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)  

Public ISBD [article]  inDevelopment and Psychopathology > 33-1 (February 2021) . - p.301-312 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 [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

Sensitive periods for psychosocial risk in childhood and adolescence and cardiometabolic outcomes in young adulthood / Jenalee R. DOOM in Development and Psychopathology, 32-5 (December 2020)  

Public ISBD [article]  inDevelopment and Psychopathology > 32-5 (December 2020) . - p.1864-1875 Titre : Sensitive periods for psychosocial risk in childhood and adolescence and cardiometabolic outcomes in young adulthood Type de document : Texte imprimé et/ou numérique Auteurs : Jenalee R. DOOM, Auteur ; Kenia M. RIVERA, Auteur ; Estela BLANCO, Auteur ; Raquel BURROWS, Auteur ; Paulina CORREA-BURROWS, Auteur ; Patricia L. EAST, Auteur ; Betsy LOZOFF, Auteur ; Sheila GAHAGAN, Auteur Article en page(s) : p.1864-1875 Langues : Anglais (eng) Mots-clés : Adolescent  Adult  Body Mass Index  *Cardiovascular Diseases  Child  Chile  Female  Humans  Infant  Longitudinal Studies  Male  Risk Factors  Young Adult  *cardiometabolic risk  *infancy  *metabolic syndrome  *psychosocial risk  *young adulthood Index. décimale : PER Périodiques Résumé : Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood. We assessed whether the timing of psychosocial risk from infancy through adolescence predicts cardiometabolic outcomes in young adulthood. Young adults and their mothers participated in a longitudinal study beginning in infancy in Santiago, Chile (N = 1040). At infancy, 5 years, 10 years, and adolescence, mothers reported on depressive symptoms, stressful experiences, support for child development in the home, father absence, parental education, and socioeconomic status (SES) to create a psychosocial risk composite at each time point. Young adults (52.1% female; 21-27 years) provided fasting serum samples and participated in anthropometric and blood pressure (BP) assessments, including a dual-energy X-ray absorptiometry (DXA) scan for measuring body fat. Greater infant psychosocial risk was associated with a greater young adult metabolic syndrome score (? = 0.07, 95% confidence intervals (CI): 0.01 to 0.13, p = 0.02), a higher body mass index and waist circumference composite (? = 0.08, 95% CI: 0.03 to 0.13, p = 0.002), and a higher body fat (DXA) composite (? = 0.07, 95% CI: 0.01 to 0.12, p = 0.02). No psychosocial risk measure from any time point was associated with BP. Infant psychosocial risk predicted cardiometabolic outcomes in young adulthood better than psychosocial risk at 5 years, 10 years, or adolescence, mean of psychosocial risk from infancy through adolescence, and maximum of psychosocial risk at any one time. Consistent with the Developmental Origins of Health and Disease model, findings suggest that infancy is a sensitive period for psychosocial risk leading to poorer cardiometabolic outcomes in young adulthood. En ligne : http://dx.doi.org/10.1017/s0954579420001248 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437 [article] Sensitive periods for psychosocial risk in childhood and adolescence and cardiometabolic outcomes in young adulthood [Texte imprimé et/ou numérique] / Jenalee R. DOOM, Auteur ; Kenia M. RIVERA, Auteur ; Estela BLANCO, Auteur ; Raquel BURROWS, Auteur ; Paulina CORREA-BURROWS, Auteur ; Patricia L. EAST, Auteur ; Betsy LOZOFF, Auteur ; Sheila GAHAGAN, Auteur . - p.1864-1875. Langues : Anglais (eng) in Development and Psychopathology > 32-5 (December 2020) . - p.1864-1875 Mots-clés : Adolescent  Adult  Body Mass Index  *Cardiovascular Diseases  Child  Chile  Female  Humans  Infant  Longitudinal Studies  Male  Risk Factors  Young Adult  *cardiometabolic risk  *infancy  *metabolic syndrome  *psychosocial risk  *young adulthood Index. décimale : PER Périodiques Résumé : Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood. We assessed whether the timing of psychosocial risk from infancy through adolescence predicts cardiometabolic outcomes in young adulthood. Young adults and their mothers participated in a longitudinal study beginning in infancy in Santiago, Chile (N = 1040). At infancy, 5 years, 10 years, and adolescence, mothers reported on depressive symptoms, stressful experiences, support for child development in the home, father absence, parental education, and socioeconomic status (SES) to create a psychosocial risk composite at each time point. Young adults (52.1% female; 21-27 years) provided fasting serum samples and participated in anthropometric and blood pressure (BP) assessments, including a dual-energy X-ray absorptiometry (DXA) scan for measuring body fat. Greater infant psychosocial risk was associated with a greater young adult metabolic syndrome score (? = 0.07, 95% confidence intervals (CI): 0.01 to 0.13, p = 0.02), a higher body mass index and waist circumference composite (? = 0.08, 95% CI: 0.03 to 0.13, p = 0.002), and a higher body fat (DXA) composite (? = 0.07, 95% CI: 0.01 to 0.12, p = 0.02). No psychosocial risk measure from any time point was associated with BP. Infant psychosocial risk predicted cardiometabolic outcomes in young adulthood better than psychosocial risk at 5 years, 10 years, or adolescence, mean of psychosocial risk from infancy through adolescence, and maximum of psychosocial risk at any one time. Consistent with the Developmental Origins of Health and Disease model, findings suggest that infancy is a sensitive period for psychosocial risk leading to poorer cardiometabolic outcomes in young adulthood. En ligne : http://dx.doi.org/10.1017/s0954579420001248 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437

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