In 1952, polio put 58,000 Americans in hospital in a single summer.

Children. Iron lungs. Whole families rearranged around a disease that arrived without warning and left without mercy. The scale of it is hard to hold in your head now. Cities closed public swimming pools. Parents kept children indoors. Terror was not too strong a word.

Jonas Salk published his vaccine in 1955. By 1979, the United States was polio-free. Globally, a 99% reduction. We look back at that story now as an obvious turning point, one of those moments where medicine crossed a permanent line and everything after it was different.

The people living through 1952, 1953, 1954 had no idea. They were managing the crisis in front of them. The polio summer of 1952 was a public health emergency, not a history lesson. The breakthrough that was three years away was invisible from inside the fear.

I keep coming back to that gap. The gap between being inside a moment and being able to see it for what it is. Because I think we are inside one of those moments right now. And I am not sure we are noticing.

This week on RTHK Radio 3 Morning Brew, Phil Whelan and I talked about two pieces of science that, on the surface, appear to have nothing in common. One is about where human language came from. The other is about how long we might live. Together, they are asking the same deeper question: what did we think we knew about being human, and what is science quietly revising?

---

The First Story: Language Did Not Begin With Us

There are tiny sequences in the human genome (they make up 0.1% of all our DNA) that researchers have now identified as the primary drivers of language capacity. They’re called HAQERs, which stands for Human Accelerated Quasi-palindromic Elements with Repeats. The naming is unwieldy. The finding is not.

These sequences have 200 times more influence on language ability than anything else in our genome. They are, in effect, genetic volume knobs for the thing that makes us human. Researchers at the University of California Santa Cruz published the finding in Science Advances on 11 June 2026.

Here is the part that should stop you: they found HAQERs in Neanderthals too. In some cases, the Neanderthal version appeared to be more pronounced than ours.

Which means language did not begin with Homo sapiens.

It began much earlier. And we may have inherited the hardware from the species we displaced, or competed out of existence.

Neanderthals emerged around 400,000 years ago. Homo sapiens arrived in Europe around 45,000 years ago. For roughly 5,000 to 10,000 years, the two species lived alongside each other. They shared territory. They interbred. Non-African humans today carry 1 to 4% Neanderthal DNA. Then Neanderthals disappeared, around 40,000 years ago.

We have spent the centuries since telling ourselves that what separates us from every other species, what makes Homo sapiens the ones who made it, is intelligence, and specifically language. Stories, culture, religion, governance, markets. The whole architecture of human civilisation sits on a foundation of language.

This research is suggesting that foundation may not have originated with us. We may have inherited it. Or out-competed people who had as good or better hardware.

Phil asked me on air whether Neanderthals were telling stories, having arguments, making plans. The research does not decode the content. It identifies capacity. And capacity for complex language implies the need for it. You do not develop the biological infrastructure for something unless there is something to communicate.

The question this opens, which I find genuinely unsettling in the best way, is: what else did we take credit for?

Language is not just communication. It is infrastructure. It shapes not just how we exchange information but how we think. Earlier this year I explored how language shapes how generations relate to time and ageing. The Neanderthal finding pushes that conversation 350,000 years further back.

If language goes further back than we thought, then the foundations of storytelling, meaning-making, and social complexity predate Homo sapiens. That is either humbling or liberating, depending on how you look at it. I lean toward liberating. If what makes us human is not unique to us, then what makes us human is something we share across deep time, something that runs through us rather than originating with us.

Australian Indigenous languages carry some of the oldest continuous linguistic traditions on Earth. More than 250 distinct languages existed at the time of European contact, with evidence of continuity going back 50,000 years or more. The HAQERs finding does not diminish that extraordinary cultural richness. It contextualises it within a much longer story of language as the fundamental technology of social life.

---

The Second Story: The Ugliest Animal Alive Has Been Quietly Extraordinary

The naked mole rat is, by objective measure, one of the least appealing animals in existence. Hairless. Wrinkled. It lives underground in colonies. It has large, prominent front teeth. It is not the creature you would expect to carry one of the most significant biological discoveries of the decade.

And yet.

A rodent comparable in size to a naked mole rat, a standard mouse or rat, lives three to four years. The naked mole rat lives approximately thirty. It almost never develops cancer. Its cognitive function is maintained well into old age. It does not appear to age in the conventional sense. For decades, biologists knew this and did not know why.

Now they do.

