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Objective: Although positive marital quality is usually associated with lower chronic low-grade inflammation, not everyone benefits equally from spousal support. Exposure to early life adversity (ELA) has been proposed as a factor that may impede the social buffering effect of positive social relationships. The goal of this study was to test whether ELA would moderate the impact of marital quality on inflammation. Method: This cross-sectional study examined 168 partnered middle-aged women who either were experiencing a current chronic caregiving stressor, raising an adolescent with an autism spectrum disorder or intellectual disability, or who had the normative parenting experience of raising a typically developing adolescent. Participants completed self-report questionnaires on marital satisfaction, dyadic coping, and perceived partner responsiveness to create a composite index of marital quality, and they filled out the Childhood Trauma Questionnaire to assess ELA exposure. Participants also provided plasma samples for the assessment of interleukin-6, tumor necrosis factor-α, and C-reactive protein, three circulating biomarkers of inflammation. Results: ELA moderated the association between marital quality and inflammation. Among individuals who endorsed lower ELA exposure, there was a significant, negative association between marital quality and interleukin-6 and tumor necrosis factor-α levels. However, this association was attenuated and not statistically significant among participants who reported higher ELA exposure. This effect was independent of current chronic stress. Conclusions: These findings suggest that ELA may impair the social buffering effect of marital quality on inflammation. This impaired social buffering effect may be another mechanism through which ELA promotes sustained elevations in inflammation over time. [ABSTRACT FROM AUTHOR]

Cognitive reactivity (CR) is a psychological vulnerability marker of depression, whereas response to acute tryptophan depletion (ATD; a serotonergic challenge procedure) is a biological vulnerability marker. The aim of this study was to investigate the relationship between these markers. Thirty-nine remitted depressed patients participated in 2 ATD sessions in a double-blind crossover design. CR, assessed prior to the ATD sessions, predicted depressive response to high-dose ATD. CR also diminished the effects of 2 known predictors of ATD response: gender and residual symptoms. Neuroticism and behavioral inhibition were unrelated to ATD response. CR is associated with an increased sensitivity to reductions of serotonin concentrations. These findings present a small step toward unifying cognitive and neurobiological theories of depression. [ABSTRACT FROM AUTHOR]