GOCHANG, South Korea, June 13 (AJP) -Three scientists who have spent careers studying people who live to 100 gather in South Korea — and find, to their surprise, that their very different methods have led them to the same place. They arrived in Gochang, a rural county on Korea's southwestern coast three very different arguments about why some people live to 100.
By the time their conversation ended, the geneticist, the epidemiologist, and the social gerontologist had reached a quiet consensus: the secret to a long life may be that there is no single secret at all.
The occasion was the 30th International Centenarian Consortium, the world's foremost gathering of researchers studying extreme old age. What follows is an edited transcript of the special closing dialogue,
convened on June 12.
______________________________________________________________________
PART I — HOW THE QUESTION CHANGED
______________________________________________________________________
SANG-CHUL PARK · Chonnam National University
When this consortium first met in Georgia in 1994, the question was simple: why do some people live to 100? Thirty years later, we are no longer asking that. We are asking something harder — how can people live healthily to 100? That is not a semantic shift. It is a moral one.
TOM PERLS · Boston University
That shift is the core of what this meeting has been about. Moving from lifespan to healthspan. We have spent a generation learning to count the years. Now we have to learn to fill them.
PETER MARTIN · Iowa State University
And that reframing changes everything — what we measure, what we treat, what we consider a success. When I started tracking people in their 90s toward becoming centenarians, I was not asking whether they would survive. I was asking what shape they would be in when they arrived.
______________________________________________________________________
PART II — ON GENES, AND THEIR LIMITS
______________________________________________________________________
PERLS
If we expected to find one longevity gene — one switch to flip — we were being naive. Longevity is polygenic. Thousands of variants, each tiny on its own, but in the right combination, powerful. It is like a lottery. You do not win by holding one ticket. You win by combining dozens of them correctly.
What is striking is that centenarians carry disease-causing variants at roughly the same frequency as the general population. What distinguishes them is a higher burden of protective variants — inimmune regulation, lipid metabolism, DNA repair. They are not genetically pristine. They are better buffered.
PARK
Our whole-genome study of 60 Korean centenarians found something that stopped us. One DNA repair gene, BRCA1, was completely intact across more than 110,000 sequences — not a single variant. Silence, in genetics, can be the loudest signal of all.
We also found that 99.74 percent of those centenarians carried the same deletion variant in a calcium-channel gene, ORAI1 — a mutation that standard databases classify as disease-causing. In our centenarians, it appears to suppress chronic inflammation. The genome knows things our databases do not yet.
PERLS
That finding matters far beyond Korea. Our reference genomes are overwhelmingly European. Variants common in Asian populations get flagged as pathological when they may be protective. We need a centenarian reference pangenome built from many ethnicities. This Korean dataset is a founding contribution to that work.
______________________________________________________________________
PART III — TEN YEARS INSIDE THE BODY
______________________________________________________________________
MARTIN
Listening to the genetics, I keep asking: how does this actually manifest, year by year, in a living person? My team tracked 516 people who would go on to reach 100, following them from age 90.
At 90, arthritis and hypertension were nearly universal. Over the next decade, disease burden grew — but it grew very differently depending on what was being managed.
The practical implication is morbidity compression. People who carried less disease burden into their early 90s retained more functional independence at 100. The interventions you make at 92 shape the person you are at 100. That window does not close as early as people assume.
PERLS
This connects directly to what I mean by resilience. Fifty-five percent of centenarians have dementia. Frailty is present in over 95 percent. They are not, by any clinical measure, super-healthy. What they have is the capacity to carry illness for longer without losing the ability to function. Telomere maintenance, low chronic inflammation, distinctive
gut microbiota — these are the molecular substrates of endurance, not immortality.
______________________________________________________________________
PART IV — WHAT THE FIELD GOT WRONG ABOUT CENTENARIANS' LIVES
______________________________________________________________________
PARK
I interviewed centenarians in Korea's longevity regions in 2001 and again in 2025. In 2001, nearly 88 percent lived with their children.
More than half were confined to their rooms. A centenarian living alone was considered a social failure — a sign that the family had abandoned its duty.
By 2025, half were living independently. Half were traveling beyond their villages. We documented a 97-year-old man who drove himself to Jeju Island. The same life circumstances that once signaled abandonment now signal agency.
MARTIN
What changed? The policy infrastructure, obviously — Korea's Long-Term Care Insurance, the community care services, the Basic Pension.
But also what changed is what centenarians expect of themselves. They now go to lunch at community centers. They write poetry. They walk an hour every morning. They have developed a self-concept that wasn't available
to their predecessors.
PERLS
And social connection has biological consequences. Loneliness and isolation elevate chronic inflammation — the same pathway that accelerates aging. The social lives of centenarians are not a soft human-interest sidebar to the real science. They are the real science.
______________________________________________________________________
CODA — WHAT WE HAVE LEARNED
______________________________________________________________________
PARK
The three of us have studied the same population for three decades using entirely different methods. Tom looked at their genes. Peter looked at their clinical trajectories. I looked at the land, the policy, the society they inhabit. Our conclusions have converged.
A centenarian is not created by a single secret.
PERLS
And that is actually good news. If there were one dominant cause, we could change nothing. Because longevity is multi-determined, there are multiple places to intervene. Lifestyle, social policy, medicine, genetics — they all move the same needle. The absence of a single answer is an invitation to act on many fronts at once.
MARTIN
For me, the reward is simpler. If our data helps one person in their early 90s reach 100 a little healthier and a little more
independently, that is sufficient reason to keep counting.
______________________________________________________________________
Sang-Chul Park is chair professor at Chonnam National University and the founder of the Korean Centenarian Study, which he has led since 1995. He was the principal organizer of the 30th International Centenarian Consortium.
Tom Perls is professor of medicine at Boston University and founder of the New England Centenarian Study, one of the world's longest-running investigations into the genetics of extreme longevity.
Peter Martin is professor of human development at Iowa State University, specializing in the clinical trajectories and psychological well-being of adults in their 90s and beyond.
*This dialogue was conducted at the close of ICC 2026 in Gochang, South Korea, and has been edited and condensed. It is published as a special feature for AJP.
Copyright ⓒ Aju Press All rights reserved.