Food, DNA, and the Ticking Clock of Life: How Our Genetic Code Shapes Ageing

Food is delicious. That’s not exactly surprising — for billions of years, life has been locked in a relentless struggle to find enough to eat. From our simplest evolutionary ancestors to the complex beings we are today, survival has always hinged on getting enough fuel to live and reproduce.
Those with a strong drive to seek and devour food had an undeniable advantage, and as a result, our brains are hardwired to love eating. Hunger demands our attention, and satisfaction brings instant reward.

But evolution didn’t fine-tune an “off switch” for overeating. In a world where the next meal was never guaranteed, stuffing ourselves whenever food appeared made perfect sense. Modern abundance, however, has left that ancient instinct working against us.

The DNA Inside Every Bite
Every mouthful of food starts a chain of events that affects you far more deeply than you might imagine. Inside almost every cell of your body, there’s a complete instruction manual for building and maintaining you: over two metres of DNA coiled into a nucleus just millionths of a metre wide.

DNA’s double-helix has become a symbol of science itself — elegant, neat, and pure in textbooks and logos. But the reality inside your cells is much messier. DNA is crammed shoulder-to-shoulder with thousands of other molecules, constantly jostled and assaulted by chemical forces. This delicate code of A, T, C, and G – the four bases – is under attack every single day.

Surprisingly, the greatest threat isn’t even from external enemies like cigarette smoke, UV light, or radiation (although they do their share of harm). Most of the damage actually comes from you — or more precisely, from your metabolism. The simple act of converting food into energy produces chemical byproducts that can batter DNA.

The result? Each cell in your body can experience up to 100,000 DNA injuries every single day.

The Copying Dilemma
As cells divide, they have to duplicate that massive two-metre stretch of DNA. Over a lifetime, your body will produce ten quadrillion near-perfect copies of your genome — enough combined length to stretch halfway to the nearest star.

Even with nature’s best proofreading machinery, mistakes — called mutations — sometimes slip through. Some mutations don’t matter, but others are dangerous. Because they alter the genetic code in ways that look “perfectly normal” to the cell, they can remain undetected indefinitely.

One rogue cell, with just the wrong mix of mutations, can spiral into uncontrolled growth — cancer.

When Fixing the Damage Causes More Damage
Oddly enough, even curing cancer can take a toll on DNA. Treatments like chemotherapy and radiotherapy work by targeting cancer cells, but nearby healthy cells often get caught in the blast.

We see the consequences in childhood cancer survivors. While modern medicine has dramatically improved survival rates, many of these survivors experience accelerated ageing in adulthood — earlier onset of heart disease, high blood pressure, stroke, dementia, arthritis, and even second cancers. In fact, their lifespan can be reduced by around a decade.

Damage done to DNA during treatment appears to speed up the body’s ticking biological clock.

The Protective Endcaps: Telomeres
On a microscopic level, our DNA is divided into 46 chromosomes, and each chromosome is capped at both ends by telomeres — repeating nonsense sequences of DNA, like “TTAGGG” over and over, that act like protective boots for shoelaces.

Why do we need them? For two reasons:

Preventing chaos – Without telomeres, the loose ends of chromosomes might be mistaken for broken DNA and glued together in disastrous tangles.

Compensating for a design flaw – Our DNA-copying machinery can’t fully duplicate the very ends of chromosomes. Each time a cell divides, a tiny piece of telomere is lost. Better to sacrifice meaningless repeats than important genes.

But telomeres aren’t endless. Over a lifetime of cell divisions, they shorten. And when they become critically short, the cell gets the signal to retire from active duty:

Sometimes it self-destructs (apoptosis).
Sometimes it stops dividing but remains alive in a kind of limbo — cellular senescence.

Both of these processes are part of the tapestry of ageing.

Food, Mutations, and Time
From the moment we take our first bite of food to our final breath, every calorie fuels more than just movement — it drives the process of life and, inevitably, decay. Our evolutionary wiring pushes us to eat, feeding not only our energy needs but also the constant churn of DNA activity inside every cell.

Mutations accumulate. Telomeres shrink. And while damage repair systems keep us functional for decades, the slow drip of errors, like whispers in a game of telephone, eventually reshapes our bodies and minds in ways that we call ageing.

The story here is profound: ageing is not just about years passing — it’s about the battle within every cell, every day.

💡 Takeaway: What we eat keeps us alive, but it also keeps our DNA busy — and sometimes under fire. Our genetic code is resilient, but it’s not invincible. Understanding how life’s most fundamental instructions change over time might be the key to unlocking longer, healthier lives.

Source : Ageless: The New Science of Getting Older Without Getting Old by Andrew Steele

Goodreads : https://www.goodreads.com/book/show/52954648-ageless

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