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Background: Exposure to adverse childhood experiences (ACE) has been associated with elevated circulating inflammatory markers in adulthood. Despite the robust effect of ACE on later health outcomes, not all individuals exposed to ACE suffer from poor health.Purpose: The goal of this study was to evaluate whether current resilience resources may attenuate the impact of ACE on inflammatory markers among individuals with elevated C-reactive protein (CRP) levels.Methods: Participants (N = 174) completed one-time self-report questionnaires assessing ACE exposure within the first 18 years of life and current resilience resources, and provided blood samples for interleukin-6 (IL-6) and CRP.Results: Individuals who were exposed to multiple ACE had greater IL-6 than participants with lesser ACE exposure. However, current resilience resources significantly moderated this effect. Among individuals who reported multiple ACE, higher resilience resources were associated with lower IL-6 levels.Conclusion: These data suggest that resilience resources might attenuate the association between ACE and later health outcomes. [ABSTRACT FROM AUTHOR]

Background: Poor social integration increases risk for poor health. The psychobiological pathways underlying this effect are not well-understood. Purpose: This study utilized a migration stress model to prospectively investigate the impact of social integration on change in high-frequency heart rate variability (HF-HRV), a marker of autonomic functioning. Methods: Sixty new international students were recruited shortly after their arrival in the host country and assessed 2 and 5 months later. At each assessment period, participants provided information on social integration and loneliness and had their resting HF-HRV evaluated. Results: There was an overall decrease in HF-HRV over time. The magnitude of the within-person and between-person effects of social integration on HRV increased over time, such that greater social integration was associated with higher HF-HRV at later follow-ups. Conclusions: These results suggest that altered autonomic functioning might represent a key pathway linking social integration to health outcomes. [ABSTRACT FROM AUTHOR]

Background: Disrupted sleep quality is one of the proposed mechanisms through which chronic stress may lead to depression. However, there exist significant individual differences in sleep reactivity, which is the extent to which one experiences sleep disturbances in response to stress.Purpose: The aim of the current study was to investigate whether low high-frequency heart rate variability (HRV), as a psychophysiological marker of poor emotional and physiological arousal regulation, predicts stress-related sleep disturbances associated with greater risk of depression symptoms.Methods: Using a chronic caregiving stress model, 125 mothers of adolescents with developmental disorders and 97 mothers of typically developing adolescents had their resting HRV and HRV reactivity recorded and completed a measure of depressive symptoms, as well as a 7 day sleep diary to assess their sleep quality. A moderated mediation model tested whether sleep quality mediated the association between chronic stress exposure and depressive symptoms and whether HRV moderated this mediation.Results: After controlling for participant age, body mass index, ethnicity, socioeconomic status, and employment status, poor sleep quality mediated the association between chronic stress and depressive symptoms. Resting HRV moderated this indirect effect such that individuals with lower HRV were more likely to report poorer sleep quality in the context of chronic stressor exposure, which, in turn, was related to greater depressive symptoms.Conclusions: Lower HRV, a potential biomarker of increased sleep reactivity to stress, is associated with greater vulnerability to stress-related sleep disturbances, which, in turn, increases the risk for elevated depressive symptoms in response to chronic stress. [ABSTRACT FROM AUTHOR]

Background: High-frequency heart rate variability (HF-HRV) reactivity was proposed as a vulnerability factor for stress-induced sleep disturbances. Its effect may be amplified among individuals with high trait worry or sleep reactivity.Purpose: This study evaluated whether HF-HRV reactivity to a worry induction, sleep reactivity, and trait worry predict increases in sleep disturbances in response to academic stress, a naturalistic stressor.Method: A longitudinal study following 102 undergraduate students during an academic semester with well-defined periods of lower and higher academic stress was conducted. HF-HRV reactivity to a worry induction, trait worry using the Penn State Worry Questionnaire, and sleep reactivity using the Ford Insomnia Stress Reactivity Test were measured during the low stress period. Sleep disturbances using the Pittsburgh Sleep Quality Index were assessed twice during the lower stress period and three times during the higher stress period.Results: Greater reductions in HF-HRV in response to the worry induction predicted increases in sleep disturbances from the lower to the higher academic stress period. Trait worry moderated this association: individuals with both higher trait worry and greater HF-HRV reactivity to worry had larger increases in stress-related sleep disturbances over time, compared to participants with lower trait worry and HF-HRV reactivity. A similar, but marginally significant effect was found for sleep reactivity.Conclusion: This study supports the role of HF-HRV reactivity as a vulnerability factor for stress-induced sleep disturbances. The combination of high trait worry and high HF-HRV reactivity to worry might identify a subgroup of individuals most vulnerable to stress-related sleep disturbances. [ABSTRACT FROM AUTHOR]