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SAN DIEGO — Scientists have long wondered what makes our bodies age. Is it like a car slowly breaking down from wear and tear? Or more like a computer whose programming gradually goes awry? A new study from the University of California San Diego suggests both perspectives might be right, and in effect, challenges current approaches to anti-aging research.

For years, researchers have debated two main theories about why we age. The first suggests aging happens because our DNA accumulates random damage over time, like a beloved book slowly collecting tears and stains. The second theory focuses on epigenetic changes. These are modifications that control which genes are active without changing the DNA sequence itself, similar to how a piano goes out of tune in a specific pattern.

In recent years, scientists and biohackers have sought out ways to “reset” our epigenetic clocks in order to slow down the aging process. This latest study, published in Nature Aging, however, suggests DNA mutations prevents this level of biohacking from becoming a reality.

“Major research institutions and companies are betting on turning back the epigenetic clock as a strategy to reverse the effects of aging, but our research suggests that this may only be treating a symptom of aging, not the underlying cause,” explains Trey Ideker, Ph.D., a professor at UC San Diego School of Medicine and the Jacobs School of Engineering, in a statement.

By examining data from over 9,300 people, researchers discovered these two aging processes are closely linked. At the heart of this discovery are special spots in our DNA called CpG sites, where scientists can attach small chemical tags (methylation marks) that help control nearby genes. These tags work like tiny volume knobs that can turn genes up or down. As we age, the pattern of these marks changes so predictably that scientists have created “biological clocks” that can estimate someone’s age just by looking at their methylation patterns.

“Epigenetic clocks have been around for years, but we’re only now beginning to answer the question of why epigenetic clocks tick in the first place,” says first author Zane Koch, a Ph.D. candidate in bioinformatics at UC San Diego. “Our study demonstrates for the first time that epigenetic changes are intricately and predictably tied to random genetic mutations.”

What makes this discovery particularly fascinating is that when DNA damage occurs at CpG sites, it doesn’t just affect that single location. Instead, it creates a ripple effect, changing how genes are controlled across surprisingly long stretches of DNA — up to 10,000 genetic letters in either direction. This finding helps explain a puzzle that has long confused scientists: DNA damage happens relatively rarely and randomly, yet the changes in gene control that occur with aging are widespread and consistent. The new research shows that each instance of DNA damage can influence hundreds of nearby control switches, amplifying its impact far beyond the original site of damage.

Even more remarkably, the research team found they could predict someone’s age almost as accurately by looking at their pattern of DNA damage as they could by examining their methylation marks. Both methods even agreed on which individuals were biologically “older” or “younger” than their actual age would suggest.

“If somatic mutations are the fundamental driver of aging and epigenetic changes simply track this process, it’s going to be a lot harder to reverse aging than we previously thought,” notes co-corresponding author Dr. Steven Cummings, executive director of the San Francisco Coordinating Center at UC San Francisco. “This shifts our focus from viewing aging as a programmed process to one that’s largely influenced by random, cumulative changes over time.”