The experiences we face early in life may leave their marks on our health in ways that echo across decades—and even across the entire body.
A new study, published today in the journal Science (DOI:10.1126/science.aea4922), examined a unique group of free-living, rhesus macaques who have been followed their entire lives to document their experiences. Pairing these histories with genomic data from 12 tissues collected in adulthood, the study provides some of the clearest molecular evidence yet that early life adversity leaves a lasting, system-wide impression at the epigenome, the biological layer on top of the human genome that regulates gene activity.
Led by researchers at Arizona State University and Vanderbilt University, along with collaborating institutions, the study examined telltale aging hallmarks of the epigenome—called DNA methylation patterns. DNA methylation is one of the most well-studied markers of aging and can be used to build "epigenetic clocks" that estimate both an organism's chronological age (how long it has been alive) and biological age (how old it appears physiologically).
"Our goal was to understand how aging unfolds across the body, and how early experiences might influence that process," said study co-senior author Noah Snyder-Mackler, a professor in Arizona State University's School of Life Sciences. "What we found is that early life adversity leaves a coordinated epigenetic signature that spans multiple tissues—but it doesn't simply accelerate aging in a uniform way."
In this study, researchers developed highly precise tissue-specific clocks, capable of predicting age within about one year of an individual's chronological age. They conducted their study of 237 macaques, who live in semi-natural conditions on Cayo Santiago (colloquially referred to as "Monkey Island"), a 38-acre island off Puerto Rico's east coast. The island is inhabited by over 1,500 free-ranging rhesus macaques and managed by the University of Puerto Rico and Caribbean Primate Research Center. By integrating multi-tissue DNA methylation collected in adulthood with detailed records of early life experiences, the team uncovered how adversity and aging interacted to shape biology at the molecular level.
What they found was that despite this epigenetic precision, aging did not occur uniformly across the body. Instead, the researchers found that age-related changes in DNA methylation were highly tissue-dependent.
"At a molecular level, aging looks very different depending on which tissue you examine," said Amanda Lea, assistant professor of Biological Sciences at Vanderbilt University, co-senior author of the study. "Blood, which is most commonly measured in human studies, only captures part of the picture." Some tissues, like the thymus and pituitary gland, showed particularly strong and distinct age-related patterns, while others exhibited more subtle changes.
Yet even amid this diversity, individuals showed a degree of internal consistency. Animals that appeared "biologically older" in one tissue tended to appear older in other tissues as well, suggesting that aging operates as a partially coordinated process across the body.
The study's most novel insights came from examining early life adversity—defined through naturally occurring conditions such as maternal loss, low maternal social status, or growing up in a crowded social group. These experiences were not only associated with changes in DNA methylation, but in a strikingly coordinated way across tissues. "We found that each type of adversity tends to affect specific regions of the genome," said Lea. "But once it targets those regions, the effects are often shared across multiple tissues."
In total, the team identified thousands of genomic regions where DNA methylation was associated with early life adversity. These regions frequently overlapped with those affected by aging—but importantly, the direction of the effects was not consistent.
"In some cases, adversity-related changes looked like accelerated aging. In others, they went in the opposite direction," explained co-lead author Rachel Petersen, a Vanderbilt postdoctoral researcher. "This tells us that early adversity doesn't simply 'speed up' aging. Instead, it reshapes the epigenome in more complex ways."
This finding challenges a common assumption that early adversity uniformly accelerates biological aging. Instead, the results suggest a more nuanced model, in which early experiences alter the trajectory of molecular aging, amplifying the effects of aging in some tissues, such as the pituitary, but not others. These findings further suggest that the well-documented effects of early adversity on health operate, at least in part, through mechanisms that are not directly linked to aging.
The study also highlights the importance of studying multiple tissues. Many previous studies have relied on blood samples, which are relatively easy to collect. However, the new findings show that this approach may miss critical aspects of how aging and environmental exposures affect the body.
"Different tissues have their own epigenetic landscapes and respond differently to both age and adversity," said co-lead author Baptiste Sadoughi, an ASU postdoctoral researcher. "To fully understand health and disease, we need to take a whole-body perspective."
The use of rhesus macaques, which share many biological and social similarities with humans, adds to the study's relevance. Unlike laboratory animals, these macaques live in complex social environments, allowing researchers to capture naturally occurring variation in life experiences.
"This kind of dataset is incredibly rare," said Lea. "It allows us to connect detailed life histories with molecular changes across the body in a way that simply isn't possible in most human studies."
Beyond its scientific contributions, the research has important implications for understanding the developmental origins of health and disease. By showing how early experiences shape the epigenome across tissues, it provides a potential mechanism linking childhood conditions to later-life outcomes.
"Early life is a critical window for biological development," said Snyder-Mackler. "Our findings suggest that experiences during this period can leave lasting marks on the genome that influence health trajectories over the lifespan."
At the same time, the complexity of the results offers a note of caution. Because all types of adversity do not have uniform effects, predicting long-term consequences will require a more detailed understanding of context, timing, and individual variation.
"This is not a simple story," Lea said. "But that's what makes it exciting. We're beginning to see how life experiences are written into our biology—and why those signatures might vary within and between individuals."
As researchers continue to explore the interplay between environment, epigenetics and aging, studies like this one are helping to redefine what it means to grow older—not just as a function of time, but as a dynamic process shaped by the unique experiences that can truly define our lives.
For a full list of authors and institutions, go to (DOI 10.1126/science.aea4922). The study was made possible by funding from the National Institutes of Health, including the National Institute on Aging (grants R01AG060931, R01AG084706, R00AG075241, and R21AG078554), the National Institute of Mental Health (R01MH118203) and the Office of Research Infrastructure Programs (P40OD012217); the National Science Foundation (SMA-2105307, BCS-2041654, and SBE-2313953); the Hevolution Foundation/American Federation for Aging Research; and The Leakey Foundation.
