Could PTSD Cause Premature Aging?

Post-traumatic stress disorder (PTSD) may increase the risk of premature senescence (aging), according to a recent study.

In the past, PTSD has been linked to other significant psychological conditions, such as depression, anger, insomnia, eating disorders, and substance abuse. Similarly, previous research has suggested a possible link between psychological conditions like schizophrenia and bipolar disorder with accelerated aging.
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In order to determine whether PTSD, a psychological condition that, unlike schizophrenia and bipolar disorder, is caused exclusively by external traumatic stress, could also be linked to accelerated aging, researchers conducted a comprehensive review of available literature, identifying 64 relevant studies.

Note: To define premature aging, a condition that has no standard definition, researchers examined conditions that incorporate it into their symptoms, like Down’s syndrome and progeria.

Of the 64 studies, 22 dealt with biomarkers of accelerated aging and 10 examined PTSD-related mortality rates.

Overall, the researchers found that patients with PTSD have shorter telomere length (considered a strong measure of the aging process), greater pro-inflammatory markers, and higher rates of age-related conditions like cardiovascular disease, diabetes, and dementia, than those without PTSD. Further, 7 of the 10 studies on mortality indicated an association between PTSD and early mortality.

“In short, evidence from multiple lines of investigation suggests that PTSD may be associated with a phenotype of accelerated senescence. Further research is critical to understand the nature of this association. There may be a need to re-conceptualize PTSD beyond the boundaries of mental illness, and instead as a full systemic disorder.”

—Michael Potts

Reference:

Lohr JB, Palmer BW, Eidt CA, et al. Is Post-traumatic stress disorder associated with premature senescence? a review of the literature [epub ahead of print]. American Journal of Geriatric Psychiatry. May 2015. DOI: http://dx.doi.org/10.1016/j.jagp.2015.04.001