The E. coli living inside you right now is a descendant of bacteria that existed three billion years ago. Not similar organisms — the same species, the same survival strategy. We, Homo sapiens, live an average of about 80 years and call it an achievement. What went wrong with evolution?

The bacterium: a genius of minimalism

• A bacterial genome is a small circular coil of DNA with roughly 400 to 500 genes. No introns, almost no “junk,” virtually nothing superfluous. The entire E. coli genome is around 4.6 million base pairs. By comparison, the human genome runs to 3 billion base pairs, of which only 1.5 percent codes for proteins.
• This is not a deficiency — it is a strategy. A small genome copies quickly and with a minimum of errors. A bacterium divides every 20 to 30 minutes. Under ideal conditions, a single cell can produce more than 70 trillion descendants in 24 hours — a mass exceeding the weight of a human body.
• Most importantly: bacteria have no internal death programme. They die from external causes — starvation, competitors, viruses, antibiotics. But not from old age. Division continues as long as resources exist.
• A bacterium does not die. It either divides or goes dormant. Death is simply not part of its biological vocabulary.
• A separate superpower: horizontal gene transfer. Bacteria exchange DNA directly — through plasmids, membrane fusion, bacteriophages. This means a useful mutation arising in one cell can spread to millions of others within hours. It is precisely how antibiotic resistance propagates — not through reproduction but through lateral copying.
• We cannot do this. Every human being is born with a fixed set of genes that changes only through sexual reproduction and random mutation — slowly, across generations. These are fundamentally different speeds of adaptation.

The price of complexity

• About two billion years ago, one of the most significant events in the history of life took place: one bacterium engulfed another — and instead of digesting it, established a symbiosis. The engulfed cell became a mitochondrion. It was a deal: the host gained a powerful energy source, the guest gained a safe haven. Both survived.
• The eukaryotic cell that arose from this partnership was incomparably more productive than a bacterial cell. It could afford to be larger, more complex, more specialised. From such cells, multicellular organisms eventually assembled — algae, fungi, plants, animals, us.
• But there was a price. A complex cell is thousands of components, any of which can fail. Signalling pathways that can misfire and trigger tumours. Mitochondria that produce energy and simultaneously produce free radicals — molecular by-products that damage everything around them. An immune system that occasionally attacks its own tissues.
• Above all, division became dangerous. Each time a cell copies its 3 billion nucleotides, there is a risk of error. Proofreading systems correct almost everything — but not quite everything. Over time, errors accumulate. This is one of the molecular foundations of aging.

The division counter: telomeres and the Hayflick limit

• In 1961, American biologist Leonard Hayflick discovered something inconvenient. He was culturing cells from human embryonic lung tissue and counting how many times they divided. After roughly 50 to 60 divisions, they simply stopped. They did not die — they froze. Hayflick called this the Hayflick limit.
• Colleagues were initially sceptical. For the first half of the twentieth century, biologists had assumed that cells in culture were potentially immortal — provided nothing went wrong. Hayflick insisted that this was not an experimental artefact but a biological fact. He was right.
• The mechanism was explained later. At the ends of every chromosome sit telomeres — repeating sequences TTAGGG, a kind of protective cap. With each division, telomeres shorten slightly. When they become critically short, the cell stops dividing — to prevent copying of damaged DNA. This is a built-in defence against mutation.
• Telomeres are a biological division counter. Each time a cell divides, the counter clicks down by one. When it reaches zero, division stops.
• At birth, telomere length in white blood cells is around 10 to 12 kilobases. By age 80, approximately 4 to 5. Cells lose 20 to 40 base pairs per year from division alone. Additional shortening comes from stress, smoking, chronic inflammation, poor sleep.
• Bacteria have no telomeres: their DNA is circular, there are no ends. The division counter was simply never installed.

Telomerase: the exception to the rule

The enzyme telomerase can restore telomeres. In germ cells and stem cells it is active — which is why they divide far more than 50 times. In most somatic cells, telomerase is almost completely switched off.

Cancer cells are one of the rare exceptions. They reactivate telomerase and become “immortal” in the literal sense: dividing again and again for as long as the host lives. This is the paradox: the mechanism that could extend the life of normal cells creates, in cancer cells, the primary threat.

Progeria: ageing at the speed of sound

• Hutchinson–Gilford progeria syndrome is a rare genetic condition in which a mutation in the LMNA gene disrupts the structure of the cell’s nuclear envelope. Cells stop dividing normally, telomeres shorten at a catastrophic rate, DNA damage accumulates.
• Children with progeria look and behave like elderly people by the age of 8 to 10. Average life expectancy is around 13 years. The cause of death is almost always a heart attack or stroke — conditions that in ordinary people take 70 to 80 years to develop.
• Progeria is an accelerated replay of normal ageing. By studying it, scientists understand which molecular processes underlie ordinary biological ageing. It is a living laboratory that nobody asked to open.

