The gradual aging of the immune system is partly marked by shortened telomeres, the DNA–protein caps at the ends of chromosomes that protect genes from degradation. This study undertakes a lifespan approach to stress and leukocyte telomere length in a nationally representative sample of US residents. By using data from 16 y of the Health and Retirement Study, childhood and adulthood life stressors were examined for their individual and combined associations with increased odds of having short telomeres. Accumulated adverse experiences in childhood significantly predicted an increased likelihood of having short telomeres later in life, suggesting a potential pathway through which childhood experiences have been previously shown to predict adulthood morbidity and mortality. 
 
 Abstract 
 
 Stress over the lifespan is thought to promote accelerated aging and early disease. Telomere length is a marker of cell aging that appears to be one mediator of this relationship. Telomere length is associated with early adversity and with chronic stressors in adulthood in many studies. Although cumulative lifespan adversity should have bigger impacts than single events, it is also possible that adversity in childhood has larger effects on later life health than adult stressors, as suggested by models of biological embedding in early life. No studies have examined the individual vs. cumulative effects of childhood and adulthood adversities on adult telomere length. Here, we examined the relationship between cumulative childhood and adulthood adversity, adding up a range of severe financial, traumatic, and social exposures, as well as comparing them to each other, in relation to salivary telomere length. We examined 4,598 men and women from the US Health and Retirement Study. Single adversities tended to have nonsignificant relations with telomere length. In adjusted models, lifetime cumulative adversity predicted 6% greater odds of shorter telomere length. This result was mainly due to childhood adversity. In adjusted models for cumulative childhood adversity, the occurrence of each additional childhood event predicted 11% increased odds of having short telomeres. This result appeared mainly because of social/traumatic exposures rather than financial exposures. This study suggests that the shadow of childhood adversity may reach far into later adulthood in part through cellular aging. 

 TIME Health For more, visit TIME Health 
 
 There are a lot of things to envy about youth: clear skin, perfect hair, boundless energy. But nothing says young like a good set of telomeres. We’ve all got them, but if you’re past a certain age, you don’t want to think about them too much. 
 
 Telomeres are the protein caps at the end of chromosomes that act as a sort of mortal fuse: the older you get the shorter they grow, a process that contributes to all manner of age-related diseases and breakdowns. Telomere length can be affected by things other than merely the number of years you’ve been around, including environmental toxins and stress and whether or not you exercise and meditate. Now, a paper published in PNAS Plus takes the impact of stress a worrisome step further: According to a study of 4,598 people, adverse experiences in childhood can hasten the telomere burn-down, leading to premature aging of cells—and of the body as a whole. 
 
 The study—a collaboration between researchers in the U.S. and Canada, led by kinesiologist Eli Puterman of the University of British Columbia—drew its sample group from the 26,000 people already participating in the U.S. Health and Retirement Study (HRS), a bi-annual health survey of adults over 50 that began in 1992. For the telomere work, the volunteers were chosen from across an age, gender and overall health spectrum, with multiple other factors including education, weight and smoking history also factored in. Saliva swabs were collected from all of the volunteers and telomere length was measured using polymerase chain reaction (PCR). 
 
 That was the easy part. 
 
 The subjects were then asked about life stressors that they either did or did not experience, either in childhood or adulthood. The experiences were divided into two categories: financial and social. The financial traumas included such things as losing a job or going on food stamps in adulthood; and a parent losing a job or a family losing a home in childhood. The social traumas included death of a child or a spouse or participation in combat for adults; and parental abuse, parental addiction, or trouble with the police in childhood. 
 
 The results were both striking and disturbing. In no event did financial adversity seem to have much impact on telomere length—whether the problems were experienced in childhood or adulthood. Adverse social experiences in adulthood initially seemed so have an effect on telomere length, with each stressor increasing the odds of telomere-shortening by 8%. But when the results were adjusted for other variables, such as genetics, education or smoking history, the effect disappeared. 
 
 That was not the case when it came to kids. The study found that every occurrence of one of the named social stressors in childhood increased the risk of shortened telomeres in adulthood by 11%. That number was stubborn and robust—sticking around even after the investigators corrected for all of the other variables that could have influenced the results. And while any study that relies on volunteers reporting their own experiences can be colored by poor recall or selective memory, most research shows that if anything, people tend to exaggerate the good in their past rather than the bad. 
 
 “Previous studies on the validity of retrospective reporting from childhood,” the researchers wrote, “suggest that people are more likely to underreport early abuse experiences than overreport them.” Additional cases of shortened telomeres among the subjects in the study might thus have been attributable to childhood stress even if the subjects themselves did not mention it. 
 
 The mechanism at work that translates a bad experience to protein changes is uncertain, but the investigators suspect it involves the epigenome, the control system that sits atop the genome and regulates which genes are expressed and which aren’t. Unlike genes, which are essentially fixed for life, the epigenome is constantly changing. Life stressors, the researchers wrote, “may embed epigenetically and alter gene expression almost permanently.” 
 
 Getting old, of course, is never easy. As Bette Davis is said to have said, it “ain’t for sissies.” It is, however, supposed to be for the old. There’s a particular cruelty in early-life traumas so severe that they get the process rolling early—one more reminder to parents of the importance of raising kids carefully, gently and well. 

 En Español 
 
 By Dennis Thompson 
 
 HealthDay Reporter 
 
 MONDAY, Oct. 3, 2016 (HealthDay News) -- Childhood trauma might promote faster cellular aging in people, a new study suggests. 
 
