MUCH of the news around the science of life-extension seems futuristic and sensational enough to be taken with a pinch of salt – overblown talk of living for 1,000 years, or cybernetic immortality. But when Sue Armstrong, an Edinburgh-based science author with decades of experience, says that there are drugs already on trial that could slow the process of ageing, it’s worth paying attention. When she talks of increasing the healthspan, rather than the lifespan, of the population, it’s clear she’s describing a serious endeavour.

Armstrong has spent the last few years travelling the world meeting and interviewing the scientists at the forefront of ageing research for her new book, Borrowed Time: The Science Of How And Why We Age, and what she has brought back not only provides hope that an increased healthspan might be available to us all, but that there are things we can all do – and not just popping pills – to give us the biggest chance at a long life, possibly even as much as 120 years.

The research she writes about is happening at a time when, in some wealthy countries, lifespan is no longer increasing but has stalled. Last year life expectancy dropped in Scotland for the first time in 35 years. A report last week revealed that the gap in life expectancy, between rich and poor women in England was widening. One of the big issues of our times is health justice, and Armstrong, having spent years working as a foreign correspondent in Africa reporting on the Aids pandemic, is familiar with the way drug availability can drive health inequality. When she first started researching the book, the narcissism among the wackier life extension gurus almost put her off. “I see how very easy it is to have a divided world – the haves and have nots. I felt that the search from extreme longevity was an elite endeavour.”

Nevertheless, the issue of how and why we age fascinated her. Armstrong, who will be talking in an event at the Edinburgh Science Festival next month, is a dynamic and energetic seventy years old. Her mother died at the age of 97, after having, she says, a “miserable last five years”, her father at the age of 87 from cancer. Genes, at least, seem to have her set up for a good few more decades.

But at 70, she is already well into her post-reproductive phase, a stage in which, according to some of the theory in her book, in evolutionary terms, our bodies are disposable. We have evolved to thrive until we produce the next generation – after that, our bodies, are essentially no longer really needed. Her bodily disposability doesn’t seem to bother her. “Physiologically,” she says, “you may rail against the infirmities of your body, but psychologically there is still a hell of a lot worth living for.”

One of the questions she starts with is what, even, ageing is? It would be neat, of course, if she came back from her explorations in the world of gerontology with some story of ageing as a single process in which we could intervene, but inevitably it's not as simple. However, what emerged from her survey of the science was that ageing can really be thought of as a disease, or as one scientist puts it in her book “a disease super-syndrome”.

Armstrong didn’t used to think of ageing as a disease – the idea was one she resisted. However, the journey she has gone on has shown to her that a lot of the diseases associated with old age are not isolated. “One of the key things that came out of my research,” she says, “is that all of the diseases associated with ageing have common roots – it’s the process itself.”

The problem with the way, therefore, that we currently deal with these diseases is that we are coming late to the game, only responding to the process when someone has heart failure, diabetes, cancer or dementia. But it’s possible that all these diseases could be treated much earlier, at their roots, potentially relieving some of the care burden and later costs. “That’s the thesis and the goal of gerontology,” she says.

Ageing is also not, says Armstrong, just a matter, as is often thought of wear and tear. Rather, more often, it involves cells getting out of control. “Cancer,” says Armstrong, “is just overblown life, as opposed to a disease that’s come from outside. And ageing, on some levels, is the same. One of the scientists I spoke to, David Gems, said it might actually be life not stopping when it should. Hyperfunction, he called it.”

The view is supported by the fact that, she says, “many of the classic pathologies of old age involve deranged and runaway growth or over enlargement of cells rather than decline and decay. This is the case with cancer and cardiovascular disease.”

Among the features of ageing responsible for a lot of the trouble is the way what are called senescent cells accumulate. These are cells that have stopped dividing but not died. Cell senescence is a necessary part of the anti-cancer mechanism. As Armstrong puts it, "Dividing cells have a natural cut-off point to guard against mistakes that might have crept into the cells during constant division from causing cancer.” Without senescence, also, wounds would not heal. But the problem with these cells is that, as we get older, they tend to stick around too long, accumulate in the wrong places, and also send out messages that trigger inflammation, which is itself one of the defining features of ageing. Inflammation increases so much as we age that it has even been dubbed “inflammaging”.

As it happens, since the publication of Armstrong’s book a key breakthrough has been made in this area in Scotland, at the University Of Edinburgh, by a team led by Professor Wendy Bickmore, director of the Medical Research Council Human Genetics Unit. Bickmore is new to the field of geroscience. She came to it almost by accident because she has always been interested in the way the genome is packaged inside cells, and her office happened to be next to that of a cancer researcher whose interest was in senescence.

