Objective The pain, depression, and fatigue symptom cluster is an important health concern. Loneliness is a common risk factor for these symptoms. Little is known about the physiological mechanisms linking loneliness to the symptom cluster; immune dysregulation is a promising candidate. Latent herpesvirus reactivation, which is reflected by elevated herpesvirus antibody titers, provides a window into immune dysregulation. Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) are two common herpesviruses. Methods Participants were 200 breast cancer survivors who were 2 months to 3 years post-treatment at the time of the study. They completed questionnaires and provided a blood sample that was assayed for CMV and EBV antibody titers. Results Lonelier participants experienced more pain, depression, and fatigue than those who felt more socially connected. Lonelier participants also had higher CMV antibody titers which, in turn, were associated with higher levels of the pain, depression, and fatigue symptom cluster. Contrary to expectations, EBV antibody titers were not associated with either loneliness or the symptom cluster. Conclusions The pain, depression, and fatigue symptom cluster is a notable clinical problem, especially among cancer survivors. Accordingly, understanding the risk factors for these symptoms is important. The current study suggests that loneliness enhances risk for immune dysregulation and the pain, depression, and fatigue symptom cluster. The present data also provide a glimpse into the pathways through which loneliness may impact health.

Objective Pain, depression, and fatigue function as a symptom cluster and thus may share common risk factors. Interpersonal relationships clearly influence health, suggesting that loneliness may promote the development of the pain, depression, and fatigue symptom cluster. We hypothesized that loneliness would be related to concurrent symptom cluster levels and increases in symptom cluster levels over time. Methods We utilized two observational studies with distinct longitudinal samples. Study 1 was a sample of cancer survivors and benign controls (N=115) assessed annually for 2 years. Study 2 was a sample of older adults caring for a spouse with dementia (caregivers) and non-caregiver controls (N=229) assessed annually for 4 years. Participants completed annual measures assessing loneliness, pain, depression, and fatigue. Results Across both samples, lonelier participants experienced more concurrent pain, depression, and fatigue and larger increases in symptom cluster levels from one year to the next than less lonely participants. Sleep quality did not mediate the results in either study. All analyses were adjusted for relevant demographic and health variables. Conclusions Two longitudinal studies with different populations demonstrated that loneliness was a risk factor for the development of the pain, depression, and fatigue symptom cluster over time. The current research helps identify people most at risk for pain, depression, and fatigue, and lays the groundwork for research about their diagnosis and treatment. These data also highlight the health risks of loneliness; pain, depression, and fatigue often accompany serious illness and place people at risk for poor health and mortality.

Objective: Everyday stressors can threaten valued aspects of the self. Self-affirmation theory posits that this threat could be attenuated if individuals affirm alternative self-resources. The present study examined whether self-affirmation would buffer cumulative stress responses to an ongoing academic stressor. Design: Undergraduate participants provided 15-hr urine samples on the morning of their most stressful examination and baseline samples 14 days prior to the examination. Participants were randomly assigned to the self-affirmation condition where they wrote two essays on important values over the 2-week period prior to exam, or a control condition. Main Outcome Measures: Samples were analyzed for urinary catecholamine excretion (epinephrine, norepinephrine), an indicator of sympathetic nervous system activation. Participants also indicated their appraisals of the examination experience. Results: Participants in the control condition increased in cumulative epinephrine levels from baseline to examination, whereas participants in the self-affirmation condition did not differ from baseline to examination. The buffering effect of self-affirmation was strongest among individuals most concerned about negative college evaluation, those most psychologically vulnerable. Conclusion: The findings demonstrate that sympathetic nervous system responses to naturalistic stressors can be attenuated by self-affirmation. Discussion centers on psychological pathways by which affirmation can reduce stress and the implications of the findings for health outcomes among chronically stressed participants.

Objectives Cancer survivors often report cognitive problems. Furthermore, decreases in physical activity typically occur over the course of cancer treatment. Although physical activity benefits cognitive function in non-cancer populations, evidence linking physical activity to cognitive function in cancer survivors is limited. In our recent randomized controlled trial, breast cancer survivors who received a yoga intervention had lower fatigue and inflammation following the trial compared to a wait-list control group. This secondary analysis of the parent trial addressed yoga’s impact on cognitive complaints. Methods Post-treatment stage 0 – IIIA breast cancer survivors (N = 200) were randomized to a 12-week twice-weekly Hatha yoga intervention or a wait-list control group. Participants reported cognitive complaints using the Breast Cancer Prevention Trial (BCPT) Cognitive Problems scale at baseline, immediately post-intervention, and 3-month follow-up. Results Cognitive complaints did not differ significantly between groups immediately post-intervention (p = .250). However, at the 3-month follow-up, yoga participants’ BCPT Cognitive Problems scores were an average of 23% lower than wait-list participants’ scores (p = .003). These group differences in cognitive complaints remained after controlling for psychological distress, fatigue, and sleep quality. Consistent with the primary results, those who practiced yoga more frequently reported significantly fewer cognitive problems at the 3-month follow-up than those who practiced less frequently (p < 0.001). Conclusions These findings suggest that yoga can effectively reduce breast cancer survivors’ cognitive complaints, and prompt further research on mind-body and physical activity interventions for improving cancer-related cognitive problems.

