The Information Theory of Aging: Why Your Cells Forget Who They Are

Short answer: Aging occurs primarily through the loss of epigenetic information - the control systems that tell cells which genes to express - rather than DNA damage itself. Your DNA sequence remains largely intact, but the "instructions for reading it" degrade over time, causing cells to lose their identity and function, which drives 80-90% of age-related diseases like heart disease, Alzheimer's, and cancer.

Common Questions Patients Ask

1. Q: Is aging actually a disease, or is it just a natural process?
2. Q: What's the difference between DNA and epigenetic information?
3. Q: Why does epigenetic information matter more than my DNA sequence?
4. Q: How does epigenetic information get corrupted over time?
5. Q: What are epigenetic clocks, and what do they tell us?
6. Q: Why do some people look younger than their age, and what does that mean for their health?

This article explains why aging happens at the cellular level, how damaged genetic information causes cells to lose their function, and what emerging science suggests we might do about it.

There's a woman I visit sometimes who keeps her mother's recipe cards in a wooden box on the kitchen counter. The cards are stained with decades of use - flour fingerprints, oil spots, the occasional coffee ring. The handwriting has faded on some of them. You can still read "chicken soup" at the top, but the measurements are barely legible now. She's had to guess at the amounts, make substitutions. The soup still tastes good, she says, but it's not quite the same.

That's aging, essentially. Not the loss of the recipe itself - that stays intact - but the loss of the instructions for reading it properly.

The Disease That Isn't Called a Disease

Here's something strange about how medicine categorises illness: if fewer than 50% of people get a condition, we call it a disease and dedicate entire research institutes to curing it. If more than 50% get it, we call it normal and accept it as inevitable.

Aging affects 100% of humans who live long enough. By that arbitrary definition, it's not a disease - it's just life. But strip away the semantics and look at what aging actually does: progressive deterioration of function, increasing susceptibility to illness, eventual death. That sounds exactly like a disease to me. Actually, it sounds like the disease - the one underlying most of what we treat in clinical practice.

Heart disease, Alzheimer's, type 2 diabetes, most cancers - 80 to 90% of their occurrence is driven by aging itself. If we could keep tissues biologically young, most of these conditions wouldn't develop in the first place. We've spent centuries treating the downstream consequences while largely ignoring the upstream cause.

Or maybe we haven't been ignoring it - maybe we just didn't have the language or the tools to address it properly until recently.

Two Types of Information (One Gets Corrupted)

Every cell in your body contains about six feet of DNA. If you unspooled all the DNA from all your cells and laid it end to end, you'd have enough to reach the moon and back eight times. That's a lot of information packed into a very small space.

There are two types of biological information at work here. The first is the DNA sequence itself - the famous double helix, the ATCG code that gets passed from parent to child. This is digital information, surprisingly stable. Mutations happen, yes, but they're relatively rare events. Most of your DNA today is identical to what it was when you were born.

The second type is what we call epigenetic information - the control systems that determine which genes get read and when. Think of DNA as a library containing every book your cells could ever need. The epigenome is the cataloguing system that tells the liver cell to read liver books and the neuron to read neuron books. Without that system, you'd have chaos - cells trying to do everything at once or forgetting what they're supposed to do entirely.

Here's the critical part: about 80% of your future longevity and health is controlled by this second system, not the DNA sequence itself. The epigenome is far more dynamic, far more responsive to environment and behaviour, and - unfortunately - far more susceptible to degradation over time.

The Scratches on the CD

The epigenome works through chemical modifications to DNA and the proteins it wraps around. Methylation - the addition of small methyl groups to specific DNA sites - is one of the main marking systems. These marks get laid down during embryonic development and are supposed to last your entire life, maintaining cellular identity. A neuron stays a neuron. A skin cell stays a skin cell.

But information degrades. It's the second law of thermodynamics - entropy increases, order decreases. Every time you photocopy a photocopy, you lose resolution. Every generation of a cassette tape recording sounds a bit muddier. (For younger readers: cassettes were these magnetic tape things we used before streaming. The quality degraded noticeably with each copy.)

DNA isn't copying itself repeatedly, but it is constantly being read, repaired, packed, and unpacked. Chemical marks get added and removed in response to stress, diet, inflammation, radiation - basically, in response to living. Over time, some of these marks get placed incorrectly or removed when they shouldn't be. The cataloguing system starts to fail.

Genes that should stay silent begin to activate. Genes that should stay on get shut down. A liver cell might start expressing genes normally found only in skin. A neuron might lose expression of genes critical for neuronal function. The cell becomes confused about its identity. It's still technically alive, still has the same DNA, but it's not functioning properly anymore.

We can measure this. There are now what we call epigenetic clocks - algorithms that analyse methylation patterns across the genome and predict biological age with surprising accuracy. Some of these clocks can predict mortality risk better than chronological age alone. When I look at someone and think they seem older or younger than their stated age, I'm probably unconsciously picking up on the outward manifestations of their epigenetic age.

