Assume a Longer Life

This is the chapter where books like this one usually lose their serious readers.

The pattern is predictable. An author has an interesting argument about the consequences of some technology, and in order to get to the interesting part, they have to first establish that the technology is coming. So they write a chapter full of exponential curves and confident dates, and anyone with domain knowledge closes the book, because they can see the author has no idea how hard the actual problem is.

I would like to avoid that, and there is a straightforward way to do it. I am going to make my premise as weak as I possibly can, and then show that the argument still runs.

So let me start by listing what this book does not need.

It does not need immortality. Nothing here requires anyone to live forever, and Chapter 6 argues at length that forever is not on the menu regardless of what medicine achieves.

It does not need uploading, digital minds, or any transfer of a person into a machine. If that becomes possible it changes the argument substantially, and I flag where, but the argument does not rest on it.

It does not need a date. I am not going to tell you when, because I do not know, and neither does anybody else who is being honest with you.

It does not need any specific intervention to work. Not senolytics, not reprogramming, not rapamycin, not anything currently in a clinical trial.

What it needs is this. At some point, healthy human lifespans reach somewhere between 150 and 300 years.

That is the whole premise. Everything in this book follows from it, and it is a far weaker claim than the ones usually made in this genre. It requires roughly a doubling to a tripling of the current healthy span, which is less than the improvement in life expectancy at birth that the developed world already achieved between 1850 and 1950.

Now let me be honest about why that comparison, which sounds so reassuring, is actually the wrong one.

The two centuries that did not extend life

Life expectancy at birth in wealthy countries went from somewhere in the thirties in 1850 to somewhere in the eighties today. That looks like a doubling of the human lifespan, and it is routinely described that way.

There is a popular correction to this, which is that the whole thing is an artifact of child mortality. For most of history a large share of people died before their fifth birthday, and when you average a great many deaths at age two with a normal number at age seventy, you get a figure in the thirties that tells you very little about how long an adult actually lived. A Roman who reached twenty had a decent chance of seeing sixty.

That correction is popular, it is repeated constantly, and it is also wrong, or at least badly overstated. I believed it myself until I went and looked.

Mortality fell at every age, not just in childhood. Take the cleanest measure, which is to start the clock after the dangerous early years have already passed. In England in 1841, a five-year-old could expect to live about fifty-five more years, reaching sixty. Today a five-year-old can expect to reach eighty-two. That is a gain of more than twenty-five years, measured from an age where infant mortality has already been excluded from the arithmetic entirely.

So we did extend adult life, substantially, and anyone who tells you the whole story is dead babies is skipping the evidence.

Here is what actually did not move.

The longest verified human life belongs to Jeanne Calment, who was born in 1875 and died in 1997 at the age of 122 years and 164 days. She remains the only person ever verified to have reached 120, and she is more than three years clear of the next name on the list. Nearly thirty years have passed since her death, medicine has transformed, and nobody has come close.

That is the shape of the thing. We have gotten steadily better at delivering people to old age intact, and modestly better at extending old age once they arrive. What we have not done is move the far edge. James Fries named the resulting pattern in 1980 and called it the compression of morbidity: instead of dying steadily across the whole span of life, more and more of us stay healthy until we hit a wall in our eighties or nineties, and then decline quickly. Demographers describe the survival curve as becoming rectangular.

A rectangle has an edge, and that edge has not moved in the lifetime of anyone reading this.

This is why the reassuring historical comparison fails. The last two centuries of gains came from pushing more people up against the wall. The next doubling requires moving the wall, and moving the wall is not a harder version of the same task. It is a different task, and it has to be done somewhere we have never worked, which is inside the aging process itself.

What is actually on the table

So where does that stand? I will give the honest version, which is less exciting than the promotional version and more interesting than the dismissive one.

The serious framing arrived in 2013, when Carlos López-Otín and colleagues published a paper identifying what they called the hallmarks of aging. They listed nine. A revision in 2023 expanded it to twelve. The specifics matter less than the move, which was to stop treating aging as one undifferentiated process and start treating it as a list: genomic instability, shortening telomeres, changes in how genes are switched on and off, mitochondrial dysfunction, cells that stop dividing but refuse to die, and so on.

This converted a philosophical problem into an engineering one, because a list is something you can work through. And the work has produced real results. I am going to give them with their actual numbers, because the numbers are considerably more modest than the coverage, and the gap between the two is the most useful thing in this chapter.

Senescent cells. These are cells that have stopped dividing but refuse to die, sitting in tissue emitting inflammatory signals. In 2016 the van Deursen group showed that genetically deleting them in mice reduced age-related tissue dysfunction and extended lifespan. Drugs that do the same thing, called senolytics, followed. The most studied combination is dasatinib with quercetin, and in 2018 a study in Nature Medicine reported that it improved physical function and increased lifespan in old mice. Human trials exist and are early, small and aimed at specific diseases rather than at aging.

Partial reprogramming. This is the strangest result in the field. Shinya Yamanaka identified four genes that can revert an adult cell all the way back to a stem cell. In 2016 Ocampo and colleagues applied them in short pulses rather than continuously, two days on and five days off, which appeared to reset markers of cellular age without erasing the cell’s identity, and without the tumors that continuous expression causes.

