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Stress, Psychological Resources, and HPA and Inflammatory Reactivity During Late Adolescence

  • Jessica J. Chiang (a1), Ahra Ko (a2), Julienne E. Bower (a3), Shelley E. Taylor (a3), Michael R. Irwin (a3) and Andrew J. Fuligni (a3)...

Abstract

Psychosocial stress during childhood and adolescence is associated with alterations in the hypothalamic–pituitary–adrenal (HPA) axis and with heightened inflammation, both of which are implicated in poor health; however, factors that may protect against these effects relatively early in life are not well understood. Thus, we examined whether psychosocial resources protect against stress-related alterations in the HPA axis and heightened inflammation in a sample of 91 late adolescents. Participants completed measures of various stressors (major life events, daily interpersonal stress, early adversity), and psychosocial resources (mastery, optimism, self-esteem, and positive reappraisal). They also completed the Trier Social Stress Test and provided saliva and blood samples for the assessment of cortisol and interleukin-6 reactivity. Each of the stressors was associated with lower cortisol reactivity. Additionally, associations with major life events and daily stress were moderated by psychological resources, such that more life events and daily stress were associated with decreased HPA reactivity among adolescents with lower levels of psychological resources, but not among those with higher levels of psychological resources. This pattern of findings was observed only for cortisol reactivity and not for interleukin-6 reactivity. Findings suggest that psychological resources may counteract the effects of certain adversity-related decreases in cortisol reactivity.

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Corresponding author

Address correspondence and reprint requests to: Jessica J. Chiang, Northwestern University, 1801 Maple Avenue, Suite 2450, Evanston, IL 60201; E-mail: jessica.chiang@northwestern.edu.

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This research was supported by funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01-HD062547), UCLA California Center for Population Research funded by the National Institute of Child Health and Human Development (R24-HD041022), and the UCLA Older Americans Independence Center funded by the National Institute of Aging (P30-AG028748), UCLA Cousins Center for Psychoneuroimmunology, University of California Institute for Mexico and the US, American Psychological Association, and Division 38 of the American Psychological Association. The authors’ efforts were supported by the National Heart, Lung, and Blood Institute Grant F32-HL134276 (to J.J.C.).

Footnotes

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