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Highlights • Inflammatory markers can distinguish bereaved spouses higher on grief severity compared with bereaved spouses with lower grief severity. • Even in a population high on depressive symptoms, there is a positive relationship between depression and inflammation. • Similar to the general population, inflammation is an important marker of elevated levels of depression among bereaved spouses. Abstract Grief is conceptualized by strong negative emotions, which include longing, sadness, and preoccupations with thoughts, recollections, and images of the spouse. In the initial months after the loss of a spouse, those who are widowed are at risk for cardiovascular problems and premature mortality. In the general population, depression is characterized by chronic low-grade inflammation, a key predictor of cardiovascular problems, morbidity, and mortality. Although depression and grief share similarities, they are distinct constructs. We aimed to identify if grief was related to inflammation among those who had a spouse recently die. We also sought to determine if those who are widowed and already experience elevated levels of depressive symptoms compared with the general population had higher levels of inflammation compared with those who are widowed who report fewer depressive symptoms. Ninety-nine recently bereaved individuals (M = 84.74 days since passing, SD = 18.17) completed a blood draw and psychological assessments. Proinflammatory T cell-derived cytokines were assessed, which included interferon gamma (IFN-γ), interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), IL17-A, and IL-2. Bereaved individuals with a higher grief severity (using an established cut-score) had higher levels of the proinflammatory cytokines IFN-γ, IL-6, and TNF-α than those with less grief severity. Those who experienced higher levels of depression exhibited elevated levels of proinflammatory cytokines compared with those who had lower levels of depression (using a continuous measure of depressive symptoms, as well as an established cut score). This is the first study to demonstrate that inflammatory markers can distinguish those who are widowed based on grief severity such that those who are higher on grief severity have higher levels of inflammation compared with those who are lower on grief severity. These findings also add to the broader literature on depression and inflammation by showing that even in a population with high levels of depressive symptoms, there is a positive relationship between depression and inflammation. [ABSTRACT FROM AUTHOR]

The loss of a spouse is a highly stressful event that puts people at excess risk of mortality. Excess mortality among those who are widowed is highest in the first six months after the death of a spouse and decreases over time. Heart disease accounts for the largest proportion of these deaths. The psychological stress associated with stressful life events can enhance inflammation and lower heart rate variability (HRV). Both lower HRV and higher inflammation are risk factors for cardiovascular morbidity and mortality. Thirty-two recently bereaved individuals (Mean = 89.68 days since death, SD = 17.09) and 33 age-matched comparisons completed a blood draw, EKG, and self-report questionnaires. In both adjusted and unadjusted models, spousal bereavement was associated with enhanced pro-inflammatory cytokine production by in vitro lipolysaccharide-stimulated peripheral blood leukocytes. Moreover, spousal bereavement was associated with lower HRV in comparison to the comparison group. This study is the first to demonstrate that bereavement is associated with a more pronounced ex vivo cytokine production and lower HRV in a population that exclusively consisted of widows and widowers. These findings add to the growing literature revealing the mechanisms that underlie bereavement-related cardiovascular problems. Future longitudinal studies are needed to determine the temporal relation between these risks. Understanding the biological mechanisms that underlie this stressful life event could allow researchers to create therapeutic targets for interventions to reduce or prevent the toll of a “broken heart.” [ABSTRACT FROM AUTHOR]

Cancer research within the fields of psychoneuroendocrinology and psychoneuroimmunology has made substantial progress in understanding how psychological factors impact cancer. Although the pathways by which stress “gets under the skin” to impact cancer incidence, progression, and quality of life are not yet fully understood, the answers to key questions about how stressful life events and the negative emotions they generate can impact cancer initiation, progression, and survivorship have advanced quite dramatically. In this review, we summarize the state of the science in a way that is accessible to a broad audience. We then discuss future directions in cancer research, with a focus on ways psychological science can contribute to the next generation of cancer care. [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 origins of modern psychology are deeply rooted in the notion that stressful early-life experiences negatively impact people’s mental health. Emerging work in the field of health psychology suggests that early-life stress also impacts physical well-being. Indeed, those who experienced severe early-life stress as children are more at risk for cardiovascular disease, type 2 diabetes, and cancer compared with those who did not have those early-life experiences. Recent work in the field of psychoneuroimmunology suggests that inflammation may be one mechanism underlying these associations. In this article, we provide a brief overview of the literature on early-life stress and inflammation and how psychological, autonomic, neuroendocrine, and epigenetic responses to the early environment lead to potentiated inflammation in adulthood. We conclude by highlighting the need for health-promotion and disease-prevention programs that are designed to reduce the frequency and severity of early-life stress. [ABSTRACT FROM PUBLISHER]

