It’s possible that I shall make an ass of myself. But in that case one can always get out of it with a little dialectic. I have, of course, so worded my proposition as to be right either way (K.Marx, Letter to F.Engels on the Indian Mutiny)
Monday, June 22, 2026
Early life adversity leaves lasting molecular imprint across the body
New primate study reveals how life experiences can shape aging in multiple tissues
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.
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.
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).
Cayo Santiago (colloquially referred to as “Monkey Island”), is 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.
Early childhood adversity is connected to poorer physical and mental health across a person’s lifespan, and the biological mechanisms that translate the lived effects of poverty and trauma into physical functions are starting to come to light.
A growing body of research has shown that psychosocial stress influences mitochondrial function, and mitochondria play a pivotal role in stress-related diseases and aging.
UCLA psychologists have now connected early childhood adversity to changes in how mitochondria produce energy, which may affect cellular function with adverse effects on mental and physical health.
Experiencing adversity early in life, such as abuse or neglect, is connected to poorer physical and mental health across a person’s lifespan. How the biological mechanisms that translate the lived effects of poverty and trauma into physical functions and mental health are starting to come to light, thanks to new research out of UCLA.
Psychologists at UCLA have discovered that mitochondria in cells have increased respiratory capacity after experiencing greater early-life adversity. This discovery, published in the journal Biological Psychiatry, suggests that mitochondria might be better able to respond to cellular stress by producing more energy. However, this kind of heightened response can be maladaptive in the long-term.
“This study is the first to examine early life adversity and mitochondrial bioenergetics in a diverse sample of adult men and women, and the first to examine distinct dimensions of threat and deprivation in relation to mitochondrial function,” said UCLA doctoral student Shiloh Cleveland, the paper’s first author. “Elucidating how adversity in childhood and adolescence relates to mitochondrial function could inform targeted intervention efforts earlier in the lifespan to promote positive health outcomes before the onset of age-related diseases.”
With colleagues in the Sumner Stress Lab at UCLA, Cleveland recruited 143 volunteers who completed a questionnaire on early-life adversity and submitted a blood sample. The researchers subjected live cells from the blood samples to a “stress test” to measure their bioenergetic function and found that cumulative experiences of early-life adversity were associated with increased respiratory capacity. The mitochondria from volunteers who had experienced early life adversity had a greater capacity to produce energy while under cellular stress, suggesting that cells respond to stress by producing more energy. However, this kind of “hypermetabolism” can be harmful to cells in the long term.
When the researchers drilled down into the analysis to consider different kinds of adversity, they found unique patterns. Threat was associated with lower cellular energy production, while also being prepared to meet the demands of potential future cellular stressors. Deprivation was associated with increased inefficient energy production, which researchers said may indicate greater cellular dysfunction.
“Under chronic stress, mitochondria may adapt in ways that supply cells with the energy needed to respond quickly to adversity, which can be useful in the short-term when they actually need to respond to these challenging experiences,” said UCLA psychologist Jennifer Sumner, the paper’s senior author. “But, over time, if the mitochondria are always working as if they’re under stress even when they’re not, it might wear them out more quickly and lead to adverse downstream effects on the cell. In the long run, performance could decrease to less than optimal levels, which can affect health in harmful ways.”
The results showed that the effects of adversity are not solely cumulative. The type of adversity experienced may be uniquely related to mitochondrial function.
“This study’s findings suggest that taking a more nuanced approach to thinking about experiences of early adversity may help to shed light on distinct mechanisms of the biological embedding of stress,” said Sumner.
The authors plan future research to explore the mechanisms by which early adversity affects health across the lifespan to inform better intervention and prevention efforts.
The research was funded by the National Heart, Lung, and Blood Institute and the National Center for Advancing Translational Sciences.
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