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Childhood adversity predicts black young adults? DNA methylation-based accelerated aging: A dual pathway model / Steven R. H. BEACH in Development and Psychopathology, 34-2 (May 2022)
[article]
Titre : Childhood adversity predicts black young adults? DNA methylation-based accelerated aging: A dual pathway model Type de document : Texte imprimé et/ou numérique Auteurs : Steven R. H. BEACH, Auteur ; Frederick X. GIBBONS, Auteur ; Sierra E. CARTER, Auteur ; Mei Ling ONG, Auteur ; Justin A. LAVNER, Auteur ; Man-Kit LEI, Auteur ; Ronald L. SIMONS, Auteur ; Meg GERRARD, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : 689-703 Langues : Anglais (eng) Mots-clés : discrimination DNAm-aging FKBP5 Life History Index. décimale : PER Périodiques Résumé : We expand upon prior work (Gibbons et al., ) relating childhood stressor effects, particularly harsh childhood environments, to risky behavior and ultimately physical health by adding longer-term outcomes ? deoxyribonucleic acid (DNA) methylation-based measures of accelerated aging (DNAm-aging). Further, following work on the effects of early exposure to danger (McLaughlin et al., ), we also identify an additional pathway from harsh childhood environments to DNAm-aging that we label the danger/FKBP5 pathway, which includes early exposure to dangerous community conditions that are thought to impact glucocorticoid regulation and pro-inflammatory mechanisms. Because different DNAm-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNAm-aging based on chronological age with later indices that focused on predicting biological outcomes. We utilize data from Family and Community Health Study participants (N = 449) from age 10 to 29. We find that harshness influences parenting, which, in turn, influences accelerated DNAm-aging through the risky cognitions and substance use (i.e., behavioral) pathway outlined by Gibbons et al. (). Harshness is also associated with increased exposure to threat/danger, which, in turn, leads to accelerated DNAm-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway). En ligne : http://dx.doi.org/10.1017/s0954579421001541 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474
in Development and Psychopathology > 34-2 (May 2022) . - 689-703[article] Childhood adversity predicts black young adults? DNA methylation-based accelerated aging: A dual pathway model [Texte imprimé et/ou numérique] / Steven R. H. BEACH, Auteur ; Frederick X. GIBBONS, Auteur ; Sierra E. CARTER, Auteur ; Mei Ling ONG, Auteur ; Justin A. LAVNER, Auteur ; Man-Kit LEI, Auteur ; Ronald L. SIMONS, Auteur ; Meg GERRARD, Auteur ; Robert A. PHILIBERT, Auteur . - 689-703.
Langues : Anglais (eng)
in Development and Psychopathology > 34-2 (May 2022) . - 689-703
Mots-clés : discrimination DNAm-aging FKBP5 Life History Index. décimale : PER Périodiques Résumé : We expand upon prior work (Gibbons et al., ) relating childhood stressor effects, particularly harsh childhood environments, to risky behavior and ultimately physical health by adding longer-term outcomes ? deoxyribonucleic acid (DNA) methylation-based measures of accelerated aging (DNAm-aging). Further, following work on the effects of early exposure to danger (McLaughlin et al., ), we also identify an additional pathway from harsh childhood environments to DNAm-aging that we label the danger/FKBP5 pathway, which includes early exposure to dangerous community conditions that are thought to impact glucocorticoid regulation and pro-inflammatory mechanisms. Because different DNAm-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNAm-aging based on chronological age with later indices that focused on predicting biological outcomes. We utilize data from Family and Community Health Study participants (N = 449) from age 10 to 29. We find that harshness influences parenting, which, in turn, influences accelerated DNAm-aging through the risky cognitions and substance use (i.e., behavioral) pathway outlined by Gibbons et al. (). Harshness is also associated with increased exposure to threat/danger, which, in turn, leads to accelerated DNAm-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway). En ligne : http://dx.doi.org/10.1017/s0954579421001541 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474 Glucocorticoid receptor signaling in leukocytes after early life adversity / Martha M. C. ELWENSPOEK in Development and Psychopathology, 32-3 (August 2020)
