A preliminary study suggests a history of childhood trauma among adults displaying post-traumatic stress disorder may cause accelerated aging.

Researchers at the San Francisco VA Medical Center and the University of California, San Francisco discovered that individuals with PTSD had altered chromosomes.

For these individuals, the part of the chromosome called the telomere — a DNA-protein complex whose function is to protect the chromosome from damage and mutation — was shortened and thus damaged.

Short telomere length is associated with an increased risk of cancer, cardiovascular disease, and autoimmune and neurodegenerative diseases, as well as early death.

The study is found in the online Articles in Press section of the journal Biological Psychiatry.

In the investigation, the authors collected DNA samples from 43 adults with PTSD and 47 matched participants without PTSD.

Initial analysis showed that many of the subjects with PTSD had shorter telomere length than those without PTSD.

“This was striking to us, because the subjects were relatively young, with an average age of 30, and in good physical health,” said lead author Aoife O’Donovan, PhD. “Telomere length was significantly shorter than we might expect in such a group.”

The authors then looked at incidence of severe childhood trauma, including neglect, family violence, physical abuse, and sexual abuse.

They found that, among the subjects with PTSD, the more childhood trauma a subject had experienced, the higher the risk of shorter telomere length. “People who had multiple categories of childhood traumas had the shortest telomere length,” said O’Donovan.

In contrast, subjects with PTSD but without childhood trauma had telomere length equal to those of the matched healthy subjects.

The results are meaningful as they may explain why some people with PTSD are more susceptible to disease and have problems with aging. Also, people with cumulative bouts of PTSD may, as a result, have a shortening of telomeres.

According to O’Donovan, however, the major drawback of the study was that, because the subjects without PTSD did not in general have high levels of exposure to childhood traumas, the authors were “unable to tease apart the relative contributions of childhood trauma and adult PTSD to shorter telomere length.”

Follow-up research will look at telomere length in subjects with and without childhood trauma and with and without PTSD in adulthood. A central question to be investigated is if treatment of PTSD can retard the rate of telomere shortening and, as a result, slow the risk for diseases of aging?

Source: University of California, San Francisco