LAUSR

S tress reactivity research has traditionally focused on the idea that exaggerated responses to stress may have adverse effects on health. Accumulating evidence suggests that attenuated responses to stress and delayed recovery may also be problematic. A review by Dr. Mustafa al’Absi focuses on response characteristics of the hypothalamic-pituitaryadrenocortical (HPA) axis, the endogenous opioid system (EOS), and the cardiovascular system as related to hypertension, pain perception, and addictive behaviors. A blunted stress response may indicate long-term physiological dysregulation that could usher in harmful consequences for cardiovascular disease, pain-related conditions, and addictive disorders. Pages 2–16; http://dx.doi.org/10.1097/PSY.0000000000000520 Slavich and Shields provide a detailed description of the recently developed Stress and Adversity Inventory (STRAIN), an online system for systematically assessing lifetime stress exposure. They summarize evidence for reliability and validity of the STRAIN and the relevance of the STRAIN to biobehavioral processes. The STRAIN demonstrated good usability and acceptability; good concurrent, discriminant, and predictive validity; and excellent test-retest reliability over 2 to 4 weeks. Pages 17–27; http://dx.doi.org/10.1097/PSY.0000000000000534 Oxidative DNA damage is associated with atherosclerosis, cardiovascular disease, cancer, and diabetes. Shimanoe et al. examined whether urinary 8-hydroxydeoxyguanosine (8-OHdG), a marker of oxidative DNA damage, was associated with perceived stress or depressive symptoms. Results showed that higher perceived stress was significantly associated with higher 8-OHdG, whereas no association was observed between depressive symptoms and 8-OHdG. Increased oxidative DNA damage may therefore play a role in the adverse risk of psychosocial stress for various diseases. Pages 28–33; http://dx.doi.org/10.1097/PSY.0000000000000513 Wu et al. investigated whether prenatal stress exposure and methylation in inflammation-related genes were associated with childhood adiposity in a Mexican birth cohort. A stress index was created based on four prenatally administered stress-related factors (exposure to violence, crisis in family systems, anxiety, and depression). Contrary to the authors’ hypothesis, prenatal stress was found to be associated with decreased childhood adiposity, while cord blood IL6 methylation was found to be associated with increased childhood adiposity. Pages 34–41; http://dx.doi.org/10.1097/PSY.0000000000000517 Wolf et al. examined trauma exposure and posttraumatic stress disorder (PTSD) in association with cellular aging among 339 veterans. Using an index of cellular age derived from DNA methylation data, they found that PTSD hyperarousal symptoms were associated with accelerated cellular age relative to chronological age. Moreover, accelerated cellular age also predicted mortality. Pages 42–48; http://dx.doi.org/10.1097/PSY.0000000000000506 Murdock et al. examined whether perceived health risk and depressive symptoms before a disaster were associated with postdisaster inflammation markers (CRP, IL6, and TNF-R1). Participants were part of a stress and health study whose baseline visits had occurred before a major petrochemical explosion nearby. Results revealed no main effect of the disaster on inflammation markers but showed an interaction between pre-disaster depressive symptoms with perceived health risk as related to post-disaster circulating inflammation markers. Pages 49–54; http://dx.doi.org/10.1097/PSY.0000000000000514 Posttraumatic stress disorder (PTSD) is associated with incident cardiovascular disease (CVD), but little is known about cardiovascular consequences of PTSD in daily life. Edmondson et al. found that PTSD was associated with higher ambulatory systolic blood pressure