Although ageing is inevitable – most likely due to the accumulation of damage at cellular level, rather than from any one specific programme – the actual rate of ageing can be modified.

Although we will all die, there is a certain amount of flexibility, known as plasticity in biology and elasticity in economics, in how fast we age and therefore how early or late we die.

We can see this around us every day, with some people dying early while others surviving to very old age. This plasticity is likely to be controlled by relatively simple mechanisms. Ageing research focusing on this plasticity has shown some encouraging results.

What does not kill you makes you stronger. These are hormetins, sometimes referred to as adaptogens – which cause a mild stress to the body that has long-term and broad beneficial effects.

Hormetins kickstart the body’s response to stress. On the same principle as vaccinations start your antibodies production, this response then has broader and longer-lasting benefits – benefits that in some cases lead to living longer.

Mild stress can be induced through a number of methods. The easiest and most common is physical activity, such as exercise, heat and radiation. There is emerging interest in psychological methods like meditation, brain exercises, juggling and balancing as well. There is also nutritional stress, where we reduce the number of calories we eat. This seems to kickstart something in all animals that has both positive healthy effects and also increased longevity.

The problem with hormesis is that sometimes we do not know what is a mild or a traumatic shock – the ‘goldilocks effect’ – not too little and not too much, just right.

Nadine Saul with Humboldt-University of Berlin and her colleagues have argued that the process of hormesis is a balance that has both positive and negative outcomes. It emerged that for every longevity improvement, there is a reduction in the capacity of the organism for growth, mobility, stress resistance or reproduction. Saul argues that longevity comes at a price, that there are other costs such as infertility. Women who reduce their calorific intake, for example, report that they stop having periods and therefore are temporarily infertile.

The mechanism of hormesis remains an enigma. In 1962, Italian geneticist Ferruccio Ritossa discovered that heat shock proteins are produced when cells are exposed to a variety of stresses. Initially identified with fruit flies that were exposed to a burst of heat, this resulted in new proteins being generated that help cells survive. A short, sharp shock to the system seems to make it more resilient.

Exercise, being content and eating a diet that includes the methyl group – broccoli, leafy green vegetables, citrus fruits and strawberries – seems to promote these good genes

Similarly, we now acknowledge that calorific restriction itself might be effective because of its hermetic qualities – giving the body a shock – rather than through diet. This might be the case since there are multiple ways of producing the same effect without sticking to a diet of low calories.

Recently, the definition has included a broader scope of interventions, including short-term starvation (two to three days of not eating, but drinking water), periodic fasting (one or two days a week/month of not eating solids), fasting-mimetic diets (reducing caloric intake down to 34 to 54 per cent, with a specific composition of proteins, carbohydrates, fats and micronutrients),  intermittent fasting (one day of not eating solids, or just eating one meal a day), normo-calorific diets with planned deficiencies (normal diets but restricting particular macronutrients, a substance required in relatively large amounts by living organisms such as proteins and carbohydrates) and time-restricted feeding (only eating at certain times of the day, for example five hours before going to sleep and having at least 12 hours in between dinner and breakfast).

The fact that most of these techniques have shown some positive outcome lead us away from the purely calorific intake to a shock mechanism. The underlying mechanism – rather than the reduction of calories – becomes important. And the underlying mechanism is a shock. If we accept this mechanism, then we should ask why? Why does a shock cause the body to build resilience?

The answer is both simple and radical. A shock causes the body to build resilience because the body is designed to do exactly that. Our body interacts with the environment in order to survive. And to accomplish this adaptation there must be plasticity, some wiggle room, in our capacity. In some cases, the mild shock prepares us for something more dangerous. The body prepares by building up defences by switching on and off some genes to produce the desired balance.

We know a lot about the switching on and off of these genes which we now call epigenes. There are two processes that the body uses to achieve this. Exercise, being content and eating a diet that includes the methyl group – broccoli, leafy green vegetables, citrus fruits and strawberries – seems to promote these good genes to be switched on and the bad genes to be switched off.

Although we make these moral judgements of good versus bad genes, it seems that in nature everything has a role. We need to ask why our body switches genes that cuts our life shorter.

Only after we stop having a quick answer can we become more appreciative of the balance we maintain with our natural world. We can then focus on the plasticity in older age.

From the average length of life (around 80 years) to the oldest possible (122) lies 42 years of unclaimed life. The fountain of youth might be a question of how much of my capacity can I use up rather than leaving it behind when I die.

Mario Garrett was born in Malta and is currently a professor of gerontology at San Diego State University in California, US.

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