The gene responsible produces a substance called high-molecular-weight hyaluronan, or HMW-HA. Think of it as a cellular bodyguard. It prevents cells from going rogue, which is what cancer is. It reduces the kind of inflammation that causes most of what we recognise as ageing: the slow degradation of tissue, organ function, and cognitive clarity that we have spent centuries treating as an inevitable feature of time.

Naked mole rats produce significantly more HMW-HA than other animals. Scientists transferred the gene into mice. The mice lived longer. They developed significantly less cancer. They maintained better health into old age.

The question nobody is saying out loud officially, but everyone is quietly asking in every longevity research lab on Earth, is: what if that works in humans?

About a year ago, Phil and I talked on air about the social and cultural shift already underway in how people are approaching ageing. That conversation became the blog post “Forget Growing Old, We’re Growing Forward”, about the Reinvented Elder, about Gen X demanding the right to live longer in good health, about the 100-year life as aspiration rather than anomaly. That was the cultural permission layer.

This is the biological layer arriving underneath it.

We spent centuries looking for the secrets of longevity in blue zones: Okinawa, Sardinia, the Nicoya Peninsula in Costa Rica. We studied diet, social connection, purpose, movement. All of it valuable. But the answer to one significant piece of the longevity puzzle may have been in a colony of wrinkled underground rodents in sub-Saharan Africa the entire time.

---

The Medicine Is Already Moving

The naked mole rat story is not sitting alone. It is landing in the middle of something larger, and that larger thing is what I want to spend time on. I do not think we are paying sufficient attention to it.

In 2024 and 2025, researchers published findings that would have seemed like science fiction twenty years ago. Let me be specific about what is actually happening.

Type 1 diabetes. Vertex Pharmaceuticals ran a clinical trial with a stem cell therapy called zimislecel. They grew insulin-producing cells in a laboratory from stem cells and transplanted them into people with Type 1 diabetes. These were people whose own pancreas had stopped working entirely, who have lived their whole adult lives measuring glucose and injecting insulin to manage a disease they were told could only be managed, never cured. Ten out of twelve patients in the trial were completely off insulin at the one-year mark. No injections. No pump. Published in the New England Journal of Medicine in 2025. Around 130,000 Australians live with Type 1 diabetes, most diagnosed as children.

Sickle cell disease. Casgevy, a CRISPR-based therapy, is now approved in the United States, the United Kingdom, the European Union, Canada, and several Middle Eastern countries. It is not a treatment. It is a cure. One dose. CRISPR edits the faulty gene in a patient’s own blood stem cells and reimplants them. Sickle cell disease causes a lifetime of severe pain crises, organ damage, and shortened life expectancy. It has been called a disease of the forgotten, affecting predominantly people of African descent, historically underfunded and under-researched. There is now a one-dose cure.

HIV. The virus hides inside DNA. That is why antiretrovirals can manage it but cannot finish the job. They cannot reach what is embedded in the cellular code itself. CRISPR can. Excision Biotherapeutics completed a Phase I/II trial using CRISPR to locate HIV DNA inside a patient’s cells and cut it out. Early stage. But the mechanism works in principle. Forty years ago, an HIV diagnosis was a death sentence. Now it is a manageable condition. The next step being worked toward is: it is gone.

Alzheimer’s. A gene variant called APOE4, carried by roughly 1 in 4 people, dramatically raises the risk of developing Alzheimer’s disease. Researchers now have the identified target and the CRISPR tools to potentially address it before symptoms begin. Trials are early. But the question has shifted from “can we find a target?” to “can we edit it?” That is a significant change in the conversation. Around 400,000 Australians currently live with dementia, with that number projected to reach 1 million by 2058. If gene therapy can intervene at the genetic level before the disease takes hold, the aged care picture, including the family caregiving picture and the superannuation picture, changes in ways we have not yet begun to account for.

And then there is KJ Muldoon. A baby born with a fatal rare genetic disease affecting fewer than 200 people on Earth. Scientists designed a CRISPR treatment specifically for him, for his exact mutation, never used before, never needed before. It worked. The era of personalised genetic medicine has already begun. Not as a prototype or a press release. It started with one baby and a condition most of us will never hear of. The template now exists for every rare disease.

In 2017 I wrote about eight frontiers in medicine that were then on the horizon. Several of those frontiers are now inside the building.

---

We Have Been Here Before

Tuberculosis killed one in every seven people in the 1800s. It was called consumption. It was a death sentence. Treatment was essentially none. People went to sanatoriums and waited. Now it is six months of antibiotics for most strains. We look back at the tuberculosis era the way you look at a photograph of someone wearing a gas mask in peacetime: distant, almost incomprehensible.