 Adults who had experienced stress as kids appeared to have an increased risk of shorter telomeres, which are found at the ends of a person's chromosomes. And that might increase the risk of illness and early death in adulthood, said lead researcher Eli Puterman. He is director of the Fitness, Aging & Stress Lab at the University of British Columbia in Vancouver, Canada. 
 
 Puterman added that the increased risk of faster cellular aging is "relative" -- and not every person who suffers childhood traumas will wind up ill later in life. 
 
 "This doesn't mean that every single person has short telomeres," he said. "It just means there's an increased risk." 
 
 Telomeres are comparable to the plastic tips on the ends of shoelaces, which keep the laces from fraying, Puterman explained. In this case, telomeres prevent human chromosomes from unraveling, which causes cells to age and die more quickly. 
 
 Each significant stressful event in a person's childhood appeared to increase the risk of shorter telomeres by 11 percent, Puterman and his colleagues determined from a review of nearly 4,600 people. 
 
 These events can include drug or alcohol abuse by parents, physical abuse, trouble with the law, having to repeat a grade or financial hardships in the family, according to the report. 
 
 "We found those psychological or social types of stressors seem to be driving the effect the most in this particular study, more so than financial stressors," Puterman said. 
 
 But the study did not prove that childhood stress causes shorter telomeres, only that there seems to be an association. 
 
 Previous studies have linked the length of a person's telomeres to risk of heart disease, lung disease, diabetes, Alzheimer's disease and some types of cancer, the study authors said in background notes. 
 
 Other research has shown that stress can accelerate aging of the immune system and cause cells to function less efficiently, the authors added. 
 
 However, there's been little research on whether stress can affect telomere lengths, which might partially explain the link between stress and illness, Puterman said. 
 
 To investigate this, Puterman and his colleagues analyzed saliva DNA samples from 4,598 people aged 50 and older who are participating in the U.S. Health and Retirement Study, a federally funded long-term project researching aging in the United States. 
 
 The study participants had been asked about stressful events throughout their lives, both as children and adults. The researchers stacked these events up and compared them against the likelihood that a person would have short telomeres. 
 
 Overall, a person with a lifetime of stressful events had a slightly increased risk of shorter telomeres, even after the researchers accounted for other factors that affect cellular aging, such as smoking, education, income, age, weight and medical history, Puterman said. 
 
 But when researchers drilled down deeper, they found that the childhood events seemed to be driving the increased risk of rapid cellular aging, rather than stress endured in adulthood, he said. 
 
 "It was the childhood events that they suffered that were driving these effects," Puterman said. 
 
 The findings were published Oct. 3 in the Proceedings of the National Academy of Sciences. 
 
 No one can fully explain this link, but Puterman said it could be due to the fight-or-flight hormones that are released during highly stressful events. These hormones can wear down the immune system, so it's not much of a leap to think they might be wearing down a person's cells and chromosomes as well. 
 
 "Events occur, and if they're chronic and they're repeated and they're severe enough, over time they are going to wear down our physiological system to be able to cope with those stressors," Puterman said. 
 
 Dr. Liron Sinvani is director of Northwell Health's Geriatric Hospitalist Service in Manhasset, N.Y. She said that as a geriatrician, she often sees patients suffering from diseases that have gradually developed over the course of their lives. 
 
 "I think this raises the issue of how we can protect our telomeres," said Sinvani. "These telomeres are really a huge treasure box in terms of how do we prevent aging, how do we prevent disease, how do we prevent dementia and even death. This is the key to what we need to study now." 
 
 It's not clear what a middle-aged or older person who suffered a troubled childhood might do to counter these effects, Sinvani said. Exercise, a healthy diet or continuing education might help ensure the health of both mind and body, but no research has been done to tie those lifestyle behaviors to cellular aging. 
 
 Dr. Brad Johnson, a spokesman for the American Federation for Aging Research, said that while telomeres do appear to be key to understanding human aging, the effects in this study were "really tiny." 
 
 "The telomeres may be contributing a little bit here, but it's not clear from these results that they are contributing in a big way," said Johnson, who is a fellow with the Institute on Aging at the University of Pennsylvania School of Medicine in Philadelphia. 
 
 More information 
 
 Visit the University of Utah Genetic Science Learning Center for more on telomeres.
– Children appear to be highly susceptible to the stress of trauma on a biological level, according to a study published in the Proceedings of the National Academy of Sciences. US and Canadian researchers led by Eli Puterman of the University of British Columbia have been studying the length of telomeres, the DNA-protein caps at the ends of chromosomes that inevitably shorten as we age and whose lengths are linked to age-related diseases. Puterman compares telomeres to the plastic tips that keep shoelaces from fraying, only here they protect genes from degrading, reports HealthDay. And while stressful events in adulthood don't seem to have an impact on telomere length, every childhood trauma appears to up the risk of having shorter telomeres by 11%. To test this, Puterman and his team reviewed the health records of 4,600 people drawn from the larger US Health and Retirement Study, which has been surveying adults over age 50 biannually since 1992. Telomere lengths were measured via saliva swabs, and volunteers provided details ranging from weight, smoking history, and education to financial and social traumas in childhood and adulthood, including a parent losing a job, child abuse, and parental drug addiction. Time notes that the exact mechanism at play remains unknown, but that the "striking and disturbing" correlation between childhood trauma and shortened telomeres could involve the epigenome, which regulates gene expression. The researchers stress that they've found a link, not a cause. (Drinking soda is also linked to shorter telomeres.)