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Auteur Lisa R. STARR |
Documents disponibles écrits par cet auteur (5)
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Childhood adversity moderates the influence of proximal episodic stress on the cortisol awakening response and depressive symptoms in adolescents / Lisa R. STARR in Development and Psychopathology, 29-5 (December 2017)
[article]
Titre : Childhood adversity moderates the influence of proximal episodic stress on the cortisol awakening response and depressive symptoms in adolescents Type de document : Texte imprimé et/ou numérique Auteurs : Lisa R. STARR, Auteur ; Kimberly DIENES, Auteur ; Catherine B. STROUD, Auteur ; Zoey A. SHAW, Auteur ; Y. Irina LI, Auteur ; Fanny MLAWER, Auteur ; Meghan HUANG, Auteur Article en page(s) : p.1877-1893 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Childhood adversity (CA) is known to predict sensitization to proximal stressors. Researchers have suggested that disruptions in hypothalamus–pituitary–adrenal axis functioning may be a biological mechanism. If so, CA may predict altered associations between proximal life stress and markers of cortisol secretion. We examined whether CA moderates associations between recent episodic stress and (a) the cortisol awakening response (CAR), and (b) depressive symptoms, in 241 adolescents aged 14–17 years (cortisol n = 196). Salivary cortisol was sampled at 0, 30, and 60 min postawakening for 2 days. The CAR was calculated as the area under the curve with respect to increase and waking cortisol. CA and episodic stress were assessed using contextual-threat-method-coded objective interviews. CA significantly interacted with episodic stress to predict both the CAR and depression. Among those with low CA, episodic stress predicted increased CAR but did not predict depression. For adolescents with high CA, episodic stress predicted lower CAR and higher depression. These interactions were found only for independent (uncontrollable, fateful) events, and not for dependent (self-generated) stress. Increased allostatic load resulting from CA exposure may interfere with adolescents' ability to optimally regulate their CAR in relation to recent stress, contributing to increased depression risk. En ligne : http://dx.doi.org/10.1017/S0954579417001468 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=324
in Development and Psychopathology > 29-5 (December 2017) . - p.1877-1893[article] Childhood adversity moderates the influence of proximal episodic stress on the cortisol awakening response and depressive symptoms in adolescents [Texte imprimé et/ou numérique] / Lisa R. STARR, Auteur ; Kimberly DIENES, Auteur ; Catherine B. STROUD, Auteur ; Zoey A. SHAW, Auteur ; Y. Irina LI, Auteur ; Fanny MLAWER, Auteur ; Meghan HUANG, Auteur . - p.1877-1893.
Langues : Anglais (eng)
in Development and Psychopathology > 29-5 (December 2017) . - p.1877-1893
Index. décimale : PER Périodiques Résumé : Childhood adversity (CA) is known to predict sensitization to proximal stressors. Researchers have suggested that disruptions in hypothalamus–pituitary–adrenal axis functioning may be a biological mechanism. If so, CA may predict altered associations between proximal life stress and markers of cortisol secretion. We examined whether CA moderates associations between recent episodic stress and (a) the cortisol awakening response (CAR), and (b) depressive symptoms, in 241 adolescents aged 14–17 years (cortisol n = 196). Salivary cortisol was sampled at 0, 30, and 60 min postawakening for 2 days. The CAR was calculated as the area under the curve with respect to increase and waking cortisol. CA and episodic stress were assessed using contextual-threat-method-coded objective interviews. CA significantly interacted with episodic stress to predict both the CAR and depression. Among those with low CA, episodic stress predicted increased CAR but did not predict depression. For adolescents with high CA, episodic stress predicted lower CAR and higher depression. These interactions were found only for independent (uncontrollable, fateful) events, and not for dependent (self-generated) stress. Increased allostatic load resulting from CA exposure may interfere with adolescents' ability to optimally regulate their CAR in relation to recent stress, contributing to increased depression risk. En ligne : http://dx.doi.org/10.1017/S0954579417001468 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=324 Differentiating Interpersonal Correlates of Depressive Symptoms and Social Anxiety in Adolescence: Implications for Models of Comorbidity / Lisa R. STARR in Journal of Clinical Child & Adolescent Psychology, 37-2 (April-June 2008)
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Titre : Differentiating Interpersonal Correlates of Depressive Symptoms and Social Anxiety in Adolescence: Implications for Models of Comorbidity Type de document : Texte imprimé et/ou numérique Auteurs : Lisa R. STARR, Auteur ; Joanne DAVILA, Auteur Année de publication : 2008 Article en page(s) : p.337-349 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Research on psychosocial correlates of depression and social anxiety often has not accounted for their comorbidity. Differentiating correlates of depression and social anxiety may inform the development of comorbidity models. Building on research linking both disorders to interpersonal dysfunction, this study examined interpersonal correlates of depressive symptoms and social anxiety in nonreferred early adolescent (M age = 13.46) girls (n = 83), controlling for comorbid symptoms. Although both showed significant bivariate correlations with peer and family variables, partial correlations revealed that social anxiety (controlling for depressive symptoms) was more strongly related to peer variables (e.g., social competence and trust and communication in friendships), whereas depressive symptoms (controlling for social anxiety) were more strongly related to family variables (e.g., lower trust and greater alienation and conflict). Comorbid girls showed heightened peer and family alienation compared to purely dysphoric or anxious girls. Implications for casual models of comorbidity and for understanding poorer outcomes associated with comorbidity and discussed. En ligne : http://dx.doi.org/10.1080/15374410801955854 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=452
in Journal of Clinical Child & Adolescent Psychology > 37-2 (April-June 2008) . - p.337-349[article] Differentiating Interpersonal Correlates of Depressive Symptoms and Social Anxiety in Adolescence: Implications for Models of Comorbidity [Texte imprimé et/ou numérique] / Lisa R. STARR, Auteur ; Joanne DAVILA, Auteur . - 2008 . - p.337-349.
