Some moments only make sense looking back. Walking into Steve Horvath’s lab at UCLA was one of them. I had no idea how much it would change my life, my work and my sense of what was possible. I only knew my career was about to change.

A few years later I was flipping through YouTube and clicked on Joe Rogan’s interview with David Sinclair, a Harvard geneticist. A couple of minutes in, Sinclair was describing a new study that had turned back biological age, measured with Horvath’s clock.

What?! Did he just say that? Epigenetics and the Horvath clock, in front of millions of listeners?

That fall Sinclair published his book, LifeSpan. I read it, listened to it, and read it again.

The idea in plain English

Here’s the book’s big idea, as best a non-scientist can put it.

Your DNA is like digital information. It’s stable, it copies accurately, and the same code sits in nearly every cell of your body from the day you were conceived. It has survived billions of years of evolution. It’s tough.

The epigenetic layer on top of your DNA is more like analog information. It decides which genes each cell uses, which is how the same code makes a nerve cell, a muscle cell or a blood cell. It responds to how you live. But analog information wears out. Picture scratches building up on a disc.

Over time, Sinclair argues, cells lose the information that tells them what to be. A skin cell gets worse at being a skin cell. That loss of epigenetic information is, in his theory, a root cause of aging.

That was my eureka moment. It explained why the clocks work. If aging is partly the slow loss of epigenetic information, then reading the epigenetic layer is reading aging itself.

What’s happened since

A theory needs evidence. Some has arrived, so far in mice.

In one experiment, Sinclair’s lab used a set of genes that reprogram cells to reset the epigenetic age of nerve cells in the eye. Old mice got their vision back.

In another, his team went the other way. They caused small breaks in unimportant stretches of DNA in young mice, forcing cells to reshuffle their epigenetic marks without changing the code itself. The mice aged fast. By ten months old they were as frail as two-year-old mice. Partial reprogramming then rolled back some of those changes.

Mice are not people. Not every scientist agrees that epigenetic loss is the main driver of aging. Some put more weight on mutations and other damage. The human proof is still ahead of us.

What I believe

I still believe the core of it. Your DNA is not your destiny, and the epigenetic layer is where much of the story of how you age gets written. The clocks built on that layer are now among the most widely used measures of biological aging.

I also believe we have more say over that second age than most people think. That’s the part I find most hopeful.

LifeSpan made a hard subject readable and exciting. Anyone curious about why we age should read it. Thank you, David Sinclair, for writing it.

This is not medical advice.

Sources

Jon Sabes is a named inventor on U.S. Patent No. 11,817,214 and managing member of LongevityFP Technologies, LLC, which holds an exclusive license to FOXO Technologies’ epigenetics technology.