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Background: Perceived neighborhood characteristics are linked to obesity, however, the mechanisms linking these two factors remain unknown.Purpose: This study aimed to examine associations between perceived neighborhood characteristics and body mass index (BMI), establish whether indirect pathways through psychological distress and inflammation are important, and determine whether these associations vary by race/ethnicity.Methods: Participants were 1,112 adults enrolled in the Texas City Stress and Health Study. Perceived neighborhood characteristics were measured using the Perceived Neighborhood Scale. Psychological distress was measured with the Center for Epidemiological Studies Depression Scale, Perceived Stress Scale and mental health subscale of the Short Form Health Survey-36. Markers of inflammation included C-reactive protein, interleukin-6, and tumor necrosis factor receptor-1. Associations were examined with Structural Equation Modeling.Results: A model linking neighborhood characteristics with BMI through direct and indirect (i.e., psychological distress and inflammation) paths demonstrated good fit with the data. Less favorable perceived neighborhood characteristics were associated with greater psychological distress (B = -0.87, β = -0.31, p < .001) and inflammation (B = -0.02, β = -0.10, p = .035). Psychological distress and inflammation were also significantly associated with BMI (Bdistress = 0.06, β = 0.08, p = .006; Binflammation = 4.65, β = 0.41, p < .001). Indirect paths from neighborhood characteristics to BMI via psychological distress (B = -0.05, β = -0.03, p = .004) and inflammation (B = -0.08, β = -0.04, p = .045) were significant. In multiple group analysis, a model with parameters constrained equal across race/ethnicity showed adequate fit suggesting associations were comparable across groups.Conclusion: Our study extends the literature by demonstrating the importance of neighborhood perceptions as correlates of BMI across race/ethnicity, and highlights the role of psychological and physiological pathways. [ABSTRACT FROM AUTHOR]

Childhood maltreatment increases the risk of depression, especially after experiencing a stressful life event, such as bereavement. Employing emotion regulation strategies can mitigate the impact childhood maltreatment has on depression later in life following the loss of a spouse. We evaluated how cognitive reappraisal and expressive suppression moderated the impact of childhood maltreatment and depressive symptoms following spousal bereavement. We examined 130 bereaved individuals 3 months after the death of a spouse, 4 months after the death of a spouse, and 6 months after the death of a spouse. We utilized a mixed model approach to test the interaction between childhood maltreatment and cognitive reappraisal and between childhood maltreatment and expressive suppression to predict depressive symptoms across 3 time points. Cognitive reappraisal moderated the relationship between childhood maltreatment and depressive symptoms (b = − 0.17, p =.003); expressive suppression did not (b = 0.06, p =.452). Participants who used less cognitive reappraisal had a positive relationship between childhood maltreatment and depressive symptoms (b = 3.27, p <.001);participants who used more cognitive reappraisal did not (b = 1.09, p =.065). Childhood maltreatment interacted with cognitive reappraisal, but not expressive suppression, to predict depressive symptoms following spousal bereavement. This study reveals how emotion regulation strategies can be utilized as a tool to buffer the impact of childhood maltreatment on mental health following a stressor later in life, which can serve as a target for future interventions for individuals experiencing a stressful life event. [ABSTRACT FROM AUTHOR]

Attachment theory provides a framework for understanding individual differences in chronic interpersonal stress. Attachment anxiety, a type of relationship insecurity characterized by worry about rejection and abandonment, is a chronic interpersonal stressor. Stress impacts cellular immunity, including herpesvirus reactivation. We investigated whether attachment anxiety was related to the expression of a latent herpesvirus, Epstein–Barr virus (EBV), when individuals were being tested for breast or colon cancer and approximately 1 year later. Participants ( N = 183) completed a standard attachment questionnaire and provided blood to assess EBV viral capsid antigen (VCA) IgG antibody titers. Individuals with more attachment anxiety had higher EBV VCA IgG antibody titers than those with less attachment anxiety. The strength of the association between attachment anxiety and antibody titers was the same at both assessments. This study is the first to show an association between latent herpesvirus reactivation and attachment anxiety. Because elevated herpesvirus antibody titers reflect poorer cellular immune system control over the latent virus, these data suggest that high attachment anxiety is associated with cellular immune dysregulation. [ABSTRACT FROM AUTHOR]

The article discusses the issue of mental health issues in the children of undocumented immigrants in the U.S. Details of the U.S. government program titled Development, Relief, and Education for Alien Minors (DREAM) along with public debates to aspects of the DREAM program and efforts towards addressing mental health issues are discussed.