Although evidence suggests that loneliness may increase risk for health problems, the mechanisms are not well understood. Immune dysregulation is one potential pathway; elevated proinflammatory cytokines such as interleukin-6 (IL-6) increase risk for health problems. Among healthy adults exposed to acute stress (N=134), lonelier participants exhibited greater synthesis of tumor necrosis factor-alpha (TNF-α) and IL-6 by lipopolysaccharide (LPS) stimulated peripheral blood mononuclear cells (PBMCs) than less lonely participants. Similarly, among post-treatment breast cancer survivors exposed to acute stress (N=144), lonelier participants exhibited greater synthesis of IL-6 and interleukin-1 beta (IL-1β) by LPS stimulated PBMCs than less lonely participants. Although in the expected direction, loneliness was unrelated to Study 2 TNF-α. Thus, two different populations demonstrated that lonelier participants' PBMCs produced more cytokines in response to stress than less lonely participants, reflecting a proinflammatory phenotype. These data provide a glimpse into the pathways through which loneliness may impact health.

Objective Pain and depressive symptoms are commonly experienced by cancer survivors. Lower social support is linked to a variety of negative mental and physical health outcomes among survivors. Immune dysregulation may be one mechanism linking low social support to the development of pain and depressive symptoms over time. Accordingly, the goal of the present study was to examine the relationships among survivors’ social support, pain, depressive symptoms, and inflammation. Methods Breast cancer survivors (N = 164, stages 0-IIIA) completed two study visits, one before any cancer treatment and the other 6 months after the completion of surgery, radiation, or chemotherapy, whichever came last. Women completed self-report questionnaires assessing social support, pain, and depressive symptoms, and provided a blood sample at both visits. Results Survivors with lower social support prior to treatment experienced higher levels of pain and depressive symptoms over time than their more socially supported counterparts. Furthermore, women with lower pretreatment social support had higher levels of IL-6 over time, and these elevations in IL-6 predicted marginally larger increases in depressive symptoms. Conclusions The results of this study suggest that social support at the time of diagnosis predicts the post-treatment development of pain, depressive symptoms, and inflammation. Consequently, early interventions targeting survivors’ social networks could improve quality of life during survivorship.

This study explored the association between one partner's attachment style and the other partner's relationship experiences (N = 305 couples). It was hypothesized that individuals would be more satisfied in their relationship when their partners were more secure (lower in attachment avoidance and anxiety), and that this association would be mediated by perceived caregiving. Results indicated that men were less satisfied when their female partners were higher in attachment anxiety, whereas women were less satisfied when their male partners were higher in avoidance. Structural equation modeling revealed that these links were partially mediated by Journal of Social and Personal Relationships

Stress and depression consistently elevate inflammation. Stress and depression are often experienced simultaneously, which is exemplified by people in troubled relationships. Troubled relationships also elevate inflammation, which may be partially explained by their ability to engender high levels of stress and depression. People who are stressed, depressed, or in troubled relationships are also at greater risk for health problems than their less distressed counterparts. Inflammation, a risk factor for a variety of age-related diseases including cardiovascular disease, Type II diabetes, metabolic syndrome, and frailty, may be one key mechanistic pathway linking distress to poor health. Obesity may further broaden the health implications of stress and depression; people who are stressed or depressed are often overweight, and adipose tissue is a major source of proinflammatory cytokines. Stress, depression, and troubled relationships may have synergistic inflammatory effects; loneliness, subclinical depression, and major depression enhance inflammatory responses to an acute stressful event. The relationship between distress and inflammation is bi-directional; depression enhances inflammation and inflammation promotes depression. Interesting questions emerge from this literature. For instance, some stressors may be more potent than others and thus may be more strongly linked to inflammation. In addition, it is possible that psychological and interpersonal resources may buffer the negative inflammatory effects of stress. Understanding the links among stress, depression, troubled relationships and inflammation is an exciting area of research that may provide mechanistic insight into the links between distress and poor health.