I want to be careful about what that study actually showed, because it is widely reported as more than it was. The large lifespan effect, roughly thirty percent, was in mice with progeria, a genetic disease of accelerated aging. That is a disease model, not normal aging. In ordinary old mice the demonstrated result was improved regeneration of damaged muscle and pancreatic tissue. Improved tissue repair in an aged animal is a genuinely exciting finding. It is not the same thing as making the animal live longer, and the study did not claim it was.

Rapamycin. In 2009 the National Institute on Aging’s Interventions Testing Program reported that rapamycin extended lifespan in mice even when started at twenty months of age, which in mouse terms is late middle age. It was the first drug ever shown to extend lifespan in a mammal. The magnitude, from that late start, was about nine percent in males and thirteen percent in females.

Nine percent. Hold that number against the tone of most writing on this subject.

Metformin. A cheap, old, off-patent diabetes drug with enough suggestive observational data behind it that researchers proposed a formal trial, called TAME, to test whether it delays aging itself rather than any single disease. The design is six years, roughly three thousand adults aged sixty-five to seventy-nine, at a cost of around seventy-five million dollars.

It has not started. It has been awaiting funding for over a decade, and the reason is worth more attention than it usually gets. Because metformin is off patent, no company can own the result, so no company will pay for it. The most direct test we have proposed of whether a drug slows human aging is stalled not on science but on the absence of anyone with a commercial reason to run it. Anybody trying to forecast this field should hold that fact next to the enthusiasm, because it tells you what the incentives actually reward, which is proprietary molecules rather than answers.

Now the caveat that applies to all of it.

Almost every result above is in mice, worms or flies. The history of this field is full of interventions that worked beautifully in short lived animals and did nothing in people. Caloric restriction extends mouse lifespan by forty percent or more; in primates the effect is far smaller and in humans there is no comparable result. Researchers in the area have a rueful saying about having cured cancer many times over in mice.

There is a structural reason to expect this, and it is not merely bad luck. Short lived species are under less evolutionary pressure to maintain themselves, which leaves more cheap repair available to an intervention. We are already an unusually long lived mammal. Much of the easy maintenance has already been built into us, which means the remaining gains are the expensive ones.

So here is the honest summary. No intervention has ever been shown to extend the maximum human lifespan. Not one. There are real mechanisms, real drugs, real effects in animals, and a field that has become a science rather than a hope. There is also no human result, and anyone who tells you otherwise is selling something.

Why I am not going to give you a date

Given all that, the temptation is to pick a year, and I am not going to, for two reasons.

The first is that I would be wrong. Forecasts in this area have a dismal record in both directions. People have been predicting imminent breakthroughs in aging since the 1970s, and they were wrong. People also confidently declared that the maximum lifespan was fixed and that most cancers were untreatable, and they were wrong too. The honest position is wide uncertainty, and wide uncertainty does not compress into a date.

The second reason is more useful. The date does not matter for this argument.

Consider the two scenarios. Suppose the aging problem is solved in forty years. Then everything in this book is a description of the world your children negotiate, and the institutional questions in Part V are urgent.

Now suppose it takes four hundred years, or never happens at all. What have you actually lost by reading this?

You have lost nothing, because the five jobs are real right now. Death is setting the discount rate today. Inheritance is redistributing capital today. Scientific fields are reorganizing after their leading figures die today, and there is data on it. Careers are queues today, and gerontocracy is a live complaint in politics, in universities and on corporate boards today, with mortality still fully operative.

This book is, among other things, an argument that we already misunderstand a set of economic mechanisms because we cannot see the constant they rest on. That misunderstanding is causing errors now. Making the constant hypothetically variable is a device for seeing it, and the device works whether or not the hypothetical ever arrives.

So if you think the biology is a fantasy, read this as a thought experiment about the hidden structure of the present. The conclusions in Part II hold either way. Only the urgency changes.

The part that is already happening

There is one more reason not to wait for a breakthrough, and it is the reason I think this book is timely rather than speculative.

The effects do not require the full transition. They scale.

Every one of the five jobs depends on mortality continuously, not as an on and off switch. The discount rate contains a mortality term, so it moves whenever mortality moves, by however much. Inheritance flows depend on when people die, so they shift when the average shifts. The age at which authority vacates a chair is a number, and it drifts. Nothing here waits for a threshold to be crossed.

Which means that if my argument is right, we should already be able to see the early, mild version of it in the data. Not the dramatic version, but a measurable tilt in the predicted direction, over the decades in which healthy old age has been quietly extending.

We should see interest rates falling for reasons monetary policy does not fully explain.

We should see inheritance becoming a larger share of national wealth, and arriving later in the lives of the people who receive it.

We should see the average age of people holding senior positions rising, and the ladder underneath them getting slower.

We should see risk tolerance declining in wealthy societies, and safety regulation ratcheting in one direction only.

All four of those are documented trends. Every one of them has its own mainstream explanation, and I am not going to claim those explanations are wrong. I am going to claim they are incomplete, and that a single mechanism sits underneath all four, and that the mechanism is the one nobody looks at because it never used to move.

That is the case I will make over the next five chapters.

I want to have been clear about the strength of the claim, so let me restate it plainly one last time. I am not forecasting immortality. I am saying that mortality is an economic input, that it has begun to drift, that it may eventually move a great deal, and that we have no theory of what it does because we have never had to have one.

Assume a longer life. Not forever. Just longer. Then follow the money.