Liesa Ilg1, Clemens Kirschbaum2, Shu-Chen Li1, Franziska Rosenlöcher3, Robert Miller2, Nina Alexander4. 1. Chair for Lifespan Developmental Neuroscience, Faculty of Psychology, Technische Universität Dresden, Dresden, Germany. 2. Chair for Biopsychology, Faculty of Psychology, Technische Universität Dresden, Dresden, Germany. 3. Vocational School for Obstetric Care, Universitätsklinikum Carl Gustav Carus Dresden, Dresden, Germany. 4. Department of Psychology, Faculty of Human Sciences, Medical School Hamburg, Hamburg, Germany.
Abstract
Context: Antenatal synthetic glucocorticoid (sGC) therapy has been identified as a potent programming factor of the hypothalamic-pituitary-adrenal (HPA) axis. We previously observed significantly increased cortisol stress responses in 6- to 11-year-old, term-born children exposed to antenatal sGCs compared with controls. These findings call for longitudinal follow-up studies to evaluate long-term effects of antenatal sGCs, given that adolescence is marked by a substantial shift of HPA axis functioning. Objective: This study aimed to longitudinally investigate the stability of antenatal sGC-related effects on cortisol stress reactivity from childhood to adolescence. Design, Setting, and Participants: To evaluate long-term trajectories of antenatal sGCs, we longitudinally followed a subsample (n = 44) of our children's cohort into adolescence (14 to 18 years old) for a second assessment. To this end, 22 adolescents with antenatal sGC exposure and 22 untreated controls underwent a standardized laboratory stressor [Trier Social Stress Test (TSST)]. Results: Besides a general increase in HPA axis reactivity from childhood to adolescence (P < 0.05), participants treated with antenatal sGCs showed significantly higher cortisol levels in response to the TSST compared with controls during both developmental stages (P < 0.05). Furthermore, we observed a moderating effect of sGCs on rank-order stability of cortisol stress reactivity from childhood to adolescence (P < 0.05) with a trend (P = 0.07) for higher rank-order stability in sGC-exposed individuals (r = 0.37) compared with controls (r = -0.20). Conclusion: These findings suggest that antenatal sGCs yield long-term changes of HPA axis reactivity that persist into adolescence and may confer increased vulnerability for developing stress-related disorders.
Context: Antenatal synthetic glucocorticoid (sGC) therapy has been identified as a potent programming factor of the hypothalamic-pituitary-adrenal (HPA) axis. We previously observed significantly increased cortisolstress responses in 6- to 11-year-old, term-born children exposed to antenatal sGCs compared with controls. These findings call for longitudinal follow-up studies to evaluate long-term effects of antenatal sGCs, given that adolescence is marked by a substantial shift of HPA axis functioning. Objective: This study aimed to longitudinally investigate the stability of antenatal sGC-related effects on cortisolstress reactivity from childhood to adolescence. Design, Setting, and Participants: To evaluate long-term trajectories of antenatal sGCs, we longitudinally followed a subsample (n = 44) of our children's cohort into adolescence (14 to 18 years old) for a second assessment. To this end, 22 adolescents with antenatal sGC exposure and 22 untreated controls underwent a standardized laboratory stressor [Trier Social Stress Test (TSST)]. Results: Besides a general increase in HPA axis reactivity from childhood to adolescence (P < 0.05), participants treated with antenatal sGCs showed significantly higher cortisol levels in response to the TSST compared with controls during both developmental stages (P < 0.05). Furthermore, we observed a moderating effect of sGCs on rank-order stability of cortisolstress reactivity from childhood to adolescence (P < 0.05) with a trend (P = 0.07) for higher rank-order stability in sGC-exposed individuals (r = 0.37) compared with controls (r = -0.20). Conclusion: These findings suggest that antenatal sGCs yield long-term changes of HPA axis reactivity that persist into adolescence and may confer increased vulnerability for developing stress-related disorders.
Authors: Hedi L Claahsen-van der Grinten; Phyllis W Speiser; S Faisal Ahmed; Wiebke Arlt; Richard J Auchus; Henrik Falhammar; Christa E Flück; Leonardo Guasti; Angela Huebner; Barbara B M Kortmann; Nils Krone; Deborah P Merke; Walter L Miller; Anna Nordenström; Nicole Reisch; David E Sandberg; Nike M M L Stikkelbroeck; Philippe Touraine; Agustini Utari; Stefan A Wudy; Perrin C White Journal: Endocr Rev Date: 2022-01-12 Impact factor: 19.871
Authors: Juliann D Jaumotte; Alexis L Franks; Erin M Bargerstock; Edwina Philip Kisanga; Heather L Menden; Alexis Ghersi; Mahmoud Omar; Liping Wang; Anthony Rudine; Kelly L Short; Neerupama Silswal; Timothy J Cole; Venkatesh Sampath; A Paula Monaghan-Nichols; Donald B DeFranco Journal: Neurobiol Dis Date: 2021-06-11 Impact factor: 7.046