This Special Communication argues for changing the definition of posttraumatic stress disorder in DSM-5. Are changes to the definition of posttraumatic stress disorder in DSM-5 a step forward?—Yes.

We take strong exception to many of the assertions, conclusions, and recommendations in the article by Hoge et al1 in this issue of JAMA Psychiatry. Although Hoge et al1 identify a number of reasons they do not support the DSM-52 workgroup’s revisions to the diagnosis of posttraumatic stress disorder (PTSD), we believe that their basic arguments are that

Background
Deployment can put soldiers at risk of developing post-traumatic stress symptoms. Despite several longitudinal studies, little is known about the timing of an increase in post-traumatic stress symptoms relative to pre-deployment. Longitudinal studies starting pre-deployment, in which participants are repeatedly measured over time, are warranted to assess the timing of an increase in symptoms to ultimately assess the timing of an increase in treatment demand after deployment.
Methods

Genomic variation in the SKA2 gene has recently been identified as a promising suicide biomarker. In light of its role in glucocorticoid receptor transactivation, we investigated whether SKA2 DNA methylation influences cortisol stress reactivity and is involved in the development of post-traumatic stress disorder (PTSD). Increased SKA2 methylation was significantly associated with lower cortisol stress reactivity in 85 healthy individuals exposed to the Trier Social Stress Test (B=−173.40, t=−2.324, p-value=0.023).

Background
Consequences of war-related traumatisation have mostly been investigated in military and predominant male populations, while research on female civilian victims of war has been neglected. Furthermore, research of post-war posttraumatic stress disorder (PTSD) in women has rarely included early-life trauma in their prediction models, so the contribution of trauma in childhood and early youth is still unexplored.
Objective