Socioeconomic disparities in health: Changes in sleep quality and inflammation during bereavement.

Widow(er)s experience significant sleep disruption that may dysregulate immune functioning. This longitudinal study aimed to determine 1) whether changes in sleep quality were associated with changes in pro-inflammatory cytokine production during the first six months of bereavement and 2) whether these relationships depended on objective socioeconomic status (SES) and/or subjective social status. One hundred and six bereaved spouses (M = 68.49 years, SD = 9.35, 69 females) completed the following assessments at approximately three months post-death and six-month post-death: a venous blood draw and self-report questionnaires on sleep quality (Pittsburgh Sleep Quality Index), SES (MacArthur Sociodemographic Questionnaire), health, and demographic information. T-cell stimulated pro-inflammatory cytokines were assessed, including IL-6, TNF-α, IFN-γ, IL-17A, and IL-2. Worsening sleep quality was associated with increased levels of pro-inflammatory activity even after adjusting for confounding variables. The present study also identified SES as an important factor for understanding health following spousal bereavement: individuals with low SES were more susceptible to sleep-related changes in immune function. Compared to more educated widow(er)s, less educated widow(er)s showed greater increases and decreases in inflammation when sleep quality worsened or improved, respectively, over time. Findings provide evidence for a biobehavioral pathway linking bereavement to disease risk, highlight SES disparities in late adulthood, and identify individuals who may require tailored interventions to offset SES-related burden that impedes adaptive grief recovery.

Inflammation and future depressive symptoms among recently bereaved spouses.

Major depressive disorder (MDD) is an important contributor to the total disease burden because of its high comorbidity with chronic illnesses. Many people with high levels of depressive symptoms exhibit elevated systemic inflammation, but inflammation is not a necessary determinant of depression onset. Among those who recently experienced the death of a spouse, we investigated whether (a) inflammation assessed early in bereavement predicted future depressive symptoms and whether (b) inflammation predicted change in depressive symptoms from baseline to follow-up. Ninety-nine spousally bereaved individuals (M=68.61, SD=10.70) from a larger study were evaluated at baseline (3 months post-death) and follow-up (6 months post-death). Subjects received a venous blood draw and completed the Center for Epidemiologic Studies Depression Scale (CES-D). Stimulated T-cell derived cytokines (IL-6, TNF-α, and IFN-γ) were assessed individually and as a pro-inflammatory composite index. After controlling for confounding factors (i.e., age, sex, body mass index, race, ethnicity, anti-inflammatory medication, days since spousal death, smoking status, comorbidities), individuals with higher levels of IL-6, TNF-α, and IFN-γ at baseline exhibited more depressive symptoms (composite index, p = .05) and an increased probability of experiencing clinical levels of depression (CES-D score ≥16) (composite index, p = .04). Inflammatory levels were not predictive of change in depressive symptoms or in clinical depression status from baseline to follow-up. Among individuals who did not experience clinical levels of depression at baseline, baseline inflammatory levels predicted clinical levels of depression 3 months later (p = .03). This study provides support for an inflammatory mechanism underlying depression following bereavement. It suggests that one's inflammatory profile following a significant social stressor in older adulthood can be prognostic of depression risk months later. These findings add to our understanding of the physiological and mental health risks experienced by the bereaved population and provide insight into identifying vulnerable widow(er)s at risk for maladaptive grief coping.

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.

Matters of the heart: Grief, morbidity, and mortality.

Spousal bereavement is associated with an elevated risk of morbidity and mortality. Several well-regarded multidisciplinary research teams have sought to understand the biopsychosocial processes underlying why widow(er)s are at elevated physical health risk. In this paper, we review research from multiple investigatory teams, including our own, showing that, on average, widow(er)s exhibit maladaptive patterns of autonomic, neuroendocrine, and immune activity compared to matched comparisons. Widow(er)s also exhibit poorer health behaviors than they did before their spouse's death. There is considerable variation in post-loss psychological adjustment trajectories among widow(er)s, which likely corresponds to physical health risk trajectories. Yet, there is little biobehavioral research on patterns of change in physical health risk after the death of a spouse. We summarize recently published work demonstrating the utility of attachment theory to characterize and predict individual differences in physical health biomarkers; we highlight the need for a biopsychosocial approach to understand and characterize post-loss trajectory patterns. We conclude by discussing the possibility that this line of inquiry could help researchers, and ultimately providers, identify adjustment trajectories earlier and thus deliver appropriate interventions when they are most needed.

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.