[article]
Titre : Glucocorticoid receptor signaling in leukocytes after early life adversity Type de document : Texte imprimé et/ou numérique Auteurs : Martha M. C. ELWENSPOEK, Auteur ; Xenia HENGESCH, Auteur ; Fleur A. D. LEENEN, Auteur ; Krystel SIAS, Auteur ; Sara Beatriz FERNANDES, Auteur ; Violetta K. SCHAAN, Auteur ; Sophie B. MÉRIAUX, Auteur ; Stephanie SCHMITZ, Auteur ; Fanny BONNEMBERGER, Auteur ; Hartmut SCHÄCHINGER, Auteur ; Claus VÖGELE, Auteur ; Claude P. MULLER, Auteur ; Jonathan D. TURNER, Auteur Article en page(s) : p.853-863 Langues : Anglais (eng) Mots-clés : DNA methylation Fkbp5 Gilz Nr3c1 early life adversity glucocorticoid receptor Index. décimale : PER Périodiques Résumé : Early life adversity (ELA) has been associated with inflammation and immunosenescence, as well as hyporeactivity of the HPA axis. Because the immune system and the HPA axis are tightly intertwined around the glucocorticoid receptor (GR), we examined peripheral GR functionality in the EpiPath cohort among participants who either had been exposed to ELA (separation from parents and/or institutionalization followed by adoption; n = 40) or had been reared by their biological parents (n = 72).Expression of the strict GR target genes FKBP5 and GILZ as well as total and 1F and 1H GR transcripts were similar between groups. Furthermore, there were no differences in GR sensitivity, examined by the effects of dexamethasone on IL6 production in LPS-stimulated whole blood. Although we did not find differences in methylation at the GR 1F exon or promoter region, we identified a region of the GR 1H promoter (CpG 1-9) that showed lower methylation levels in ELA.Our results suggest that peripheral GR signaling was unperturbed in our cohort and the observed immune phenotype does not appear to be secondary to an altered GR response to the perturbed HPA axis and glucocorticoid (GC) profile, although we are limited in our measures of GR activity and time points. En ligne : http://dx.doi.org/10.1017/s0954579419001147 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=429
in Development and Psychopathology > 32-3 (August 2020) . - p.853-863[article] Glucocorticoid receptor signaling in leukocytes after early life adversity [Texte imprimé et/ou numérique] / Martha M. C. ELWENSPOEK, Auteur ; Xenia HENGESCH, Auteur ; Fleur A. D. LEENEN, Auteur ; Krystel SIAS, Auteur ; Sara Beatriz FERNANDES, Auteur ; Violetta K. SCHAAN, Auteur ; Sophie B. MÉRIAUX, Auteur ; Stephanie SCHMITZ, Auteur ; Fanny BONNEMBERGER, Auteur ; Hartmut SCHÄCHINGER, Auteur ; Claus VÖGELE, Auteur ; Claude P. MULLER, Auteur ; Jonathan D. TURNER, Auteur . - p.853-863.
Langues : Anglais (eng)
in Development and Psychopathology > 32-3 (August 2020) . - p.853-863
Mots-clés : DNA methylation Fkbp5 Gilz Nr3c1 early life adversity glucocorticoid receptor Index. décimale : PER Périodiques Résumé : Early life adversity (ELA) has been associated with inflammation and immunosenescence, as well as hyporeactivity of the HPA axis. Because the immune system and the HPA axis are tightly intertwined around the glucocorticoid receptor (GR), we examined peripheral GR functionality in the EpiPath cohort among participants who either had been exposed to ELA (separation from parents and/or institutionalization followed by adoption; n = 40) or had been reared by their biological parents (n = 72).Expression of the strict GR target genes FKBP5 and GILZ as well as total and 1F and 1H GR transcripts were similar between groups. Furthermore, there were no differences in GR sensitivity, examined by the effects of dexamethasone on IL6 production in LPS-stimulated whole blood. Although we did not find differences in methylation at the GR 1F exon or promoter region, we identified a region of the GR 1H promoter (CpG 1-9) that showed lower methylation levels in ELA.Our results suggest that peripheral GR signaling was unperturbed in our cohort and the observed immune phenotype does not appear to be secondary to an altered GR response to the perturbed HPA axis and glucocorticoid (GC) profile, although we are limited in our measures of GR activity and time points. En ligne : http://dx.doi.org/10.1017/s0954579419001147 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=429