Study finds early life adversity doesn't just speed up aging — it changes how the body ages

When people talk about aging, they often picture it as a single process unfolding throughout the body. But new research involving rhesus macaques suggests the reality is much more complex.

An international team of researchers, including scientists from Arizona State University's School of Life Sciences and Center for Evolution and Medicine, found that different organs age in different ways at the molecular level. Their findings also challenge a common assumption about early-life adversity: Rather than simply accelerating aging, difficult experiences early in life appear to alter how aging unfolds across the body.

Published in Science, the study examined DNA methylation, which are chemical markers that regulate how genes are expressed without changing the underlying DNA sequence across multiple tissues in rhesus macaques. The work provides one of the most detailed maps to date of how aging affects the body's epigenome.

"We often say that someone is aging, as if it's one universal process," said Baptiste Sadoughi, a postdoctoral researcher in Professor Noah Snyder-Mackler's lab and co-first author of the study. "But there is more and more evidence that the decline in different functions doesn't necessarily happen at the same speed or at the same time."

Because researchers have decades of life-history data for the monkeys, they were able to examine how DNA methylation changed across the lifespan while also accounting for early-life experiences. Sadoughi's role focused on organizing and analyzing vast amounts of genomic data to build an atlas of DNA methylation across different tissues before investigating how those patterns changed with age.

The team expected to find many of the same molecular changes occurring throughout the body. Instead, aging looked different depending on the organ.

"It's a mosaic," Sadoughi said. "The areas that change are not the same."

For example, regions of the genome that changed in the heart were often different from those changing in the liver or other organs. The discrepancies suggest that hardships early in life can shorten lifespan in ways that are not simply explained by faster aging.

At the same time, the researchers found that those organs were still broadly aging together. By developing biological "clocks" based on DNA methylation, they discovered that individuals who appeared biologically older in one organ generally appeared older in others as well, even though the molecular changes producing those estimates differed from tissue to tissue.

The study also offers a more nuanced understanding of how early-life adversity influences long-term health.

Previous research has linked childhood adversity with higher risks of disease and earlier death, leading many scientists to hypothesize that difficult early experiences simply accelerate biological aging. To test that idea, the researchers examined several forms of adversity experienced by the macaques early in life, including the loss of a mother and challenging social conditions.

The results were more complicated than expected. Rather than making every tissue appear biologically older, early-life adversity produced different effects across the body. Some tissues appeared younger, one appeared older and most showed no significant difference in biological age.

"Early-life adversity and aging overlap, but they're not exactly the same thing," said Rachel Petersen, a postdoctoral researcher at Vanderbilt University and co-lead author on this study.

The findings suggest that aging is only one biological pathway through which early experiences influence later health. Other mechanisms, many of which scientists have yet to identify, likely play important roles as well.

Although the research helps explain how early experiences become biologically embedded, Sadoughi cautioned against interpreting the findings to mean that childhood adversity permanently determines a person's future health. While early adversity is an important risk factor, many later-life influences, including social support and access to resources, can shape long-term outcomes.

"We know people are not doomed," he said. "If we support people and acknowledge they're at greater risk, there is good evidence that we can buffer those early traumatic experiences."

Beyond improving scientists' understanding of aging, the work could also help advance new biomarkers of health. Researchers hope that one day, DNA methylation patterns measured from a simple blood sample could provide clues about the health of less accessible organs throughout the body.

For now, the study highlights just how much remains to be learned about aging. Rather than following a single clock, the body's organs appear to keep time in different ways, revealing a more intricate picture of how experiences across a lifetime shape health.