Langues : Anglais (eng)
in Journal of Clinical Child & Adolescent Psychology > 37-2 (April-June 2008) . - p.337-349
Index. décimale : PER Périodiques Résumé : Research on psychosocial correlates of depression and social anxiety often has not accounted for their comorbidity. Differentiating correlates of depression and social anxiety may inform the development of comorbidity models. Building on research linking both disorders to interpersonal dysfunction, this study examined interpersonal correlates of depressive symptoms and social anxiety in nonreferred early adolescent (M age = 13.46) girls (n = 83), controlling for comorbid symptoms. Although both showed significant bivariate correlations with peer and family variables, partial correlations revealed that social anxiety (controlling for depressive symptoms) was more strongly related to peer variables (e.g., social competence and trust and communication in friendships), whereas depressive symptoms (controlling for social anxiety) were more strongly related to family variables (e.g., lower trust and greater alienation and conflict). Comorbid girls showed heightened peer and family alienation compared to purely dysphoric or anxious girls. Implications for casual models of comorbidity and for understanding poorer outcomes associated with comorbidity and discussed. En ligne : http://dx.doi.org/10.1080/15374410801955854 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=452 Genetic moderation of the association between adolescent romantic involvement and depression: Contributions of serotonin transporter gene polymorphism, chronic stress, and family discord / Lisa R. STARR in Development and Psychopathology, 28-2 (May 2016)
[article]
Titre : Genetic moderation of the association between adolescent romantic involvement and depression: Contributions of serotonin transporter gene polymorphism, chronic stress, and family discord Type de document : Texte imprimé et/ou numérique Auteurs : Lisa R. STARR, Auteur ; Constance HAMMEN, Auteur Article en page(s) : p.447-457 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Studies support a link between adolescent romantic involvement and depression. Adolescent romantic relationships may increase depression risk by introducing chronic stress, and genetic vulnerability to stress reactivity/emotion dysregulation may moderate these associations. We tested genetic moderation of longitudinal associations between adolescent romantic involvement and later depressive symptoms by a polymorphism in the serotonin transporter linked polymorphic region gene (5-HTTLPR) and examined contributory roles of chronic stress and family discord. Three hundred eighty-one youth participated at ages 15 and 20. The results indicated that 5-HTTLPR moderated the association between age 15 romantic involvement and age 20 depressive symptoms, with strongest effects for short homozygotes. Conditional process analysis revealed that chronic stress functioned as a moderated mediator of this association, fully accounting for the romantic involvement–depression link among short/short genotypes. Also, romantic involvement predicted later depressive symptoms most strongly among short-allele carriers with high family discord. The results have important implications for understanding the romantic involvement–depression link and the behavioral and emotional correlates of the 5-HTTLPR genotype. En ligne : http://dx.doi.org/10.1017/S0954579415000498 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=288
in Development and Psychopathology > 28-2 (May 2016) . - p.447-457[article] Genetic moderation of the association between adolescent romantic involvement and depression: Contributions of serotonin transporter gene polymorphism, chronic stress, and family discord [Texte imprimé et/ou numérique] / Lisa R. STARR, Auteur ; Constance HAMMEN, Auteur . - p.447-457.
