Adapted from a press release written by Arizona State University
The experiences we face early in life may leave lasting marks on our health that echo across decades—even throughout the body.
A new study published in Science (DOI), “Age and early life adversity shape heterogeneity of the epigenome across tissues in macaques,” examined a unique group of free-living rhesus macaques that researchers have followed throughout their lives. The study, which was co-led by Vanderbilt Postdoctoral Scholar in Biological Sciences Rachel Petersen and Arizona State University postdoctoral researcher Baptiste Sadoughi, and co-authored by Assistant Professor of Biological Sciences Amanda Lea and ASU School of Life Sciences Professor Noah Snyder-Mackler, paired detailed life histories with genomic data from 12 adult tissues.
The findings provide some of the clearest molecular evidence that early life adversity leaves a lasting, body-wide imprint on the epigenome, or the layer of biological information that regulates gene activity without changing the DNA sequence itself. The findings could help researchers better understand the factors that contribute to healthy aging.
“There has been a great deal of interest in understanding how early life experiences become biologically embedded and influence health decades later,” said Lea. “Our study shows that early-life conditions can leave lasting molecular traces across the body. More broadly, the findings suggest that understanding healthy aging requires looking beyond chronological age to consider how an individual’s life experiences shape biological processes over time.”
The researchers focused on DNA methylation, an epigenetic process that regulates how genes are expressed and one of the best-studied biological markers of aging. They analyzed DNA methylation patterns from 237 macaques living in semi-natural conditions on Cayo Santiago, a 38-acre island off Puerto Rico’s eastern coast that is home to more than 1,500 free-ranging rhesus macaques. From this data, the researchers built tissue-specific “epigenetic clocks,” which estimate both an individual’s chronological age, or how long an organism has lived, and biological age, or how old it appears physiologically.
Because rhesus macaques share many biological and social characteristics with humans, they provide a valuable model for studying how life experiences shape health. By combining DNA methylation data from multiple adult tissues with detailed records of early-life experiences, the researchers uncovered how adversity and biological aging interact at the molecular level.
“The complex social environment in which these animals live is another major strength of this work,” Petersen said. “Unlike studies of laboratory animals, we can characterize the effects of naturally occurring variation in life experiences. This type of dataset is extremely rare and allows us to link detailed individual histories to molecular changes across the body in a way that is not possible in most human studies.”
The team found that aging does not affect all tissues equally. Age-related DNA methylation changes varied significantly across the body. Tissues such as the thymus and pituitary gland showed especially strong age-related patterns, while others changed more gradually. Despite those differences, researchers also found evidence of coordination across tissues. Animals that appeared biologically older in one tissue often appeared older in others, suggesting that aging functions as a partially connected process throughout the body.
The study’s most striking findings emerged when researchers examined early life adversity, including maternal loss, low maternal social status, and growing up in crowded social groups. These experiences left measurable signatures in DNA methylation across multiple tissues.
“One of the most exciting and surprising findings was that early-life adversity leaves signatures in our cells that can be detected across many different tissues, and long after the adversity has occurred,” Lea said. “Further, while some researchers have proposed that adversity might accelerate the aging process, we found that early life adversity signatures do not consistently look like accelerated aging at the molecular level. Instead, early life experiences impact our biology in more complex ways.”
The researchers identified thousands of genomic regions where DNA methylation was associated with early life adversity. Many overlapped with regions affected by aging, but the effects did not follow a consistent pattern.
“In some cases, adversity-related changes looked like accelerated aging. In others, they went in the opposite direction,” Petersen said. “This tells us that early adversity doesn’t simply ‘speed up’ aging. Instead, it reshapes the epigenome in more complex ways.”
These findings challenge the common assumption that adversity uniformly accelerates biological aging. Instead, the results suggest that early experiences alter the trajectory of molecular aging in different ways across tissues. The findings also suggest that adversity influences long-term health through mechanisms that extend beyond aging alone. By showing how early experiences shape the epigenome across tissues, the study identifies a potential biological mechanism linking childhood conditions to health later in life.
At the same time, the findings highlight the complexity of those relationships. Different forms of adversity do not produce identical biological effects, meaning researchers must consider context, timing, and individual variation when predicting long-term outcomes.
“This is not a simple story, but that’s what makes it exciting,” Lea said. “We’re beginning to see how life experiences are written into our biology—and why those signatures might vary within and between individuals.”
The National Institute on Aging, part of the National Institutes of Health, funded the study.