24 processes that decide how you age.

The cell breaking down and recycling its own damaged parts, so the material can be reused. It is one of the few repair systems we can reliably switch on from the outside.

Your body’s clean-up crew. It takes old, broken cell parts, breaks them down, and uses the pieces to build new ones. When it slows, the debris accumulates, and that accumulation is a big part of what ageing looks like from the inside.

Going without food for a stretch is the strongest everyday lever — time-restricted eating or a longer fast. Hard exercise does it too. Coffee, green tea and olive oil each nudge it. Rapamycin is the most convincing pharmacological route and remains a prescription drug under study.

mTOR is the switch that tells a cell to grow rather than repair. Turning it down periodically shifts cells into maintenance, which in animals extends life.

A manager that decides whether the cell builds or cleans. Left on permanently you get growth without maintenance. The goal is not to switch it off — you need it to build muscle — but to stop it running all day.

Periods without food and without constant protein. This one has a real tension in it: the same signal that drives ageing also builds the muscle that keeps you alive after seventy. Most people over fifty need more protein, not less, and the cycling matters more than the average.

A family of proteins involved in DNA repair, inflammation and metabolic control, dependent on NAD+ to work.

A repair crew that only clocks in if there is enough of a particular fuel around. Much of the last decade of longevity supplements has been an attempt to top up that fuel.

This is where the story has changed most since 2023. NAD+ precursors reliably raise NAD+ in blood; what they have not yet shown is that this makes healthy people live longer or better. Treat the supplement claims with more caution than the 2023 version of this page did. Exercise and sleep remain the unglamorous route.

Reducing energy intake without malnutrition. It extends life across many species; in humans the evidence is for metabolic health rather than lifespan.

Eating less, but not eating badly. The body shifts from processing a constant surplus to maintaining itself.

For most people, time-restricted eating and the occasional fasting-mimicking cycle capture most of the benefit without the cost. Sustained severe restriction carries real risks — muscle and bone loss especially — and is a poor trade after sixty.

Low-grade immune activation that persists without an infection to fight. It is implicated in nearly every age-related disease, and the field now calls it inflammaging.

A fire that never quite goes out. You do not feel it day to day, which is exactly why it does so much damage over decades.

Sleep, weight, muscle, oral health, and treating the obvious sources. Omega-3s have decent evidence. This is also one of the few processes where a simple blood test — high-sensitivity CRP — tells you something useful and cheap.

Chemical marks that decide which genes are read, without changing the DNA underneath. The pattern of those marks tracks age closely enough to estimate it.

Switches on top of your genes. The sequence is fixed; which parts are switched on is not, and that is where lifestyle actually reaches your biology.

Epigenetic age tests have become widely available and remain noisy — useful as a trend over years, not as a single reading. Partial reprogramming, which resets these marks, is the most exciting thing in the field and is not yet a human therapy.

How readily your cells respond to insulin and take up glucose. Losing it precedes type 2 diabetes by many years and quietly worsens almost everything else.

How well your body handles what you eat. When it slips, blood sugar stays high for longer after every meal, and the damage is cumulative.

Muscle is the largest glucose sink you own, so resistance training matters as much as diet. Walking after meals works. A continuous glucose monitor worn for a few weeks is one of the few pieces of consumer tech that reliably changes behaviour, because you see your own response rather than a general rule.

The set of mechanisms that fix the thousands of DNA lesions each cell accumulates every day. Repair capacity declines with age; unrepaired damage drives both cancer and ageing.

A maintenance crew working constantly on damage you never notice. Ageing is partly the crew getting slower than the damage.

Reduce the load rather than chase the repair: sun sensibly, do not smoke, keep alcohol modest, sleep. The single most useful thing here is not a supplement but screening — finding what went wrong early, which is the whole point of the Bridge of Prevention.

Every tissue keeps a small reserve of unspecialised cells that divide to replace what wears out. With age the reserve shrinks, and the cells left in it divide less readily and less accurately. It is one of the twelve hallmarks of ageing, and it sits downstream of most of the others — senescence, DNA damage and chronic inflammation all wear the reserve down.

A workshop keeps a rack of good blank timber for repairs. Every year the rack holds a little less, and what is left is harder to work. Nothing looks wrong until something needs mending.

Nothing yet reliably rebuilds a reserve in a human. Protecting it is well established: resistance training keeps the satellite cells in muscle active, sleep and control of chronic inflammation reduce the drain. Stem cell transplants are standard care in a few blood cancers and are not an anti-ageing treatment — clinics selling infusions for ageing are selling ahead of the evidence, and some of what they sell is dangerous.

Chronological age is how long you have been alive. Biological age is an estimate of how worn the body is, read from the pattern of methyl marks on DNA. Steve Horvath built the first clock that worked across tissues in 2013; the later ones predict disease and death better than the first generation did, and one of them measures the rate of ageing rather than the amount.

Two watches on a table. One counts birthdays and cannot be argued with. The other counts wear, and it can be running fast or slow.

The honest answer is that the clocks are better at measuring than at being moved. They respond to the things that already have hard outcome data behind them — exercise, sleep, not smoking, body composition — and a few small trials have shown a year or two of reversal. On consumer tests: the same sample sent twice can come back with different answers, so read one result as a rough position and a trend over years as the number that means something.

A protein named after Clotho, the Greek Fate who spun the thread of a life. Mice bred without it age rapidly and die young; mice given more of it live longer. In people, higher levels track better kidney function, better cognition and lower mortality, and a variant carried by roughly a fifth of the population is associated with sharper thinking in later life.

A thread being spun. How much of it there is seems to set how long, and how evenly, the spinning goes on.

Exercise raises it modestly, and so does looking after your kidneys, which is where most of it is made. There is nothing to buy: klotho does not survive being swallowed, and injected forms are in early trials. What it is genuinely useful for today is as a marker — something to measure rather than something to move.

A protein the body already makes, whose job is to hold back another one. Myostatin is the brake on muscle: it decides how much a body will build and then stops it. Follistatin blocks the brake. That began as a story about strength and stopped being one when it became clear how much else moves with muscle — insulin sensitivity, the fat that sits around the organs, bone, the risk of frailty at eighty. In mice, raising it has been reported to add roughly a third to lifespan. In people it has been through trials in Becker’s muscular dystrophy, and it is the gene therapy most often offered to healthy adults who have nothing wrong with them.

A coil of rope bound tight so that it cannot open. Myostatin is the binding. Untie it and the body builds more of the one tissue that also burns sugar, holds the skeleton up, and decides whether you can get out of a chair at eighty.

Resistance training is the settled part: it raises follistatin and lowers myostatin, it costs nothing, and it has forty years of outcome data behind it. Everything beyond that is gene therapy — a harmless virus carries the gene in so your own cells make the protein steadily. It is gene transfer and not gene editing: nothing is altered in the DNA you would pass to a child. But the human evidence is thin, much of it unpublished, and some of the people offering it work outside the approval systems of their own countries and have been criticised for it. The mice are real. The market is ahead of the science, and the gap between the two is where the money is being made. Patrick Sewell and Liz Parrish both talk about it in the book.