Sensitizing effect of early adversity on depressive reactions to later proximal stress: Moderation by polymorphisms in serotonin transporter and corticotropin releasing hormone receptor genes in a 20-year longitudinal study / Lisa R. STARR in Development and Psychopathology, 26-4 (Part 2) (November 2014)  

Public ISBD [article]  inDevelopment and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1241-1254 Titre : Sensitizing effect of early adversity on depressive reactions to later proximal stress: Moderation by polymorphisms in serotonin transporter and corticotropin releasing hormone receptor genes in a 20-year longitudinal study Type de document : texte imprimé Auteurs : Lisa R. STARR, Auteur ; Constance HAMMEN, Auteur ; Christopher C. CONWAY, Auteur ; Elizabeth RAPOSA, Auteur ; Patricia A. BRENNAN, Auteur Année de publication : 2014 Article en page(s) : p.1241-1254 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Previous research supports gene–environment interactions for polymorphisms in the corticotropin hormone receptor 1 gene (CRHR1) and the serotonin transporter gene linked polymorphic region (5-HTTLPR) in predicting depression, but it has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life. The current study tested a gene–environment–environment interaction (G × E × E; specifically, gene–EA–proximal stress interaction) model of depression in a 20-year longitudinal study. Participants were assessed prospectively for EA up to age 5 and recent chronic stress and depressive symptoms at age 20 and genotyped for CRHR1 single nucleotide polymorphism rs110402 and 5-HTTLPR. EA predicted stronger associations between recent chronic stress and depression, and the effect was moderated by genes. CRHR1 A alleles and 5-HTTLPR short alleles were associated with greater stress sensitization (i.e., greater depressive reactivity to chronic stress for those also exposed to high levels of EA). The results are consistent with the notion that EA exposure results in neurobiological and cognitive–emotional consequences (e.g., altered hypothalamic–pituitary–adrenal axis functioning), leading to emotional distress in the face of recent stressors among those with certain genetic characteristics, although further research is needed to explore explanatory mechanisms. En ligne : http://dx.doi.org/10.1017/S0954579414000996 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=245 [article] Sensitizing effect of early adversity on depressive reactions to later proximal stress: Moderation by polymorphisms in serotonin transporter and corticotropin releasing hormone receptor genes in a 20-year longitudinal study [texte imprimé] / Lisa R. STARR, Auteur ; Constance HAMMEN, Auteur ; Christopher C. CONWAY, Auteur ; Elizabeth RAPOSA, Auteur ; Patricia A. BRENNAN, Auteur . - 2014 . - p.1241-1254. Langues : Anglais (eng) in Development and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1241-1254 Index. décimale : PER Périodiques Résumé : Previous research supports gene–environment interactions for polymorphisms in the corticotropin hormone receptor 1 gene (CRHR1) and the serotonin transporter gene linked polymorphic region (5-HTTLPR) in predicting depression, but it has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life. The current study tested a gene–environment–environment interaction (G × E × E; specifically, gene–EA–proximal stress interaction) model of depression in a 20-year longitudinal study. Participants were assessed prospectively for EA up to age 5 and recent chronic stress and depressive symptoms at age 20 and genotyped for CRHR1 single nucleotide polymorphism rs110402 and 5-HTTLPR. EA predicted stronger associations between recent chronic stress and depression, and the effect was moderated by genes. CRHR1 A alleles and 5-HTTLPR short alleles were associated with greater stress sensitization (i.e., greater depressive reactivity to chronic stress for those also exposed to high levels of EA). The results are consistent with the notion that EA exposure results in neurobiological and cognitive–emotional consequences (e.g., altered hypothalamic–pituitary–adrenal axis functioning), leading to emotional distress in the face of recent stressors among those with certain genetic characteristics, although further research is needed to explore explanatory mechanisms. En ligne : http://dx.doi.org/10.1017/S0954579414000996 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=245

Transdiagnostic pathways from early social stress to psychopathology: a 20-year prospective study / Christopher C. CONWAY in Journal of Child Psychology and Psychiatry, 59-8 (August 2018)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 59-8 (August 2018) . - p.855-862 Titre : Transdiagnostic pathways from early social stress to psychopathology: a 20-year prospective study Type de document : texte imprimé Auteurs : Christopher C. CONWAY, Auteur ; Elizabeth B. RAPOSA, Auteur ; Constance HAMMEN, Auteur ; Patricia A. BRENNAN, Auteur Article en page(s) : p.855-862 Langues : Anglais (eng) Mots-clés : Classification  comorbidity  early adversity  stress  transdiagnostic Index. décimale : PER Périodiques Résumé : BACKGROUND: Adverse family environments confer susceptibility to virtually all psychiatric problems. This study evaluated two possible models to explain this diversity of associations. Stressful family circumstances during childhood could either activate general, transdiagnostic liabilities to mental disorder or promote numerous disorder-specific liabilities. METHODS: We recruited a high-risk sample of 815 mother-offspring pairs and assessed social stressors in the family context prospectively from the perinatal period through offspring age 5. We factor analyzed offspring mental disorder diagnoses at age 20 to parse transdiagnostic and disorder-specific dimensions of psychopathology. RESULTS: Structural analyses revealed nearly equivalent prospective effects of early family stress on overarching Internalizing (beta = .30) and Externalizing (beta = .29) dimensions. In contrast, there was no evidence of disorder-specific effects. CONCLUSIONS: Social stressors early in life activate transdiagnostic, and not disorder-specific, liabilities to psychopathology. A focus on higher-order dimensions of psychopathology could accelerate etiological research and intervention efforts for stress-linked mental disorders. En ligne : http://dx.doi.org/10.1111/jcpp.12862 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=368 [article] Transdiagnostic pathways from early social stress to psychopathology: a 20-year prospective study [texte imprimé] / Christopher C. CONWAY, Auteur ; Elizabeth B. RAPOSA, Auteur ; Constance HAMMEN, Auteur ; Patricia A. BRENNAN, Auteur . - p.855-862. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 59-8 (August 2018) . - p.855-862 Mots-clés : Classification  comorbidity  early adversity  stress  transdiagnostic Index. décimale : PER Périodiques Résumé : BACKGROUND: Adverse family environments confer susceptibility to virtually all psychiatric problems. This study evaluated two possible models to explain this diversity of associations. Stressful family circumstances during childhood could either activate general, transdiagnostic liabilities to mental disorder or promote numerous disorder-specific liabilities. METHODS: We recruited a high-risk sample of 815 mother-offspring pairs and assessed social stressors in the family context prospectively from the perinatal period through offspring age 5. We factor analyzed offspring mental disorder diagnoses at age 20 to parse transdiagnostic and disorder-specific dimensions of psychopathology. RESULTS: Structural analyses revealed nearly equivalent prospective effects of early family stress on overarching Internalizing (beta = .30) and Externalizing (beta = .29) dimensions. In contrast, there was no evidence of disorder-specific effects. CONCLUSIONS: Social stressors early in life activate transdiagnostic, and not disorder-specific, liabilities to psychopathology. A focus on higher-order dimensions of psychopathology could accelerate etiological research and intervention efforts for stress-linked mental disorders. En ligne : http://dx.doi.org/10.1111/jcpp.12862 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=368

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