Langues : Anglais (eng)
in Development and Psychopathology > 28-2 (May 2016) . - p.447-457
Index. décimale : PER Périodiques Résumé : Studies support a link between adolescent romantic involvement and depression. Adolescent romantic relationships may increase depression risk by introducing chronic stress, and genetic vulnerability to stress reactivity/emotion dysregulation may moderate these associations. We tested genetic moderation of longitudinal associations between adolescent romantic involvement and later depressive symptoms by a polymorphism in the serotonin transporter linked polymorphic region gene (5-HTTLPR) and examined contributory roles of chronic stress and family discord. Three hundred eighty-one youth participated at ages 15 and 20. The results indicated that 5-HTTLPR moderated the association between age 15 romantic involvement and age 20 depressive symptoms, with strongest effects for short homozygotes. Conditional process analysis revealed that chronic stress functioned as a moderated mediator of this association, fully accounting for the romantic involvement–depression link among short/short genotypes. Also, romantic involvement predicted later depressive symptoms most strongly among short-allele carriers with high family discord. The results have important implications for understanding the romantic involvement–depression link and the behavioral and emotional correlates of the 5-HTTLPR genotype. En ligne : http://dx.doi.org/10.1017/S0954579415000498 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=288 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)
[article]
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 et/ou numérique 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
in Development and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1241-1254[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 et/ou numérique] / 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 Stress sensitization to depression following childhood adversity: Moderation by HPA axis and serotonergic multilocus profile scores / Lisa R. STARR in Development and Psychopathology, 33-4 (October 2021)
[article]
Titre : Stress sensitization to depression following childhood adversity: Moderation by HPA axis and serotonergic multilocus profile scores Type de document : Texte imprimé et/ou numérique Auteurs : Lisa R. STARR, Auteur ; Catherine B. STROUD, Auteur ; Zoey A. SHAW, Auteur ; Suzanne VRSHEK-SCHALLHORN, Auteur Article en page(s) : p.1264-1278 Langues : Anglais (eng) Mots-clés : childhood adversity depression gene-by-environment interaction genetic stress sensitization stressful life events Index. décimale : PER Périodiques Résumé : Childhood adversity appears to sensitize youth to stress, increasing depression risk following stressful life events occurring throughout the lifespan. Some evidence suggests hypothalamic–pituitary–adrenal (HPA) axis-related and serotonergic genetic variation moderates this effect, in a “gene-by-environment-by-environment” interaction (G × E × E). However, prior research has tested single genetic variants, limiting power. The current study uses a multilocus genetic profile score (MGPS) approach to capture polygenic risk relevant to HPA axis and serotonergic functioning. Adolescents (N = 241, Mage = 15.90) completed contextual-threat-based interviews assessing childhood adversity and acute life events, and diagnostic interviews assessing depression. Established MGPSs indexed genetic variation linked to HPA axis (10 single nucleotide polymorphisms [SNPs]) and serotonergic (five SNPs) functioning. Results showed significant MGPS × Childhood Adversity × Recent Life Stress interactions predicting depression for both HPA axis and serotonergic MGPSs, with both risk scores predicting stronger Childhood Adversity × Recent Stress interactions. Serotonergic genetic risk specifically predicted sensitization to major interpersonal stressors. The serotonergic MGPS G × E × E was re-tested in an independent replication sample of early adolescent girls, with comparable results. Findings support the notion that genetic variation linked to these two neurobiological symptoms alters stress sensitization, and that gene-by-environment (G × E) interactions may be qualified by environmental exposures occurring at different points in development. En ligne : http://dx.doi.org/10.1017/S0954579420000474 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457
in Development and Psychopathology > 33-4 (October 2021) . - p.1264-1278[article] Stress sensitization to depression following childhood adversity: Moderation by HPA axis and serotonergic multilocus profile scores [Texte imprimé et/ou numérique] / Lisa R. STARR, Auteur ; Catherine B. STROUD, Auteur ; Zoey A. SHAW, Auteur ; Suzanne VRSHEK-SCHALLHORN, Auteur . - p.1264-1278.
Langues : Anglais (eng)
in Development and Psychopathology > 33-4 (October 2021) . - p.1264-1278
Mots-clés : childhood adversity depression gene-by-environment interaction genetic stress sensitization stressful life events Index. décimale : PER Périodiques Résumé : Childhood adversity appears to sensitize youth to stress, increasing depression risk following stressful life events occurring throughout the lifespan. Some evidence suggests hypothalamic–pituitary–adrenal (HPA) axis-related and serotonergic genetic variation moderates this effect, in a “gene-by-environment-by-environment” interaction (G × E × E). However, prior research has tested single genetic variants, limiting power. The current study uses a multilocus genetic profile score (MGPS) approach to capture polygenic risk relevant to HPA axis and serotonergic functioning. Adolescents (N = 241, Mage = 15.90) completed contextual-threat-based interviews assessing childhood adversity and acute life events, and diagnostic interviews assessing depression. Established MGPSs indexed genetic variation linked to HPA axis (10 single nucleotide polymorphisms [SNPs]) and serotonergic (five SNPs) functioning. Results showed significant MGPS × Childhood Adversity × Recent Life Stress interactions predicting depression for both HPA axis and serotonergic MGPSs, with both risk scores predicting stronger Childhood Adversity × Recent Stress interactions. Serotonergic genetic risk specifically predicted sensitization to major interpersonal stressors. The serotonergic MGPS G × E × E was re-tested in an independent replication sample of early adolescent girls, with comparable results. Findings support the notion that genetic variation linked to these two neurobiological symptoms alters stress sensitization, and that gene-by-environment (G × E) interactions may be qualified by environmental exposures occurring at different points in development. En ligne : http://dx.doi.org/10.1017/S0954579420000474 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457