Increases in maternal depressive symptoms during pregnancy and infant cortisol reactivity: Mediation by placental corticotropin-releasing hormone / Jennifer A. SOMERS ; Isabel F. RAMOS ; Kharah M. ROSS ; Mary COUSSONS-READ ; Christine DUNKEL SCHETTER in Development and Psychopathology, 35-4 (October 2023)  

Public ISBD [article]  inDevelopment and Psychopathology > 35-4 (October 2023) . - p.1997-2010 Titre : Increases in maternal depressive symptoms during pregnancy and infant cortisol reactivity: Mediation by placental corticotropin-releasing hormone Type de document : Texte imprimé et/ou numérique Auteurs : Jennifer A. SOMERS, Auteur ; Isabel F. RAMOS, Auteur ; Kharah M. ROSS, Auteur ; Mary COUSSONS-READ, Auteur ; Christine DUNKEL SCHETTER, Auteur Article en page(s) : p.1997-2010 Langues : Anglais (eng) Mots-clés : depressive symptoms  HPA axis  infancy  placental corticotropin-releasing hormone  pregnancy Index. décimale : PER Périodiques Résumé : Background:Maternal depressive symptoms in pregnancy may affect offspring health through prenatal programming of the hypothalamic-pituitary-adrenal (HPA) axis. The biological mechanisms that explain the associations between maternal prenatal depressive symptoms and offspring HPA axis regulation are not yet clear. This pre-registered investigation examines whether patterns of maternal depressive symptoms in pregnancy are associated with infant cortisol reactivity and whether this association is mediated by changes in placental corticotropin-releasing hormone (pCRH).Method:A sample of 174 pregnant women completed assessments in early, mid, and late pregnancy that included standardized measures of depressive symptoms and blood samples for pCRH. Infant cortisol reactivity was assessed at 1 and 6 months of age.Results:Greater increases in maternal depressive symptoms in pregnancy were associated with higher cortisol infant cortisol reactivity at 1 and 6 months. Greater increases in maternal depressive symptoms in pregnancy were associated with greater increases in pCRH from early to late pregnancy which in turn were associated with higher infant cortisol reactivity.Conclusions:Increases in maternal depressive symptoms and pCRH over pregnancy may contribute to higher infant cortisol reactivity. These findings help to elucidate the prenatal biopsychosocial processes contributing to offspring HPA axis regulation early in development. En ligne : https://dx.doi.org/10.1017/S0954579422000621 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=515 [article] Increases in maternal depressive symptoms during pregnancy and infant cortisol reactivity: Mediation by placental corticotropin-releasing hormone [Texte imprimé et/ou numérique] / Jennifer A. SOMERS, Auteur ; Isabel F. RAMOS, Auteur ; Kharah M. ROSS, Auteur ; Mary COUSSONS-READ, Auteur ; Christine DUNKEL SCHETTER, Auteur . - p.1997-2010. Langues : Anglais (eng) in Development and Psychopathology > 35-4 (October 2023) . - p.1997-2010 Mots-clés : depressive symptoms  HPA axis  infancy  placental corticotropin-releasing hormone  pregnancy Index. décimale : PER Périodiques Résumé : Background:Maternal depressive symptoms in pregnancy may affect offspring health through prenatal programming of the hypothalamic-pituitary-adrenal (HPA) axis. The biological mechanisms that explain the associations between maternal prenatal depressive symptoms and offspring HPA axis regulation are not yet clear. This pre-registered investigation examines whether patterns of maternal depressive symptoms in pregnancy are associated with infant cortisol reactivity and whether this association is mediated by changes in placental corticotropin-releasing hormone (pCRH).Method:A sample of 174 pregnant women completed assessments in early, mid, and late pregnancy that included standardized measures of depressive symptoms and blood samples for pCRH. Infant cortisol reactivity was assessed at 1 and 6 months of age.Results:Greater increases in maternal depressive symptoms in pregnancy were associated with higher cortisol infant cortisol reactivity at 1 and 6 months. Greater increases in maternal depressive symptoms in pregnancy were associated with greater increases in pCRH from early to late pregnancy which in turn were associated with higher infant cortisol reactivity.Conclusions:Increases in maternal depressive symptoms and pCRH over pregnancy may contribute to higher infant cortisol reactivity. These findings help to elucidate the prenatal biopsychosocial processes contributing to offspring HPA axis regulation early in development. En ligne : https://dx.doi.org/10.1017/S0954579422000621 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=515

Testing the biological embedding hypothesis: Is early life adversity associated with a later proinflammatory phenotype? / Katherine B. EHRLICH in Development and Psychopathology, 28-4 pt2 (November 2016)  

