Matters of the heart: Grief, morbidity, and mortality

Abstract

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.

Keywords: attachment theory; bereavement; health; heart disease; immune system.

Figure 1.

Autonomic, neuroendocrine, and immunological mechanisms underlying the association between bereavement and heart disease. The sympathetic nervous system increases heart rate and blood pressure. The parasympathetic nervous system counteracts the sympathetic nervous system via the vagus nerve. The HPA axis releases cortisol through a cascade of hormones (CRH and ACTH) to suppress the immune system. But under chronic stress conditions, the HPA axis can promote inflammation. The innate (macrophage, neutrophils, natural killer cells) and adaptive immune system (T cells) release proinflammatory cytokines that promote inflammation. Feedback mechanisms link peripheral systems to the brain, increasing grief and depressive symptoms and emotional sensitivity to future stressors which perpetuate the cycle again. Chronic stress as a result of bereavement dysregulate these systems and creates an internal environment susceptible to heart disease and mental illness. Abbreviations: CRH=Corticotropin releasing hormone; ACTH=Adrenocorticotropic hormone; HPA axis = hypothalamic-pituitary-adrenal axis

Figure 2.

Factors influencing physical and mental health outcomes in spousally bereaved individuals over time. After the death of the spouse, bereaved individuals experience a number of emotional, behavioral, and physiological changes. Stress related to bereavement (a), including loss-oriented and restoration-oriented stressors, may encourage negative health behavior, disrupt homeostasis within physiological systems, or create emotional instability. All of these impacting elements affect and are affected by each other. Months or years later (b), individuals who still exhibit high levels of depressive or grief symptoms are at increased risk for cardiovascular disease, depression, or grief-related disorders. Preexisting factors (c) such as attachment patterns influence how susceptible individuals are to physiological, behavioral, and emotional dysregulation as a result of bereavement-related stress. High attachment anxiety is a risk factor for poor emotional and physical health. The five grief trajectories identified by Bonanno et al. (2004) are represented in (d), with pink and blue representing individuals who are symptomatic and nonsymptomatic 18 months after their loss.