Jeanne Calment and the Gompertz law

• Jeanne Calment of Arles lived for 122 years and 164 days — the verified world record. She gave up smoking at 117 (“because it had become inconvenient to ask someone to light my cigarette”). She took up fencing at 85. She cycled until she was 100.
• The Calment case is interesting precisely because she followed no strict longevity regimen. This suggests that genetics plays a substantial role — in particular, polymorphisms in FOXO3 (a regulator of cellular longevity) and APOE (linked to vascular disease and dementia risk).
• According to the Gompertz–Makeham law, first described in 1825, the human mortality rate doubles approximately every 8 to 9 years after the age of 30. The risk of dying at 40 is twice what it was at 31. At 49, twice what it was at 40. This is exponential growth that admits no exceptions in any species with a finite lifespan.
• Jeanne Calment lived to 122 and never gave us an answer as to why. Perhaps because there is no single answer: longevity is a combination of hundreds of small pieces of luck.

The paradox of the smoking centenarian

Among documented long-lived individuals there are smokers with 50 to 60 year tobacco histories. This looks like a mockery of every health recommendation in existence. How to explain it?

Barely at all — in individual cases. But the statistics are merciless: only around 1 percent of all smokers reach age 100. Those who do are almost certainly carrying rare protective gene variants — for example, in the CETP gene, which regulates “good” HDL cholesterol. Genetic luck allowed them to survive what would have killed 99 percent of people with the same history.

This is not an argument for smoking. It is a demonstration of how important genetics is in ageing — and how dangerous it is to draw conclusions from individual cases.

Blue Zones: what the world’s longest-lived people have in common

• The “Blue Zones” are several geographic regions with an unusually high concentration of centenarians: Sardinia (Italy), Okinawa (Japan), Ikaria (Greece), the Nicoya Peninsula (Costa Rica), and Loma Linda (California, USA).
• Demographer Michel Poulain and journalist Dan Buettner, who studied these regions from the 2000s onward, identified several common patterns. None of them is magical:
• Natural movement. Not a gym, but walking, gardening, herding — physical activity built into daily life.
• A plant-forward diet with moderate meat consumption. Legumes are a dietary staple almost everywhere.
• Absence of chronic stress, or the presence of rituals to discharge it: the afternoon nap in Ikaria, prayer among the Loma Linda Adventists.
• Strong social bonds. The Okinawan concept of “moai” — a lifelong mutual support group of 5 to 7 people.
• A sense of purpose. In Japanese: ikigai — the reason to get up in the morning. In Costa Rican: plan de vida.
• The common denominator is not a specific diet or a longevity gene. It is an environment in which healthy behaviour is the default, not an effort.

What happens in the gut of centenarians

• One of the unexpected discoveries of the last decade: long-lived individuals have significantly more diverse gut microbiomes compared to their peers. Their intestines more often contain Akkermansia muciniphila and Bifidobacterium — bacteria that strengthen the gut barrier and reduce systemic inflammation.
• Chronic inflammation — “inflammaging” (from inflammation and aging) — is now considered one of the central mechanisms of accelerated ageing. A constantly, mildly activated immune system slowly degrades tissues and raises the risk of cardiovascular disease, dementia and cancer.
• A diverse microbiome counteracts this. It produces short-chain fatty acids — butyrate, propionate — that nourish intestinal cells and support an anti-inflammatory immune profile.
• This explains why the high-fibre diets of Blue Zone populations work: not because they are the “right food,” but because they feed the right bacteria.

What all this means for those planning to become parents

• The biology of ageing is not an abstract subject for those thinking about having a child. Several direct connections:
• Age and the quality of reproductive cells. Telomeres shorten in eggs with every passing year. Mitochondrial function in oocytes declines. Paternal age increases the frequency of de novo mutations in sperm — by roughly 1 to 2 new mutations per year. This is not a reason for panic, but it is a biological reality.
• Preconception lifestyle affects the epigenetics of offspring. Chronic stress, smoking and sleep deprivation shorten telomeres in reproductive cells and alter DNA methylation patterns. More detail in the Epigenetics and Unseen Inheritance articles in the Learn section.
• Mitochondrial diseases are inherited through the maternal line. If the mother’s family has a history of mitochondrial myopathies, neurodegenerative conditions, or unexplained pregnancy losses — this is an indication for genetic consultation and possibly preimplantation genetic testing.
• Antioxidant support during preconception preparation is not marketing. CoQ10, vitamin D and omega-3 reduce oxidative stress in reproductive cells. Specific doses and indications are in Module 3 (Biohacking & Preconception).

The key point

• Bacteria are immortal because they are simple. We are mortal because we are complex. This is not an accident or an evolutionary error — it is a trade-off: in exchange for the ability to think, feel and build civilisations, we accepted a biological expiry date.
• But that date is not fixed. Telomeres shorten more slowly in people who move, sleep, maintain social bonds and reduce chronic inflammation. Jeanne Calment lived to 122 — which tells us that the biological ceiling is still far away.
• A bacterium divides forever because it can do nothing but divide. We age because we can do almost everything else.

Glossary