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Auteur Jeffry A. SIMPSON |
Documents disponibles écrits par cet auteur (1)
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Life stress and cortisol reactivity: An exploratory analysis of the effects of stress exposure across life on HPA-axis functioning / Ethan S. YOUNG in Development and Psychopathology, 33-1 (February 2021)
[article]
Titre : Life stress and cortisol reactivity: An exploratory analysis of the effects of stress exposure across life on HPA-axis functioning Type de document : Texte imprimé et/ou numérique Auteurs : Ethan S. YOUNG, Auteur ; Jenalee R. DOOM, Auteur ; Allison K. FARRELL, Auteur ; Elizabeth A. CARLSON, Auteur ; Michelle M. ENGLUND, Auteur ; Gregory E. MILLER, Auteur ; Megan R. GUNNAR, Auteur ; Glenn I. ROISMAN, Auteur ; Jeffry A. SIMPSON, Auteur Article en page(s) : p.301-312 Langues : Anglais (eng) Mots-clés : Trier Social Stress Test cortisol reactivity cumulative stress development life stress Index. décimale : PER Périodiques Résumé : Stressful experiences affect biological stress systems, such as the hypothalamic-pituitary-adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity. En ligne : http://dx.doi.org/10.1017/s0954579419001779 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=442
in Development and Psychopathology > 33-1 (February 2021) . - p.301-312[article] Life stress and cortisol reactivity: An exploratory analysis of the effects of stress exposure across life on HPA-axis functioning [Texte imprimé et/ou numérique] / Ethan S. YOUNG, Auteur ; Jenalee R. DOOM, Auteur ; Allison K. FARRELL, Auteur ; Elizabeth A. CARLSON, Auteur ; Michelle M. ENGLUND, Auteur ; Gregory E. MILLER, Auteur ; Megan R. GUNNAR, Auteur ; Glenn I. ROISMAN, Auteur ; Jeffry A. SIMPSON, Auteur . - p.301-312.
Langues : Anglais (eng)
in Development and Psychopathology > 33-1 (February 2021) . - p.301-312
Mots-clés : Trier Social Stress Test cortisol reactivity cumulative stress development life stress Index. décimale : PER Périodiques Résumé : Stressful experiences affect biological stress systems, such as the hypothalamic-pituitary-adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity. En ligne : http://dx.doi.org/10.1017/s0954579419001779 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=442