Objective A cancer diagnosis provokes significant levels of emotional distress, with intrusive thoughts being the most common manifestation among breast cancer survivors. Cancer-related intrusive thoughts can take the form of emotional memories, flashbacks, nightmares, and intrusive images. Emotional arousal after a severe life stressor prolongs adrenergic activation, which in turn may increase risk for post-traumatic symptomatology. However, antihypertensive beta-blockers block adrenergic activation and are known to reduce traumatic memories and related psychological distress. Thus, the current study examined the association between beta-blocker use and the severity of cancer-related intrusive thoughts and related symptoms following a cancer diagnosis. Methods The 174 breast and 36 female colorectal cancer patients who had recently undergone diagnostic screening or biopsy included 39 beta-blocker users and 171 non-users. Prior to any cancer treatment including surgery, participants completed questionnaires that included the Impact of Events Scale and the Center for Epidemiological Studies Depression Scale. Analyses controlled for age, education, cancer stage, cancer type, days since diagnosis, marital status, depression, and comorbidities. Results Although the high rates of cancer-related distress in this sample were similar to those of other studies with recently diagnosed patients, beta-blocker users endorsed 32% fewer cancer-related intrusive thoughts than non-users. Conclusions Recently diagnosed cancer patients using beta-blockers reported less cancer-related psychological distress. These results suggest that beta-blocker use may benefit cancer patients' psychological adjustment following diagnosis, and provide a promising direction for future investigations on the pharmacological benefits of beta-blockers for cancer-related distress. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Abstract: Depression is a risk factor for morbidity and mortality, and immune dysregulation may be partially responsible for this link. Proinflammatory cytokines such as interleukin 6 (IL-6) are reliable predictors of quality of life, morbidity, and many causes of mortality. The current study evaluated relationships between depressive symptoms, as assessed by the CES-D, and stress-induced inflammation. The participants, 138 healthy adults, were evaluated at rest, and after a standardized laboratory speech and mental arithmetic stressor. Compared with individuals with fewer depressive symptoms, those with more depressive symptoms produced more IL-6 in response to the stressor, as well as significantly higher levels of IL-6 both 45min and 2h after the stressor. These findings add to our emerging understanding of the complex interactions among stress, depression, and immune dysregulation, and provide one potential pathway to explain relationships between depressive symptoms and disease. [Copyright &y& Elsevier]

Objective: Childhood adversity has been linked to greater emotional and physiological sensitivity to stress. Stress has well-documented effects on cellular immunity, including enhanced herpesvirus reac- tivation. This study assessed whether childhood adversity was associated with the expression of two latent herpesviruses, Epstein-Barr virus (EBV) and cytomegalovirus (CMV) in adults, and whether this association could be detected beyond the psychological distress women experienced in the aftermath of a breast cancer diagnosis and its treatment. Methods: One hundred and eight breast cancer survivors completed questionnaires and provided blood samples to assess EBV virus capsid antigen (VCA) IgG antibody titers and CMV IgG antibody titers. Results: Breast cancer survivors who experienced more childhood adversities had higher EBV and CMV antibody titers than those with fewer childhood adversities. Those who experienced more childhood adversities also had more depressive symptoms, less education, and poorer sleep quality than those with fewer childhood adversities. Depressive symptoms, education, sleep quality, age, BMI, cancer stage, comorbidities, and weekly alcohol consumption were not related to EBV or CMV antibody titers. Time since last treatment was negatively associated with EBV and CMV antibody titers. Elevated antibody titers to latent herpesviruses represent poorer cellular immune system control over viral latency; these data suggest that those with more childhood adversities have poorer cellular immune function. Conclusions: These findings add to the emerging literature suggesting that adverse early experiences may make people more vulnerable to immune dysregulation in adulthood. The consequences of early adversity appear to persist across the life span. [ABSTRACT FROM AUTHOR]

The social-signal-transduction theory of depression asserts that people who experience ongoing interpersonal stressors and mount a greater inflammatory response to social stress are at higher risk for depression. The current study tested this theory in two adult samples. In Study 1, physically healthy adults (N = 76) who reported more frequent interpersonal tension had heightened depressive symptoms at Visit 2, but only if they had greater inflammatory reactivity to a marital conflict at Visit 1. Similarly, in Study 2, depressive symptoms increased among lonelier and less socially supported breast-cancer survivors (N = 79). This effect was most pronounced among participants with higher inflammatory reactivity to a social-evaluative stressor at Visit 1. In both studies, noninterpersonal stress did not interact with inflammatory reactivity to predict later depressive symptoms. [ABSTRACT FROM AUTHOR]

