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An unhappy marriage increases disease and mortality risks. Discordant couples exhibit stronger links to their partner’s autonomic fluctuations–that is, stronger covariation–than do satisfied couples, but whether this physiological signature plays a role in marriage’s health effects is unknown. To examine associations between couples’ heart rate variability (HRV) covariation during conflict and their inflammation levels, 43 married couples engaged in a marital problem discussion while wearing heart rate monitors and provided blood samples throughout the day. Multilevel models treated log-transformed interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS) stimulated IL-6 and TNF-alpha, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) as outcomes, accounting for morning baseline HRV levels, age, gender, trunk fat, marital satisfaction, hostility observed during the problem discussion, and study design features. Couples whose moment-to-moment HRV changes tracked more closely together during conflict had higher serum IL-6 ( p = 0.04), LPS-stimulated IL-6 ( p = 0.02), VCAM- 1 ( p = 0.01), and at a trend level, LPS-stimulated TNF-alpha ( p = 0.06) across the day. Thought to result in part from couples’ exchange of negative emotion during disagreement, stronger HRV covariation predicted a heightened inflammatory profile beyond the roles of general marital quality and observed negativity. These data highlight partners’ conflict-related HRV linkage as a novel social-biological mechanism explaining marital discord’s connection to inflammation-related disease. [ABSTRACT FROM AUTHOR]

Although evidence suggests that attachment anxiety may increase risk for health problems, the mechanisms are not well understood. Married couples (N =85, M age =38.67) provided saliva samples over three days and blood samples on two occasions. Participants with higher attachment anxiety produced more cortisol and had fewer numbers of CD45+ T cells, CD3+ T cells, CD3+CD4+ helper T cells, and CD3+CD8+ cytotoxic T cells than those with lower attachment anxiety. Higher cortisol was also related to fewer numbers of CD45+, CD3+, CD3+CD4+, and CD3+CD8+, which is mechanistically consistent with research showing that cortisol alters the cellular immune response. These data suggest that attachment anxiety may have physiological costs and provide a glimpse into the pathways through which social relationships impact health. The current study also extends attachment theory in an important new direction by utilizing a psychoneuroimmunological approach to the study of attachment anxiety, stress, and health. [ABSTRACT FROM AUTHOR]