The polio summer of 1952. The vaccine in 1955. The eradication by 1979.

Our grandchildren will look back at Type 1 diabetes and sickle cell disease and HIV the way we look at polio and tuberculosis. The medicine is moving. We are living inside one of those moments right now. The difference between 1952 and now is not that progress is faster. There are more fronts opening simultaneously.

---

The Ripple Effects

When I wrote about the future of medicine and predictive health scoring last year, the conversation was about diagnostics, about knowing earlier. This week’s signals are about something upstream of diagnostics. They are about rewriting the biological code itself.

The ripple effects from that are significant and, in many cases, have not been thought through.

Superannuation systems were designed for a 65 to 85 retirement window. That window was built around life expectancy data from a world where most people aged in ways we may be on the edge of fundamentally altering. A 100-year healthy lifespan breaks the maths of every pension system on Earth. Not eventually. Within the working lifetimes of people currently in the workforce.

Aged care, as an industry, is predicated on a specific model of old age: frailty, cognitive decline, increasing dependency. If HMW-HA gene therapy eventually delays or prevents the cellular processes that drive that model, the aged care sector is not disrupted. It is restructured from the ground up. What it becomes, we do not yet have a name for.

The workforce. If you are healthy at 80, when do you retire? What does a career look like across 60 working years? The graduate-to-retirement arc that most organisational structures are built around was designed for lifespans and health spans we may be about to significantly extend.

Relationships. Marriages designed around a life expectancy of 70 look different when you are planning for 110. Not better or worse. Different. The social infrastructure of partnership, family, community, friendship: all of it was built around assumptions about how long people live and in what condition.

And there is the equity question, which I think is the most important one and the one least likely to be asked in boardrooms. Every major medical intervention in history has been wealth-stratified first. Vitamins, statins, preventive imaging, advanced diagnostics. Access precedes equity by years, sometimes decades. If longevity gene therapy reaches humans in 10 to 15 years, the gap between those who can access it early and those who cannot will be wider than any wealth gap we have previously encountered. This connects to a question I explored last year about what it means to know in advance how long you will live. Because if longevity becomes a purchasable extension, the existential stakes of that question change completely.

---

What This Means for How You Prepare

None of what I have described is certain. The gap between mice and humans is real. The gap between a CRISPR trial and a globally approved therapy is real. The pace of regulatory approval, manufacturing scale, and equitable access means that even the most promising science takes longer to reach people than the headlines suggest.

But the direction is clear. And direction, in foresight work, matters as much as timeline.

Here is what I think this demands of leaders, organisations, and individuals right now.

First, update your assumptions. The actuarial tables, retirement models, workforce planning frameworks, and healthcare cost projections that most organisations operate on were built around assumptions about human lifespan and healthspan that may be ten to fifteen years out of date. The signals arriving this week suggest those assumptions need reviewing, not eventually but now.

Second, follow the biology, not the hype. The headlines about AI and longevity are loud. The actual science is quieter, more specific, and more credible than the noise around it. The HMW-HA finding is peer-reviewed. The CRISPR sickle cell approval is regulatory fact, not announcement. Separating signal from noise in this space matters more than in almost any other.

Third, take the equity question seriously before it becomes a crisis. The access patterns for any longevity intervention that reaches humans will reproduce the access patterns of every previous medical breakthrough, unless organisations, governments, and health systems make deliberate choices to break that pattern early. The time to design for equity is before demand becomes apparent, not after.

Fourth, hold the human question. If you live to 150, you will outlive almost everyone you love. Multiple times. That is not a medical outcome. It is an existential one. The social, psychological, and relational dimensions of a longer lifespan have received almost none of the attention that the biological dimensions have. They need it.

We are somewhere around 1953 right now. The Salk vaccine is not published yet. But somewhere in a laboratory at the University of California, or a biotech in Brisbane, or a CRISPR lab in Seoul, the science that will change what ageing means is being assembled. And the question for organisations and leaders is not whether to wait and see. The question is whether you are paying attention clearly enough to see it while you still have time to prepare.

The naked mole rat had no idea it was extraordinary. It was just living its best life underground for three decades.

We should probably start taking it more seriously than it takes itself.

Choose Forward.

This post is based on my segment with Phil Whelan on RTHK Radio 3 Morning Brew, 17 June 2026.

Sources: Science Advances (11 June 2026); Nature World News (11 June 2026).