Scientists make a breakthrough in measuring aging through DNA

What if your body’s age wasn’t just the number of birthdays you’ve had? Scientists are now exploring a new way to track the passage of time inside your cells—by measuring how unpredictable certain patterns in your DNA become as you grow older.

Researchers from the University of California, Los Angeles have introduced a fresh tool that may one day improve how we measure biological aging. Instead of just counting chemical tags on DNA like before, this method focuses on the randomness of those tags. It’s called methylation entropy—a measure of how varied and disordered these chemical patterns become over time. Their findings suggest that this entropy could be just as accurate as current age prediction methods—and, in some cases, even better.

The new study, published in the journal, Aging-US, looked at over 3,000 regions of DNA from people between the ages of 7 and 84. These samples came from cells inside the cheek, collected through simple buccal swabs. The scientists then used a technique called targeted bisulfite sequencing to read the DNA and examine the methylation patterns.

What they found was both surprising and promising. As people aged, the randomness—or entropy—of these methylation patterns changed in clear, repeatable ways. Sometimes the DNA became more chaotic, and sometimes it became more orderly. These shifts didn’t always match how much methylation was happening, showing that entropy could give new insight into aging that traditional methods miss.

To understand this new discovery, it helps to know how DNA methylation works. Think of your DNA as a long instruction manual. Some instructions are meant to be read often, others only at special times. Methylation is like placing bookmarks on certain pages—it helps control which parts of the DNA are active or silent.

Over time, the placement of these bookmarks starts to change. Some may get lost, others added in new places. These changes are known to be tied to aging and have led to the creation of what are called epigenetic clocks. These clocks estimate how old your body really is, based on your DNA.

Until now, most clocks focused on the average number of bookmarks, or methyl groups, found in certain DNA regions. But this approach may overlook an important part of the story. As the new research suggests, the pattern and disorder of these bookmarks might matter just as much as how many there are.

According to the research team, “[…] methylation entropy is measuring different properties of a locus compared to mean methylation and CHALM, and that loci can become both more or less disordered with age, independently of whether the methylation is increasing or decreasing with age.”

The researchers used a method that tracks the arrangement of methylated and unmethylated sites on individual DNA strands. Each region studied had four CpG sites—places in the DNA where methylation commonly happens. With four sites, there are 16 possible patterns. The more spread-out these patterns were across a population, the higher the entropy.

They studied samples from 100 people and found that entropy changed with age in consistent ways. At some locations, patterns became more random, while others grew more ordered. Importantly, these changes were not always tied to whether methylation levels were rising or falling. This means entropy provides new and separate information.

To test how well this entropy measure could estimate age, the scientists used both statistical models and machine learning techniques. On its own, entropy performed well. But when combined with average methylation levels and another method called CHALM (Cellular Heterogeneity-Adjusted cLonal Methylation), predictions improved even more. In some cases, the average error between predicted and actual age was just five years.

The results connect with a growing theory: aging may partly result from a gradual breakdown of the biological “instructions” that keep your cells functioning. These instructions, stored in the form of epigenetic information, can be disrupted by time, stress, or damage. When that happens, cells may forget how to behave—and the body begins to show signs of aging.

Past research has shown that DNA methylation plays important roles beyond aging. It helps silence the second X chromosome in females, regulates imprinted genes, and suppresses harmful gene expression. But when methylation goes off course, it can also contribute to problems like cancer.

Many methylation changes seen with age are called epigenetic drift. Some CpG sites become more methylated, especially in key regulatory regions, while others lose their marks. These shifts can silence developmental genes, similar to what happens in some tumors.

Because of this, scientists have been developing better tools to track these changes. Epigenetic clocks created by earlier teams have shown strong links between methylation and age, with correlations above 0.90. But those clocks focused on averages. This new study adds a deeper layer by showing that how methylation is distributed across sites—the entropy—may offer unique and useful signals.

What makes this discovery exciting is its potential to improve the precision of biological age estimates. Current models might miss subtle changes that entropy can detect. And if age-related diseases are tied to these disruptions, spotting them earlier could help in treatment or prevention.

Entropy-based analysis could also support recent studies exploring how to reverse signs of aging. One mouse study triggered aging by causing breaks in DNA. When key factors were added to the cells, some of the aging signs reversed. If methylation entropy reflects that loss—and possibly the recovery—of epigenetic information, it might become a valuable way to track therapies.

Another study showed that slow-dividing cells maintain more ordered methylation patterns over time than fast-dividing ones. This adds to the idea that methylation disorder builds up randomly with age. By measuring this randomness directly, entropy could become a new tool in the search for treatments that slow or even reverse aging.

Still, more research is needed. This study used cheek cells. Scientists will need to explore whether the same patterns hold true in other tissues like blood, skin, or organs. And while entropy appears promising, it may need to be paired with other metrics for the best results.

In the meantime, this work opens a new chapter in how we think about aging. Rather than just counting how many changes happen in our DNA, we may need to look at how organized or disordered those changes are. In other words, aging might not just be about what’s added or lost—but about how much sense the DNA still makes.

Note: The article above provided above by The Brighter Side of News.

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