• Several stress-mediated pathways relevant to the formation of brain metastases have been identified. • Stress-induced activation of the neuroendocrine system, noradrenergic pathways and β-adrenergic signaling contribute to inflammation, impaired cellular immune response, and tumor angiogenesis. • Pharmacological blockade of stress- and inflammatory pathways, and immune stimulation, may provide a viable pharmacological strategy for suppressing many of the pathways through which the SNS can stimulate tumor progression and the formation of brain metastasis. Chronic stress can promote tumor growth and progression through immunosuppressive effects and bi-directional interactions between tumor cells and their microenvironment. β-Adrenergic receptor signaling plays a critical role in mediating stress-related effects on tumor progression. Stress-related mechanisms that modulate the dissemination of tumor cells to the brain have received scant attention. Brain metastases are highly resistant to chemotherapy and contribute considerably to morbidity and mortality in various cancers, occurring in up to 20% of patients in some cancer types. Understanding the mechanisms promoting brain metastasis could help to identify interventions that improve disease outcomes. In this review, we discuss biobehavioral, sympathetic, neuroendocrine, and immunological mechanisms by which chronic stress can impact tumor progression and metastatic dissemination to the brain. The critical role of the inflammatory tumor microenvironment in tumor progression and metastatic dissemination to the brain, and its association with stress pathways are delineated. We also discuss translational implications for biobehavioral and pharmacological interventions. [ABSTRACT FROM AUTHOR]

• Spousal caregivers and widow(er)s have worse cognitive outcomes than controls. • Spousal caregivers and widow(er)s have increased long-term risk for dementia. • Stress-related pathways may contribute to abnormal cognitive decline. • We propose a biopsychosocial model linking partner loss to increased ADRD risk. • Longitudinal research on stress, health, and cognition in this population is needed. Accumulating research suggests that stressful life events, especially those that threaten close intimate bonds, are associated with an increased risk of dementia. Grieving the loss of a spouse, whether in the form of caregiving or after the death, ranks among 'life's most significant stressors', evoking intense psychological and physiological distress. Despite numerous studies reporting elevated dementia risk or poorer cognition among spousal caregivers and widow(er)s compared to controls, no review has summarized findings across cognitive outcomes (i.e., dementia incidence, cognitive impairment rates, cognitive performance) or proposed a theoretical model for understanding the links between partner loss and abnormal cognitive decline. The current systematic review summarizes findings across 64 empirical studies. Overall, both cross-sectional and longitudinal studies revealed an adverse association between partner loss and cognitive outcomes. In turn, we propose a biopsychosocial model of cognitive decline that explains how caregiving and bereavement may position some to develop cognitive impairment or Alzheimer's disease and related dementias. More longitudinal studies that focus on the biopsychosocial context of caregivers and widow(er)s are needed. [ABSTRACT FROM AUTHOR]

• Married couples provided 5 salivary cortisol samples during a 9.5 h visit. • Coding of couples' conflicts provided data on positive and negative behavior. • A stressed spouse was associated with slower declines in one's own cortisol. • Negative and less positive behaviors and a stressed spouse related to higher cortisol. • We show how partners "get under the skin" to influence stress-related health risk. Perceived stress can lead to dysregulated cortisol patterns, including blunted peaks and flatter slopes, which are associated with increased morbidity and mortality risks. Couples' interdependence provides a prime opportunity for partners' stress to disrupt a healthy cortisol pattern. This study examined how individuals' own perceived stress and their partners' perceived stress shape cortisol levels and slopes across the day, as well as how positive and negative behaviors during conflict discussions impact associations between stress and cortisol. Both partners of a married couple (n = 43 couples, 86 individuals) completed a full day in-person visit. Each partner completed the Perceived Stress Scale, and all couples engaged in a 20-min marital problem discussion which was recorded and later coded for positive and negative behaviors using the Rapid Marital Interaction Coding System (RMICS). Partners also provided five salivary cortisol samples across the day, two samples before the conflict and three after the conflict. The dyadic design and analyses provided a way to account for the interdependent nature of married couples' data, as well as to use the Actor-Partner Interdependence Model (APIM) to assess the mutual influence of spouses' stress on cortisol. Individuals with more stressed partners had flatter cortisol slopes than individuals with less stressed partners, who showed steeper and thus healthier declines across the day. Individuals' cortisol levels at the beginning of the day were similar regardless of their partners' perceived stress, but individuals with more stressed partners had higher cortisol levels 30-min, 1 h, and 4 h after the conflict discussion than those with less stressed partners. Couples' behavior during the conflict moderated the relationship between partner perceived stress and average cortisol; when couples used more negative and less positive behaviors, individuals with more stressed partners had higher average cortisol levels than those with less stressed partners. On a day couples experienced conflict, having a partner with higher perceived stress is associated with dysregulated cortisol patterns, including higher levels and flatter slopes, but having a partner with lower perceived stress is linked to steeper and thus healthier cortisol declines. A partner's stress was particularly consequential for one's own cortisol when couples used more negative and fewer positive behaviors during a conflict discussion. This research adds to the growing literature on pathways connecting marital interactions to important biorhythms and health. [ABSTRACT FROM AUTHOR]