still not holding back. Shripad Tuljapurkar, a population studies expert at Stanford University, told a recent meeting of the American Association for the Advancement of Science that as new anti-ageing treatments become available, people will get even older. Soon, the average age of death will jump by a year every year – five times the present rate.

While few would argue that living longer is an attractive idea, the rapid increase in the number of years raises a question: what will life be like for our increasingly elderly population? Is it such a good idea to live for an extra decade if it simply means 10 more years of illness or frailty?

"What we really want is our health expectancy to be as close as possible to our life expectancy, so that we live long and die quickly," says Lorna Layward, a research manager at the charity Research into Ageing. "In other words, we [want to] compress the time we are ill at the end of our lives."

But is that possible? Getting into the specifics of this is difficult because each individual will have different diseases and suffer in a different way. The state of our bones, muscles, hearts, brains and immune systems over time depends on a range of factors, from genetics and the environment we have lived in to the medical care available to us and our level of education. But there is no doubt age is the biggest single risk factor in a host of diseases, from dementia to cancer.

Calculating a person’s chances of good health in old age is therefore tricky. But scientists are finding that, generally, the time we are likely to spend ill at the end of our ever-increasing lives will drop thanks to medical advances and growing awareness of how to stay healthy.

Quality of life is improving for the elderly. "If you look at what a 70-year-old person is doing now versus what a 70-year-old person was doing 50 years ago, it’s totally different," says Arlan Richardson, director of the Barshop Institute for Ageing and Longevity Studies at the University of Texas. "All you’ve got to look at is [the astronaut] John Glenn, who went [into space] when he was 77. Three out of four of my grandparents died before they were 75 years of age, let alone going [into space]."

But most elderly people will have to endure long-term illness, says Ann Bowling, a population scientist at University College London. "Whether it’s cancers or heart disease, they’re not going to go away, but they are becoming more treatable. People are less likely to die from those, but we’re more likely to have to live with them."

Predictions for health expectancy have changed over the past few decades. "In the 1980s, life expectancy was increasing and the best data that we had suggested that for every increased year of life expectancy, a greater fraction was disabled life expectancy," says Richard Suzman, director of the social and behavioural research program at the US National Institute on Ageing. "That led to a pessimistic perception that what we would see was a piling up of chronic illness and related disability; that medical science could extend life but it couldn’t prevent disability or cure it."

But that world view changed suddenly in the early 1990s, after a study by researchers at Duke University, who had been following the health of 20,000 people for almost a decade. They showed that disability among the elderly was dropping at an ever-increasing rate.

Looking at their volunteers in 1994, the Duke researchers had expected a quarter of their volunteers to be disabled if rates had stayed the same as those in 1982. Instead, only 21 per cent of the people were disabled – equivalent to 1.2 million fewer disabled people than forecast. The researchers said this represented a relative decline of almost 15 per cent, most of it thanks to improved education on health risks and better health care.

The slew of drugs and treatments dealing with the problems of age continue to arrive. Researchers in the US are studying the use of anabolic steroids to build up muscle mass, for example. In Britain, Malcolm Jackson, of the University of Liverpool, is looking for drugs that prevent deterioration of muscle mass. Stem cells, the master cells that can grow into any type of tissue, could also help. "The people doing work in that area believe that it will be possible, certainly in disease states, to help replace diseased muscle. It’s not a big step from that to the ageing muscle," says Jackson.

Heart damage could be repaired by stem cells. Understanding how the cells are made will allow the development of treatments to induce a mature heart cell to start dividing, something it would not normally do.

Tim Skerry, a professor of orthopaedic biology at Sheffield University, says that drugs to stop bones wasting away are available. "If you have a fracture because of osteoporosis, you can prevent further bone loss. But by the time you’ve got a fracture, much of your skeleton is already weaker than it should be. So stopping further loss is good, but it’s not the whole answer," he says. Stimulating bone to grow again is the goal. "Current research is going very much in that direction and there are a few drugs that stimulate bone formation."

Arthritis, the result of wear and tear on the joints of the body, causes many long-term problems. Scientists suspect that several genes could be implicated in the development of this and related conditions – how that information will be used to improve life for sufferers is still an open question.

There is good news in other areas, however. Mortality rates with hip fractures are already improving: nowadays, 20 per cent of people die a year after fracturing their hip; 10 years ago, 35 per cent died. As hip-replacements improve, the trauma for the patients (who will be healthier in their old age, anyway, and better able to cope with such surgery) will decrease.

The sticking point to this progress could be the brain. There is no cure for dementia yet and leads are thin on the ground. Laboratory-based techniques for immunising against certain types of brain degeneration, or slowing down the degradation, have worked in animals but not in humans. Carol Brayne, a professor of public health medicine at Cambridge University, believes it is "very unlikely that [any present technique] is going to make an impact on old-age dementia, certainly in the near future and maybe in the longer term".

Richardson has further reservations. "We have people living now who are older than we’ve ever had. The question is whether we’ve done anything about the ageing process or we’re treating diseases more effectively," he says. "People in their 70s are healthier than they were 50 years ago but, on the other hand, I don’t see, unless we do something about ageing, that, 20 years from now, a 70- or an 80-year-old person will be any healthier than they are now."

He argues that quality of life will not improve dramatically until scientists look further at the mechanisms behind, rather than the symptoms of, ageing. "Until the past five years, there was not a lot of interest in putting money into ageing research – one reason was the belief that you couldn’t do anything about it. The other thing is if you do slow down the ageing process, maybe that’ll be bad because we’ll just have more people in nursing homes."

But the tide is turning. Studies into genetic factors behind ageing have shown that no single gene is responsible. Rather, several parts of our genome have been linked to the cumulative effect that makes us age. Restrict how much an animal eats, for example, and it will live longer. In lab experiments, rats on calorie-restricted diets were found to be physiologically younger, got diseases later in life and had less severe cases. "From the rodent models that have been looked at, the increase in life span is usually in the range of 15 to 30 per cent maximum," says Richardson.

Cutting calories is thought to trigger a switch in an animal’s behaviour from normal to a state of stasis, in which growth and ageing are temporarily put on hold. When food becomes available again, the animal’s behaviour switches back.

Richardson predicts that understanding the mechanisms behind calorie restriction, and other genetic reasons for ageing, could be used within two decades to give people several extra healthy years of life. He argues that none of the illnesses related to ageing should be inevitable and that achieving longer healthy life — an average of 100 or more — is all about good maintenance.

"Possibly you could stop ageing in its tracks," he says. Start with a high-quality body (eating your greens, not smoking and doing lots of exercise in your younger days) and you can keep it going for longer with due care and attention. "It’s like the difference between a Rolls-Royce and a cheap car."

 

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