TY - JOUR
T1 - Spousal bereavement is associated with more pronounced ex vivo cytokine production and lower heart rate variability
T2 - Mechanisms underlying cardiovascular risk?
AU - Fagundes, Christopher P.
AU - Murdock, Kyle W.
AU - LeRoy, Angie
AU - Baameur, Faiza
AU - Thayer, Julian F.
AU - Heijnen, Cobi
N1 - Funding Information:
This work was supported by the National Heart, Lung, and Blood Institute ( 1R01HL127260-01 ). The technical assistance of Mr. Jia Liu is gratefully acknowledged. We are very grateful to Patricia Morales and Kristi Parker for project coordination, and Levi Saucedo for data management. Finally, we appreciate DeWayne Williams and Derek Spangler for cleaning and scoring the HRV and Lani DuFresne for editing. Appendix A
Publisher Copyright:
© 2018
PY - 2018/7
Y1 - 2018/7
N2 - 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.”
AB - 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.”
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U2 - 10.1016/j.psyneuen.2018.04.010
DO - 10.1016/j.psyneuen.2018.04.010
M3 - Article
C2 - 29702444
AN - SCOPUS:85046348675
SN - 0306-4530
VL - 93
SP - 65
EP - 71
JO - Psychoneuroendocrinology
JF - Psychoneuroendocrinology
ER -