Stressful experiences during youth seem to leave a mark on a person’s genome decades later, in the form of withered chromosomal caps. As reported in PNAS, childhood stress correlates with increased odds to have shortened telomeres, the chromosome tips that protect essential genes from degradation but that shrink with age. Shortened telomeres have been linked to cardiovascular disease, diabetes, cancer, and early death.

“This is the first large, nationally representative dataset that has looked at this accumulation of stress,” says co-author Eli Puterman, a health psychologist at the University of British Columbia in Vancouver, Canada.

The authors used data from the ongoing University of Michigan Health and Retirement Study (HRS), which has been tracking people older than 50 since 1992. The study records 17 possible stressors ranging from the death of a spouse to being wounded in combat to requiring food stamps. The researchers simply totaled up how many stressors each subject experienced.

Of the 20,000 people in the study, 5,808 offered up saliva samples in 2008. From these, HRS researchers used PCR to measure telomere length. The study authors categorized the bottom quartile of telomere length as “short” telomeres, a common practice in epidemiology.

Each additional stressor raised a person’s odds of short telomeres by six percent. When the authors analyzed the data with respect to either 10 adult or seven childhood adversities, they found that adult stressful events, alone, did not significantly correlate with telomere length. Every additional childhood event, however, raised chances of short telomeres by 11 percent.

The childhood stressors that correlated most with shorter telomeres were trouble with the law, repeating a grade, being physically abused, and problems due to parent’s drug or alcohol use. “Those four seem to be the ones driving a lot of these effects,” says Puterman. Childhood instances of financial strain appeared to have little effect on telomeres.

Unlike previous studies, the new report considered a variety of stressors across lifespan, notes Idan Shalev, a health biologist at the Pennsylvania State University in University Park, not involved in this study. “This confirms what we think about stress in early life, that it can program some of the biological systems permanently, over and above stress and lifestyle behaviors you experience later on.” Scientists suspect that stress might lead to stunted telomeres by wearing down the immune system, or by making epigenetic changes to the genome.

Audrey Tyrka, a psychiatrist and neuroscience researcher at Butler Hospital in Providence, Rhode Island, praised the size and range of adverse items in the study but noted that many kinds of adverse events—such as neglect or parental separation—were absent from the HRS dataset. “I do think if they were able to measure more adversities, there would likely be a stronger effect,” says Tyrka, who was not involved with the research.

It will be important to validate the results in other large study groups, Puterman says. He’s also analyzing whether other life factors, such as exercise or diet, could mitigate or compound the effects of stress.

If the pattern holds true, there are societal implications. “We can’t really say that people should just pull themselves up by their bootstraps and move on when they’ve experienced significant adversity,” says Tyrka, “because they’re biologically at risk for a whole host of diseases.”