Perceived income inadequacy is associated with Epstein-Barr Virus latency and mental health outcomes in informal caregivers who are also employed in the healthcare industry.

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.

Immune and Epigenetic Pathways Linking Childhood Adversity and Health Across the Lifespan.

Childhood adversity is associated with a host of mental and physical health problems across the lifespan. Individuals who have experienced childhood adversity (e.g., child abuse and neglect, family conflict, poor parent/child relationships, low socioeconomic status or extreme poverty) are at a greater risk for morbidity and premature mortality than those not exposed to childhood adversity. Several mechanisms likely contribute to the relationship between childhood adversity and health across the lifespan (e.g., health behaviors, cardiovascular reactivity). In this paper, we review a large body of research within the field of psychoneuroimmunology, demonstrating the relationship between early life stress and alterations of the immune system. We first review the literature demonstrating that childhood adversity is associated with immune dysregulation across different indices, including proinflammatory cytokine production (and its impact on telomere length), illness and infection susceptibility, latent herpesvirus reactivation, and immune response to a tumor. We then summarize the growing literature on how childhood adversity may alter epigenetic processes. Finally, we propose future directions related to this work that have basic and applied implications.

Biological mechanisms underlying widowhood's health consequences: Does diet play a role?

The loss of a spouse is a highly stressful event that puts older adults at increased risk for morbidity and mortality. The risk is highest in the first year to 18 months post-loss; nevertheless, widow(er)s, in general, are at heightened risk of cardiovascular disease (CVD) related morbidity and mortality, and to a lesser extent, non-CVD related morbidity and mortality. The primary goal of this article is to argue for a perspective that considers diet and emotion-induced autonomic, neuroendocrine, and immune dysregulation, in unison, to understand the mechanisms underlying morbidity and mortality in early widowhood. Toward this end, we first summarize our previously published work, as well as work from other investigatory teams, showing that compared with those who were not bereaved, widow(er)s have higher levels of pro-inflammatory cytokine production and more dysregulated autonomic and neuroendocrine activity than non-widow(er)s, independent of health behaviors such as diet. We highlight that a major gap in our current understanding of the biobehavioral mechanisms that underlie the widowhood effect is the role of diet and hypothesize that the adverse health impact of grief and associated negative emotions and diet may be more than additive. Therefore, we propose that diet may be a pathway by which widow(er)s are at higher CVD risk requiring further investigation.

Bereavement among widowed Latinos in the United States: A systematic review of methodology and findings.

This study systematically reviewed the methodology and findings of 19 peer-reviewed studies on the experience of bereavement among widowed Latinos, including risk and protective factors to the health of this vulnerable population. Of these studies, 10 included quantitative data, 3 were qualitative studies, and 6 were narrative reviews. Results emphasized the relevance of cultural beliefs about death, rituals, religion, and Latino values (i.e., familismo, respeto, simpatía, personalismo) as common themes in the included studies, along with expressions of grief (e.g., Ataque de nervios, somatization) that vary by gender and acculturation. Risk factors associated with diminished well-being in this population included being a male, financial strain, cultural stressors, having an undocumented legal status, experiencing widowhood at a younger age, and having poor physical health. Effective coping strategies identified included having adequate social support primarily from family, religion and religious practices, the use of folk medicine, volunteering, and the use of emotional release strategies. Moreover, the results highlight that researches informing the health needs of widowed Latinos in the US is limited, and studies with enhanced methodological rigor are needed to better understand the complex needs of this vulnerable population.

Feasibility and acceptability of a faith-based mind-body intervention among African American adults.

Physical activity reduces cancer risk, yet African American adults remain insufficiently active, contributing to cancer health disparities. Harmony & Health (HH) was developed as a culturally adapted mind-body intervention to promote physical activity, psychosocial well-being, and quality of life among a church-based sample of overweight/obese, insufficiently active African American adults. Men and women were recruited to the study through an existing church partnership. Eligible participants (N = 50) were randomized to a movement-based mind-body intervention (n = 26) or waitlist control (n = 24). Participants in the intervention attended 16 mind-body sessions over 8 weeks and completed a physical assessment, questionnaires on moderate-to-vigorous physical activity (MVPA) and psychosocial factors, and accelerometry at baseline (T1), post-intervention (T2), and 6 week follow-up (T3). Eighty percent of participants (94% women, M age = 49.7 ± 9.4 years, M body mass index = 32.8 ± 5.2 kg/m2) completed the study, and 61.5% of intervention participants attended ≥10 mind-body sessions. Participants self-reported doing 78.8 ± 102.9 (median = 40.7, range: 0-470.7) min/day of MVPA and did 27.1 ± 20.7 (median = 22.0, range: 0-100.5) min/day of accelerometer-measured MVPA at baseline. Trends suggest that mind-body participants self-reported greater improvements in physical activity and psychosocial well-being from baseline to post-intervention than waitlist control participants. HH is feasible and acceptable among African American adults. Trends suggest that the mind-body intervention led to improvements in physical activity and psychosocial outcomes. This study extends the literature on the use of mind-body practices to promote physical and psychological health and reduce cancer disparities in African American adults.

