Background: A central problem in posttraumatic stress disorder (PTSD) is a reduced capacity to suppress fear under safe conditions. Previously, we have shown that combat‐related PTSD patients have impaired inhibition of fear‐potentiated startle (FPS). Given the high comorbidity between PTSD and depression, our goal was to see whether this impairment is specific to PTSD, or a non‐specific symptom associated with both disorders. Methods: Fear‐potentiated startle was assessed in 106 trauma‐exposed individuals divided into four groups: (a) No diagnosis control, (b) PTSD only, (c) major depression (MDD) only, and (d) comorbid PTSD and MDD. We used a novel conditional discrimination procedure, in which one set of shapes (the danger signal) was paired with aversive airblasts to the throat, and different shapes (the safety signal) were presented without airblasts. The paradigm also included fear inhibition transfer test. Results: Subjects with comorbid MDD and PTSD had higher FPS to the safety signal and to the transfer test compared to controls and MDD only subjects. In contrast to the control and MDD groups, the PTSD and comorbid PTSD and MDD groups did not show fear inhibition to safety cues. Conclusions: These results suggest that impaired fear inhibition may be a specific biomarker of PTSD symptoms. Depression and Anxiety, 2010.

Epigenetic processes, including DNA methylation, change reliably with age across the lifespan, such that DNA methylation can be used as an “epigenetic clock”. This epigenetic clock can be used to predict age and age acceleration, which occurs when methylation-based prediction of age exceeds chronological age and has been associated with increased mortality. In the current study we examined epigenetic age acceleration using saliva samples collected from children between ages 6–13 (N = 101). Children’s exposure to neighborhood violence and heart rate during a stressful task were assessed. Age acceleration was associated with children’s direct experience of violence (p = 0.004) and with decreased heart rate (p = 0.002). Children who were predicted to be older than their chronological age had twice as much violence exposure as other children and their heart rate was similar to that of adults. The results remained significant after controlling for demographic variables, such as sex, income and education. This is the first study to show the effects of direct violence exposure on epigenetic aging in children using salivary DNA. Although longitudinal studies are needed to determine whether accelerated epigenetic aging leads to adverse health outcomes later in life, these data point to DNA methylation during childhood as a putative biological mechanism.