Why Appearance Correlates With Longevity

People from families that produce centenarians - individuals who live past 100 - often look younger than their chronological age. At 70, they might appear 50 or younger. It's not just vanity or good skincare. Skin is a reasonable proxy for systemic aging because the same epigenetic degradation affecting internal organs is also affecting the skin's ability to maintain structure, produce collagen, and retain moisture.

I grew up in Australia, where the sun is particularly unforgiving. UV radiation accelerates epigenetic aging in skin, which is why sun-damaged skin can look decades older than protected skin on the same person. But in general, if someone looks significantly older than their years, that appearance reflects deeper systemic changes. The inverse is also true.

Grey hair by itself won't kill you - it's mostly just pigment cells losing function. But the overall maintenance of tissue architecture, the resilience of skin, the clarity of someone's eyes and gait - these things tell you something real about biological age.

The Reductionist View

There's been a lot of work in gerontology - the scientific study of aging - to identify the major mechanisms driving the aging process. Depending on who you ask, there are somewhere between eight and twelve "hallmarks of aging." These include things like cellular senescence (old cells that stop dividing but don't die), mitochondrial dysfunction (the cell's power plants losing efficiency), genomic instability (accumulated DNA damage), and so on.

It's useful to have a comprehensive list. It helps organise research efforts. But I think there's value in reduction - in asking whether one mechanism sits upstream of the others. If aging is fundamentally a loss of epigenetic information, then many of these other hallmarks might be downstream consequences rather than parallel causes.

Senescent cells, for instance, might accumulate partly because cells have lost their epigenetic identity and can no longer properly regulate their cell cycle. Mitochondrial dysfunction might reflect epigenetic changes in the genes controlling mitochondrial maintenance. Inflammation - chronic, low-grade inflammation that accelerates aging - might be driven by cells expressing inappropriate genes due to epigenetic drift.

I'm not saying other factors don't matter. They clearly do. But if you had to point to one primary driver, the loss of epigenetic information is the strongest candidate. It's also, intriguingly, one of the most potentially reversible.

The Possibility of Reversal

Here's where things get interesting. If aging is fundamentally about information loss rather than structural damage, and if that information still exists in the genome (which it does - the DNA sequence remains mostly intact), then theoretically we could restore it.

Early experiments in model organisms have shown that you can partially reset the epigenome and reverse markers of biological age. In mice, researchers have managed to restore vision in old animals by reprogramming eye cells to a more youthful epigenetic state. The same principles have been applied to other tissues with similar results.

In humans, we're not there yet. But the concept is no longer science fiction. We're talking about reading the original recipe properly again, not just making do with faded instructions.

This is fundamentally different from how we've traditionally approached aging. Instead of trying to treat each age-related disease separately - putting out fires one by one - we'd be addressing the underlying process that creates vulnerability to all of them at once.

What This Means Practically

For now, the interventions we have are relatively straightforward and somewhat unglamorous: regular exercise, caloric restriction or periodic fasting, stress management, adequate sleep, avoidance of chronic inflammation.

These aren't sexy recommendations, but they work at the epigenetic level. Exercise, for instance, triggers changes in methylation patterns that appear protective. Caloric restriction - eating less without malnutrition - is one of the most reliable interventions for extending lifespan across species, and much of its effect seems mediated through epigenetic changes.

We're also learning more about specific molecules that might help preserve epigenetic information. NAD+ (nicotinamide adenine dinucleotide - a molecule critical for cellular energy production and DNA repair) declines with age, and boosting NAD+ levels appears to have protective effects in animal models. Resveratrol, metformin, rapamycin - all are being studied for their potential to slow epigenetic aging. The evidence is still accumulating, and I wouldn't recommend anyone start self-medicating based on preliminary data, but the research is genuinely promising.

More important than any single intervention is the shift in thinking. If aging is a disease - a condition with identifiable mechanisms and potential treatments - then it becomes something we can study, measure, and potentially modify, rather than something we simply accept.

The Scratched Recipe

I don't know if that woman's chicken soup really tastes different from her mother's original, or if memory is doing its usual work of idealising the past. But the metaphor holds: the recipe is still there, complete and intact in her mother's handwriting. What's faded is the legibility, the clarity of instruction.

The genome is the recipe. The epigenome is the handwriting. And aging, in this model, is the slow fading of ink.

The good news is that we're getting better at reading faded text. We're developing tools to enhance contrast, restore clarity, maybe even rewrite portions that have become illegible. We're not there yet - nowhere close, really. But the direction is clear.

Whether aging is a disease or just the human condition probably matters less than the practical question: can we do something about it? Increasingly, the answer seems to be yes. Or at least, yes in principle. The details will take decades to work out.

In the meantime, I keep coming back to that wooden box on the kitchen counter. The stains, the wear, the evidence of use. The soup still tastes good, even if it's not quite the same. That counts for something too.