Death seems like a design flaw. If natural selection builds bodies capable of healing wounds, fighting infections, and regenerating cells, why does it permit the slow decay we call aging? Why would evolution, that relentless optimizer, tolerate such obvious deterioration?

The answer reveals something profound about how natural selection actually works. It doesn't care about you—it cares about your genes making it into the next generation. And that single-minded focus creates a blind spot, a shadow where harmful processes can accumulate unchecked.

Understanding why we age isn't just academic. It reframes how we think about our own bodies, our life stages, and the fundamental trade-offs written into every living thing. Aging isn't a mistake. It's the price of being alive in the particular way we are.

Imagine two genetic mutations. One kills its carrier at age five. The other causes identical harm but only strikes at age seventy. From natural selection's perspective, these mutations are not equivalent—not even close.

The first mutation is ruthlessly eliminated. Carriers die before reproducing, so the gene vanishes. But the second? By seventy, most individuals have already raised offspring. The damage arrives too late to affect reproductive success. Selection barely notices.

This insight, first articulated by Peter Medawar in the 1950s, explains why harmful late-acting genes can accumulate in populations. Selection's power to remove deleterious mutations declines with the age at which they act. It's not that evolution wants you to age. It's that evolution increasingly doesn't care what happens to you as you get older.

The result is a genome littered with time-delayed problems. Genes that cause Huntington's disease, certain cancers, and cardiovascular decline persist because their effects manifest after the reproductive years. Selection, which sculpts the young with exquisite precision, becomes progressively myopic about later life.

Takeaway

Natural selection's power fades with age—not because evolution intends decay, but because reproduction matters more than longevity to gene transmission.

George Williams proposed something more troubling in 1957. What if aging isn't just selection looking away? What if the very genes that make us vigorous when young cause our decline when old?

This is antagonistic pleiotropy—genes with opposite effects at different life stages. A gene boosting testosterone might enhance mate competition in youth but promote prostate cancer decades later. Genes driving rapid cell division support growth and healing but increase cancer risk over time.

Selection faces a devil's bargain. Given a choice between early vigor and late vitality, it chooses early vigor every time. A gene that doubles your reproductive success at twenty but halves your survival at sixty will spread through the population. The math is merciless.

This means aging might be actively built into successful organisms. The traits that made your ancestors successful reproducers—strong immune responses, rapid healing, high metabolic rates—may carry delayed costs that manifest as aging. Youth and decay aren't separate phenomena. They're two faces of the same coin.

Takeaway

The genes that make us thrive early may be the same ones that break us down later—vitality and decay are often biologically intertwined.

If this evolutionary logic is universal, why does a mayfly live for a day while a Greenland shark can survive for centuries? The answer lies in ecology—specifically, in what kills you besides aging.

Consider a mouse. Predators, cold, and starvation claim most mice within months, regardless of how well their bodies resist aging. Why invest in long-term maintenance when you'll likely be eaten next week? Evolution doesn't build durable mice because durability doesn't pay off.

Now consider a tortoise. Protected by armor, free from most predators, a tortoise that dies young from aging leaves fewer offspring than one that lives longer. Selection favors durability because tortoises actually survive long enough for durability to matter.

This explains the pattern we see across species. Animals with high external mortality—small rodents, most insects—age rapidly. Animals protected by shells, flight, or social living—tortoises, birds, humans—age slowly. The Greenland shark, dwelling in the cold deep with few threats, barely seems to age at all. Evolution calibrates the aging rate to match ecological reality.

Takeaway

Species age at rates calibrated to their ecological circumstances—when external threats are low, natural selection favors investing in a longer-lasting body.

Aging, then, isn't a flaw in the evolutionary machinery. It's an inevitable consequence of how natural selection operates—weakening with age, making trade-offs that favor the young, and calibrating lifespans to ecological realities.

This perspective doesn't make growing old easier. But it does make it comprehensible. Your body isn't failing you; it's operating exactly as selection shaped it to operate, with all the trade-offs that entails.

Perhaps there's something clarifying in knowing that mortality isn't a bug but a feature—the shadow cast by the very processes that built us.