Matter Bio: Learning from 400-Year-Old Sharks to Protect the Human Blueprint

A longevity study like no other

Matter Bio is launching what CEO Christopher Bradley calls “the largest study of its kind.” On the human side, the project will include up to 10,000 centenarians and 20,000 of their relatives, a cohort ten times larger than any ever assembled.

On the animal side, the study will cover dozens of long-lived and short-lived species, with around 30 individual animals per species. Each animal contributes nine different tissues, and each tissue is analyzed with three omics readouts, creating a dataset of unprecedented density and scale.

Crucially, the comparisons are not just between humans and animals. As Bradley explains: “We are not comparing sharks to people. We're comparing sharks that live 400 years to sharks that live 20, whales that live 200 years to whales that live 15, and then that difference we're comparing to us and to see what's going on.”

This design isolates the genetic and molecular factors that distinguish longevity even within the same species — a powerful way of teasing apart correlation from causation before extrapolating those mechanisms to human biology.

The goal is ambitious: to uncover the genetic and molecular machinery that keeps DNA stable in the longest-lived organisms on Earth — and then translate those strategies into therapies for humans.

Why DNA stability?

Bradley’s first-principles lens treats aging as information loss driven by damage and entropy. “I believe that time is kept in the DNA of the cell, the blueprint of the ship, of Theseus' ship. The blueprint… gets scratched, aged, changed, broken, rearranged. Then things start to go wrong. And that is not programmed. I think it's random.”

Damage, he argues, is inevitable—both endogenous and exogenous. “Life, humans and cells and all life on Earth is busy maintaining order despite the universe wanting to create disorder and destroy the order that exists.”

Within that frame, telomere attrition, epigenetic drift, and protein misfolding are all forms—or consequences—of information loss: “So I think telomere attrition is another form of information loss… If you solved telomere attrition, great. You wouldn't solve the loss of information in between those two ends.”

Comparative mutation work also shapes his view: across animals, end-of-life mutation burden clusters within a range, but the rate of accumulation tracks lifespan. “A mouse will get hundreds of mutations a year, and a human will get dozens… at the end of life, they'll both have 2,000 to ...