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Even if I didn’t know my birthday, I’d still know 30 is on the horizon. If it’s not the subtle but unmistakeable lines on my face, it’s the aches that linger after workouts I once considered cakewalks, or the punishment even the most mild hangovers bring.

These corporeal signs tell me, in no uncertain terms, that it’s time to round up from “my mid-20s” to “my late-20s," and drop the "young" from young adult. I can be vigilant about fitness, skincare and vodka-only nights out, but my whippersnapper days are behind me. 

Still, signs of aging aren’t measures of aging. New wrinkles may announce my march toward the grave, but they can’t tell me the rate at which I’m heading there. In fact, not much can. Even if we have the scientific capability to extend life, we can’t necessarily slow down the aging process. Phenomenologically, they’re distinct processes.

There’s a cruel irony at work. Increasing one’s longevity, as science currently understands it, probably translates to more years as an octogenarian (if you’re lucky) — not an extra decade to spend in one’s prime.

But scientists have stumbled on a breakthrough that may give us valuable insights into the aging process and, eventually, the chance to pump the brakes during young adulthood. It may eventually be possible to spend more time in our body’s good years. In 2007, researchers at the Scripps Research Institute (TSRI) in California found that an antidepressant called mianserin — a psychoactive drug in the tricyclic family — could extend the lifespan of ringworms by 30 to 40 percent.

Their findings were unexpected. Roundworms that received mianserin within the first 10 days of their lives (roughly through young adulthood, in worm-years) lived seven to eight days longer than their un-drugged intestine-dwelling mates. Once the worms were 12 days old, mianserin no longer had the same life-extending impact; the opportunity to game the game of life came with an expiration date.

There are known physiological changes to explain this. For one, there’s a newly discovered epigenetic phenomenon called transcriptional drift, whereby certain linked genes (that play a role in the same function) fall out of sync with one another as an organism ages.

“The orchestration of gene expression no longer seemed coordinated as the organism aged and the results were confusing because genes related to the same function were going up and down at the same time,” said lead study author Michael Petrascheck in a press release.

Got that? No? Okay, let’s try an analogy.

Imagine genes as wheels on a go-cart. Initially, the wheels all spin together, propelling the cart toward the finish line. Then, after a few years of hard use, one of the wheels comes loose and spins faster; another gets rusty and spins slower. Everything is the same age — including the go-kart’s body — but because they no longer work together, this older vehicle runs more slowly.

To be clear, transcriptional drift is the norm. This may be how we age — certain parts fall out of sync, lagging and dragging on the body as a whole. For the study in question, the worms that did not get mianserin exhibited such signs. The findings open the doors for a lot of exciting research. For example, how does transcriptional drift affect individual organs? How does the phenomenon respond to environmental and behavioral changes?

More importantly, we may eventually be able to use transcriptional drift as an objective measurement of aging.

These are early days, of course. Even the study authors aren’t even remotely prepared to translate these findings to the human experience. But, as crazy as it sounds, it’s possible that administering a psychoactive drug to young adults could prevent the dreaded transcriptional drift, granting them a few more years — in good health, at the prime of their lives.