Bickmore’s team devised a way to stop cells from growing, effectively making them senesce, and discovered that when they did, they turned on an “inflammatory programme”. “Why do they do that?” she says. “In the short term it is a really good thing for stopping cancer progression. It also stops the surrounding cells growing as well - and then the immune system can come in and clear up the bad cells. But in the long term, if this persists, it can be really bad. And in the context of ageing it’s thought that a lot of the associated damage and disease comes from this persistent inflammatory programme that senescent cells send out.”

Their breakthrough was the discovery of how, in the cell, those inflammation messages were controlled. Could such knowledge be the first step along the road to an anti-ageing pill? Bickmore urges caution. “I wouldn’t say anti-ageing pill. The research opens up the possibility of finding ways to intervene to tune down that damage, which might have some benefit. But you don’t want to stop all inflammation – you need inflammation to heal wounds deal with infections.”

But there are, in fact, already in-use drugs that appear to affect ageing. Among them, for instance, is Metformin, a commonly used drug for Type II diabetes, which has been shown to extend the lifespan and improve the health of rats and mice, and also looks to do the same in humans. The drug’s mechanism is still being researched, but it appears to enhance the activity of an enzyme within cells that inhibits the process of burning glucose for energy. Armstrong observes that the impact of this is very like the “effects of calorie restriction” diet – one of the more extreme lifestyle methods of tackling ageing encountered in her book.

Currently, Metformin is set to be the focus of a huge ageing-related clinical trial in the United States. “The thing about Metformin,” says Armstrong, “is that it’s so widely used that it already has a safety record. It hasn’t got to go through the whole process of approval.” Another commonly-used set of drugs, statins, have been found to slow the deterioration of the immune system that is part of ageing.

Although Armstrong tells a story about some of the ways in which drugs might be used to tackle ageing, in fact, her stronger message lies in the way we lifestyle really does have an impact on ageing. For instance, we know that a sedentary lifestyle isn’t good for us, but she explains why that is the case. Inflammation is a key factor in ageing and when we sit down and our muscles are resting, they release, says Armstrong, pro-inflammatory messages, while active muscles send out anti-inflammatory messages to keep the balance.

Armstrong talked to Janet Lord, director of the Institute of Inflammation and Ageing in Birmingham, who said, “That’s why exercise is so good for you – and why it’s bad to sit for any length of time. There are now independent studies that show that how much time you spend sedentary is an independent risk factor for ill health. So you can go out, as I do, for my morning run. But if I then sit for ten hours, I might as well not have bothered.” Armed with this knowledge, Lord had shifted to using a standing desk.

Meanwhile, research is showing that eating fewer calories could indeed help fight ageing. Armstrong features a chapter on calorie restriction advocates who live on a very low calorie diet, in the hope – partly inspired by experiments in calorie restriction in rodents which showed increased longevity – that it will extend their lives. However, she says, “more recent research in monkeys showed that you get as good a bang for your buck not by extreme dieting by a more measured approach.”

Even Alzheimer’s, Armstrong finds, is starting to be perceived as a symptom of a wider system breakdown. Pioneering neurologist, Dale Bredesen, for instance, describes neurodegenerative diseases as “systemic problems with neurological read-outs… not isolated brain problems.” Bredesen and his colleagues are advocates of a holistic approach to the disease. Armstrong lists, for instance, his treatments as including dietary instructions, vitamin and dietary supplements, seven to eight hours’ sleep per night, periods of fasting between meals and yoga and meditation.

Some of the lifestyle messages coming out of this current research will come as a surprise to anyone who has been aware of current health advice. But as Armstrong puts it, it can be empowering to know the reasons why our bodies are reacting as they do. “I now know,” she says, “why it’s good not to be sedentary. Or why it’s good to eat without stress around you – because stress can weaken the walls of your gut and then you get the gut bacteria leaking into the bloodstream and contributing to the inflammation. It helps to know the science behind a lot of the common messages.”

Sue Armstrong will be speaking at the Edinburgh Science Festival at 8pm on April 14.

Youth Hacks

How to keep brain and body young

Naveed Sattar, professor of metabolic medicine at the University of Glasgow: “Sadly, the answers are the boring truths: keep physically active with things you enjoy or need to do (commute to and from work – try to add 1,000 steps to daily amount for example), eat a healthier diet, and if overweight, then try to lose some weight by making sustainable, often small, changes to diet, and cut down on alcohol if drinking too much or stop smoking."

Dr Alan Gow, associate professor in psychology at Heriot-Watt University: “The evidence that 'heart smart' lifestyles might also be good for brain health is generally supported. So, for example, it is often recommended that people might try to get a bit more physical activity. I’m interested in the growing number of studies looking at how engagement in real-world activities involving new learning might be beneficial for our thinking skills.”

Professor Wendy Bickmore, director of the Human Genetics Unit at University of Edinburgh: “The best way to stop ageing is to have a healthy lifestyle and an unhealthy lifestyle also is a trigger for inflammation, so it all speaks to the same thing at the end of the day.”