Grief, depressive symptoms, and inflammation in the spousally bereaved.

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.

Neural mechanisms of emotion regulation and their role in endocrine and immune functioning: A review with implications for treatment of affective disorders.

In the past century, medical progress has helped increase life expectancy and improve health outcomes more generally. Despite this progress, psychiatric disorders-especially affective disorders including depressive and anxiety disorders-are quite common and have been linked to dysfunction in endocrine and immune systems. In this review, we discuss neurobiological correlates of emotion regulation strategies and their effects on mental and physical health. Some of these correlates, namely sub-regions of prefrontal cortex, also play a key regulatory role in autonomic, endocrine, and immunological processes. Given this functional overlap, we propose a novel neuro-immuno-affective framework that targets improving emotion regulation, in order to: (1) reduce negative affect associated with depressive and/or anxiety disorders; and (2) alter endocrine and immune system functioning (e.g., reduce inflammation)-via changes in activity within (and connectivity between) brain systems that support (successful) emotion regulation. We conclude by arguing that such a framework can be adapted for psychiatric treatment protocols that holistically incorporate neural and immunological biomarkers to promote mental and physical health.

Spousal bereavement is associated with more pronounced ex vivo cytokine production and lower heart rate variability: Mechanisms underlying cardiovascular risk?

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."

Mending the heart and mind during times of loss: A review of interventions to improve emotional well-being during spousal bereavement.

Spousal loss is one of life's greatest stressors. Bereaved spouses are at risk for aberrant cognitive and affective processing. Recent work in psychoneuroimmunology and cognitive neuroscience reveals physiological biomarkers and neural mechanisms underlying acute distress and grief during bereavement that may represent targets for future interventions. We review evidence from existing pharmacological and psychotherapeutic treatment approaches for normal bereavement, complicated grief, and bereavement-related depression. We propose promising future directions, namely the development and empirical validation of novel, personalised cognitive and neurostimulatory interventions to promote adaptive emotion regulation and reduce depressive symptoms following spousal loss. Future work may substantiate which interventions to improve emotional and physical health will be best matched to the needs of a particular surviving spouse.

Inflammation: depression fans the flames and feasts on the heat.

Depression and inflammation fuel one another. Inflammation plays a key role in depression's pathogenesis for a subset of depressed individuals; depression also primes larger cytokine responses to stressors and pathogens that do not appear to habituate. Accordingly, treatment decisions may be informed by attention to questions of how (pathways) and for whom (predispositions) these links exist, which are the focus of this article. When combined with predisposing factors (moderators such as childhood adversity and obesity), stressors and pathogens can lead to exaggerated or prolonged inflammatory responses. The resulting sickness behaviors (e.g., pain, disturbed sleep), depressive symptoms, and negative health behaviors (e.g., poor diet, a sedentary lifestyle) may act as mediating pathways that lead to further, unrestrained inflammation and depression. Depression, childhood adversity, stressors, and diet can all influence the gut microbiome and promote intestinal permeability, another pathway to enhanced inflammatory responses. Larger, more frequent, or more prolonged inflammatory responses could have negative mental and physical health consequences. In clinical practice, inflammation provides a guide to potential targets for symptom management by signaling responsiveness to certain therapeutic strategies. For example, a theme across research with cytokine antagonists, omega-3 fatty acids, celecoxib, and exercise is that anti-inflammatory interventions have a substantially greater impact on mood in individuals with heightened inflammation. Thus, when inflammation and depression co-occur, treating them in tandem may enhance recovery and reduce the risk of recurrence. The bidirectional links between depression, inflammation, and disease suggest that effective depression treatments could have a far-reaching impact on mood, inflammation, and health.

Attachment anxiety is related to Epstein-Barr virus latency.

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.

Loneliness promotes inflammation during acute stress.

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-1ß) 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.