FASTER, PLEASE: Can we delay ageing?

Quietly, over the past few decades, remarkable discoveries have been made about the biology of ageing. Since we all get older, it might seem that ageing “just happens” and can’t really be changed. In contrast, age-related disease does not seem inevitable, since not everyone gets cancer, heart disease or dementia. Accordingly, much research funding has been directed towards individual diseases, whereas very little has been directed towards ageing itself.

This is regrettable, since ageing is the greatest risk factor for many diseases; far greater than, say, smoking. If we could gain control over the ageing process, we should be able to maintain health and youthfulness for longer, and increase our resistance to age-related disease.

Ageing is a natural progressive decline that affects all organ systems and coincides with an increased risk of death. Many processes in biology, like the formation of muscles in an embryo, are governed by key “regulatory genes”, genes that can co-ordinate an entire programme of events. Evolutionary biologists long argued that regulatory genes for ageing would not exist. Ageing happens after reproduction, they argued, so a gene controlling ageing should have no effect on reproductive fitness, and so would have no way to arise by natural selection.

Thus it was surprising to discover that the rate of ageing of an entire animal could be changed dramatically by altering single genes. . . .

So far, we do have life-extending drugs for mice. Rapamycin, which targets a stress sensor called TOR, extends the average lifespan of mice by about 25 per cent, and experiments with pet dogs are under way, co-ordinated by scientists at the University of Washington in Seattle. But rapamycin can have side effects in humans (where it is used to modulate the immune system following organ transplants), so its usefulness may be limited for now.

The lifespan of a mouse can also be increased by feeding it nicotinamide riboside (NR), a nutraceutical that raises energy levels (but buyer beware: clinical trials have not been carried out). On the other, more pessimistic, hand, it is possible that we humans, with our long lifespans, have an already-active cell-protection system. Like small dogs and bats, we live longer than expected for our body size. (Among most species of mammals, a larger body size correlates with longer lifespan.)

Right now, many researchers, even those not thinking about ageing, are trying to make drugs that boost this cell-protective network. Their motivation stems from the fact that this network not only counteracts ageing, it also counteracts age-related disease. For example, elevating the levels of FGF21, a hormone normally made in response to starvation, has beneficial effects on overweight mice fed a “western diet”, and thus might counteract diseases associated with obesity, such as diabetes. Activating this cell-protection system suppresses many types of cancer in laboratory mice, and several of its components are targets for cancer interventions. Activating the system can also improve the weakened response that elderly people have to flu vaccinations. So the wheel is turning and, before too long, we should learn whether humans are broadly susceptible to the pro-longevity, healthful effects of this system.

Faster, please. I take the nicotinamide riboside, in the form of Niagen. Does it work? Ask me in 20 years.