Although evidence suggests that loneliness may increase risk for health problems, the mechanisms responsible are not well understood. Immune dysregulation is one potential pathway: Elevated proinflammatory cytokines such as interleukin-6 (IL-6) increase risk for health problems. In our first study (N = 134), lonelier healthy adults exposed to acute stress exhibited greater synthesis of tumor necrosis factor-alpha (TNF-α) and IL-6 by peripheral blood mononuclear cells (PBMCs) stimulated with lipopolysaccharide (LPS) than their less lonely counterparts. Similarly, in the second study (N = 144), lonelier posttreatment breast-cancer survivors exposed to acute stress exhibited greater synthesis of IL-6 and interleukin-1 beta (IL-1β) by LPS-stimulated PBMCs than their counterparts who felt more socially connected. However, loneliness was unrelated to TNF-α in Study 2, although the result was in the expected direction. Thus, two different populations demonstrated that lonelier participants had more stimulated cytokine production in response to stress than less lonely participants, which reflects a proinflammatory phenotype. These data provide a glimpse into the pathways through which loneliness may affect health. [ABSTRACT FROM PUBLISHER]

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]

Abstract: There is considerable evidence that stressful early life events influence a variety of physical health problems later in life. Childhood adversity has been linked to elevated rates of morbidity and mortality from a number of chronic diseases. Immune dysregulation may be one potential pathway that explains this link. In this mini-review, we summarize human studies demonstrating that severe early life stressors have lasting immune consequences. We propose a model outlining potential biobehavioral pathways that explain how early life stressors leave people vulnerable to these maladaptive outcomes. Finally, we suggest ideas for future work to test different aspects of this model. [Copyright &y& Elsevier]

Objective: Both higher socioeconomic status (SES) and supportive personal relationships confer health benefits, including better immune function. This study assessed the joint impact of SES and social support on the expression of a latent herpesvirus, Epstein-Barr virus (EBV), in a group of highly stressed women. Methods: Two-hundred and twenty four women either awaiting further evaluation following an abnormal mammogram or newly diagnosed with breast cancer completed questionnaires and provided blood samples to assess EBV viral capsid antigen (VCA) IgG antibody titers. Results: More highly educated women with more support from friends had lower EBV VCA antibody titers, reflecting a stronger cellular immune response to the latent virus; however, among less educated women, friend support was not associated with EBV antibody titers. As revealed in an ancillary analysis, more highly educated women with more friend support had lower systolic blood pressure (SBP); however, friend support was not associated with SBP among less educated women. Neither depression nor perceived stress mediated these associations. Neither cancer status nor cancer stage among those diagnosed with cancer was significantly related to these outcomes. Conclusion: Lower SES women may not reap the same immunological benefits from friend support when experiencing a stressful life event as their higher SES counterparts. [ABSTRACT FROM AUTHOR]

Finances are a prevalent source of stress. In a sample of 799 nursing home workers measured multiple times over 18 months, we found that higher perceived income inadequacy, the perception that one's expenses exceeds one's incomes, was associated with poorer self-reported mental health indicators and Epstein-Barr Virus antibody titers (a marker of cell-mediated immune function). Perceived income inadequacy predicted outcomes over and above the role of other socioeconomic status variables (objective household income and education). Mental health variables were not related to Epstein-Barr Virus antibody titers. Additionally, we found an interaction between perceived income inadequacy and informal caregiver status on our mental health outcomes; informal caregivers with higher perceived income inadequacy had poorer mental health than non-caregivers with the same perceived income inadequacy. Our findings may add nuance to the reserve capacity model, which states that those at lower socioeconomic levels are at higher risk of adverse health outcomes partly because they have fewer resources to address demands and strain. Perceived income inadequacy may significantly predict mental and physical well-being beyond other socioeconomic status variables, especially among lower-income employees. Caregiving stress and perceived income inadequacy may have synergistic effects on mental health. • Perceived income inadequacy predicted stress and distress beyond household income. • Perceived income inadequacy predicted Epstein-Barr virus antibody titers. • Informal caregivers had poorer mental health at high perceived income inadequacy. [ABSTRACT FROM AUTHOR]