Post-traumatic stress disorder (PTSD) is a common and debilitating condition, affecting between 10–20% of soldiers returning from combat zones, and with even higher prevalence rates in Veterans Affairs healthcare settings. PTSD is associated with an increased risk for various medical illnesses, many of which are commonly seen with older age. This raises the possibility that PTSD is associated with accelerated biological aging at the cellular level. Accelerated biological aging occurs when biological age outpaces chronological age, and this process is driven by a number of biological mechanisms including immune activation, oxidative stress, and mitochondrial dysfunction.

In this workshop I will present data from our research group and others pertaining to the biological mechanisms underlying accelerated cellular aging in PTSD. Most, but not all, studies have found that PTSD is associated with shorter mean leukocyte telomere length, an indicator of accelerated cellular aging. Mitochondrial dysfunction has been implicated in PTSD and our research group found evidence of a “u-shaped” relationship between PTSD symptom severity and mitochondrial DNA copy number. For what concerns immunity, we have recently found that PTSD subjects have increased blood levels of pro-inflammatory markers, a more senescent and dysfunctional profile of NK cells and impaired synthesis of nitric oxide. Finally, I will discuss the possibility of accelerated epigenetic aging in combat-exposed individuals with and without PTSD, using DNA methylation data.