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Article Summaries for September 2018 Psychosomatic Medicine, Volume 80, Issue 7

doi: 10.1097/PSY.0000000000000631
In This Issue

Chronic pain disorder has been associated with brain changes, especially in limbic circuits. In the majority of patients with chronic pain, depression and anxiety are common comorbidities. Using magnetic resonance imaging, Magon et al. investigated brain cortical thickness differences between patients with chronic pain disorder and healthy controls, with consideration of concurrent psychiatric symptoms. The results indicate that brain morphological differences between patients with chronic pain disorder and healthy controls are localized to regions that correspond to sensory as well as affective dimensions of pain processing.

Pages 592–598;

Exposure to adverse childhood experiences increases the risk of depression in adults, but the underlying mechanisms remain poorly understood. Using a gene-based approach, Peng et al. found that altered DNA methylation of five stress-related genes jointly contribute to depression. The association was partially mediated by two genes regulating stress responses (BDNF and NR3C1). The results highlight the importance of testing the combined effects of DNA methylation in multiple genes and may help to unravel a molecular mechanism through which adverse early life experiences become biologically embedded in risk of depression later in life.

Pages 599–608;

Short immune cell telomere length predicts cardiovascular-related diseases. In adults with a body mass index of 30 to 45 kg/m2 who were participants in a weight loss intervention, Mason et al. evaluated whether weight loss and weight-loss maintenance affect telomere length. Weight loss was not contemporaneously related to telomere lengthening, but maintaining weight loss of 10% for 1 year, regardless of weight-loss intervention type, was related to telomere lengthening (peripheral blood mononuclear cells, CD8+ T cells). This suggests a pathway through which weight-loss maintenance may slow immune system and cellular aging.

Pages 609–619;

Diaz et al. investigated the association of daily psychological stress with objectively measured sedentary behavior over the course of 1 year. The source of stress (e.g., work-related or argument-related) rather than its level was associated with sedentary behavior. Furthermore, the association of stress with sedentary behavior varied widely from person to person. The results provide evidence that a precision-medicine approach may be warranted to target reductions in sedentary time.

Pages 620–627;

Gebreab et al. assessed the association between psychosocial factors and cardio-metabolic risk in an adult population. They found negative psychosocial factors over the life course, i.e., childhood adversity and adulthood life-event stress, to be independently associated with increased adiposity markers and levels of blood lipids. Individual psychological traits or a history of major depressive disorder did not account for the associations. These findings provide additional insight into the complex relationship between psychosocial factors and cardio-metabolic risk.

Pages 628–639;

Carson et al. investigated racial differences and psychological stress-related associations with gut microbiota of healthy women (47 black women and 33 white women). Primary analyses focused on colorectal cancer–associated taxonomic microbiotic groups. Analyses revealed racial differences in the overall composition of gut microbiota. White women reported more stressful life events and greater distress than black women. After analyses were adjusted for stress measures, black women displayed a higher abundance of Bacteroides, which has been associated with colorectal cancer. This result highlights the need for more investigation of factors that influence gut microbiota and ways to cultivate an optimal gut environment.

Pages 640–648;

Beis et al. investigated potential mechanisms underlying stress-induced increases in innate immune cells in the blood of healthy men. They found that the stress-induced increase in norepinephrine (NE) related to simultaneous increases in granulocyte and monocyte cell counts. In a subsequent placebo-controlled study, they confirmed that an NE infusion, mimicking a stress reactivity effect, induced monocyte and neutrophil increases that were partly inhibited by prior blockade of α-adrenergic receptors. This would indicate partial mediation by α-adrenergic mechanisms.

Pages 649–658;

Using three large national samples from the United States, Stephan et al. examined the relation between subjective age and mortality. They showed that feeling older than one’s age is associated with increased risk of mortality across adulthood and old age. Depressive symptoms, disease burden, functional limitations, cognition, and physical inactivity accounted for the association and are potential pathways by which feeling older may culminate in higher mortality risk.

Pages 659–664;

Patients with motor neuron disease (MND) and coexisting frontotemporal dementia have reduced survival. Garcia-Willingham et al. investigated the relationships between subclinical executive and self-regulatory difficulties and survival among 37 patients with MND. Patients reporting more self-regulatory difficulties at baseline had higher mortality risk during 6 year follow-up. In contrast, performance on the Wisconsin Card Sorting Test and caregiver ratings of patient self-regulation did not significantly predict survival.

Pages 665–672;

A large, prospective population-based cohort study by Askim et al. examined whether anxiety and depression symptoms constitute increased risk of bloodstream infection (BSI). Severe anxiety and depression symptoms were associated with moderately increased BSI risk. Adjustment for comorbidities, BMI, and lifestyle attenuated the association. To reduce the burden of BSI, an early focus on physical health and health behaviors in people with severe anxiety and depression symptoms may be warranted.

Pages 673–679;

Trauma and/or symptoms of posttraumatic stress disorder (PTSD) have been linked to cardiovascular disease (CVD). Using data from the Collaborative Psychiatric Epidemiology Surveys, Vidal et al. found an increased likelihood of cardiovascular events for those with a diagnosis of PTSD compared to other categories of participants (no trauma, trauma but no PTSD symptoms, or subclinical symptoms of PTSD) as well as for non-Latino black participants. Optimal health interventions should focus on these populations.

Pages 680–688;

Copyright © 2018 by American Psychosomatic Society