Public ISBD [article]  inDevelopment and Psychopathology > 28-4 pt2 (November 2016) . - p.1273-1283 Titre : Testing the biological embedding hypothesis: Is early life adversity associated with a later proinflammatory phenotype? Type de document : Texte imprimé et/ou numérique Auteurs : Katherine B. EHRLICH, Auteur ; Kharah M. ROSS, Auteur ; Edith CHEN, Auteur ; Gregory E. MILLER, Auteur Article en page(s) : p.1273-1283 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Accumulating evidence suggests that the experience of early life adversity is a risk factor for a range of poor outcomes across development, including poor physical health in adulthood. The biological embedding model of early adversity (Miller, Chen, & Parker, 2011) suggests that early adversity might become embedded within immune cells known as monocytes/macrophages, programming them to be overly aggressive to environmental stimuli and insensitive to inhibitory signals, creating a “proinflammatory phenotype” that increases vulnerability to chronic diseases across the life span. We tested this hypothesis in the present study. Adolescent girls (n = 147) had blood drawn every 6 months across a 2.5-year period. To assess inflammatory responses to challenge, their monocytes were stimulated in vitro with a bacterial product, and production of the cytokine interleukin-6 was quantified. Hydrocortisone was added to cultures to assess the cells’ sensitivity to glucocorticoids’ anti-inflammatory signal. Using cluster analyses, we found that early life adversity was associated with greater odds of displaying a proinflammatory phenotype characterized by relatively larger interleukin-6 responses and relatively less sensitivity to glucocorticoids. In contrast, ongoing social stress was not associated with increasing odds of being categorized in the proinflammatory cluster. These findings suggest that early life adversity increases the probability of developing a proinflammatory phenotype, which, if sustained, could forecast risk for health problems later in life. En ligne : http://dx.doi.org/10.1017/s0954579416000845 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294 [article] Testing the biological embedding hypothesis: Is early life adversity associated with a later proinflammatory phenotype? [Texte imprimé et/ou numérique] / Katherine B. EHRLICH, Auteur ; Kharah M. ROSS, Auteur ; Edith CHEN, Auteur ; Gregory E. MILLER, Auteur . - p.1273-1283. Langues : Anglais (eng) in Development and Psychopathology > 28-4 pt2 (November 2016) . - p.1273-1283 Index. décimale : PER Périodiques Résumé : Accumulating evidence suggests that the experience of early life adversity is a risk factor for a range of poor outcomes across development, including poor physical health in adulthood. The biological embedding model of early adversity (Miller, Chen, & Parker, 2011) suggests that early adversity might become embedded within immune cells known as monocytes/macrophages, programming them to be overly aggressive to environmental stimuli and insensitive to inhibitory signals, creating a “proinflammatory phenotype” that increases vulnerability to chronic diseases across the life span. We tested this hypothesis in the present study. Adolescent girls (n = 147) had blood drawn every 6 months across a 2.5-year period. To assess inflammatory responses to challenge, their monocytes were stimulated in vitro with a bacterial product, and production of the cytokine interleukin-6 was quantified. Hydrocortisone was added to cultures to assess the cells’ sensitivity to glucocorticoids’ anti-inflammatory signal. Using cluster analyses, we found that early life adversity was associated with greater odds of displaying a proinflammatory phenotype characterized by relatively larger interleukin-6 responses and relatively less sensitivity to glucocorticoids. In contrast, ongoing social stress was not associated with increasing odds of being categorized in the proinflammatory cluster. These findings suggest that early life adversity increases the probability of developing a proinflammatory phenotype, which, if sustained, could forecast risk for health problems later in life. En ligne : http://dx.doi.org/10.1017/s0954579416000845 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294

Threat vigilance and socioeconomic disparities in metabolic health / Camelia E. HOSTINAR in Development and Psychopathology, 29-5 (December 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-5 (December 2017) . - p.1721-1733 Titre : Threat vigilance and socioeconomic disparities in metabolic health Type de document : Texte imprimé et/ou numérique Auteurs : Camelia E. HOSTINAR, Auteur ; Kharah M. ROSS, Auteur ; Meanne CHAN, Auteur ; Edith CHEN, Auteur ; Gregory E. MILLER, Auteur Article en page(s) : p.1721-1733 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : A quarter of the global population meets diagnostic criteria for metabolic syndrome (MetS). MetS prevalence stratifies by socioeconomic status (SES), such that low SES is associated with higher MetS risk starting in childhood. Despite this trend, some low-SES children maintain good metabolic health across the life span, but the factors responsible for their resilience are not well understood. This study examined the role of threat vigilance as either a moderator or a mediator of the effects of low early life SES on adult metabolic risk. Three hundred twenty-five Canadians aged 15–55 participated (M = 36.4 years, SD = 10.7; 55.4% female). We coded parental occupational status between the ages of 0 and 5 to index early life SES. We used the International Diabetes Federation case definition for MetS based on waist circumference, blood pressure, triglyceride levels, HDL cholesterol, and glycosylated hemoglobin measures. Threat vigilance was assessed using the Weapons Identification Procedure, a visual discrimination paradigm that captures implicit perceptions of threat. Analyses supported the moderator hypothesis: low early life SES was associated with MetS diagnosis exclusively among those with high levels of threat vigilance. This suggests that low early life SES environments that heighten vigilance to threat might be particularly detrimental for metabolic health. Conversely, low threat vigilance may buffer against the metabolic risks associated with socioeconomic disadvantage. En ligne : http://dx.doi.org/10.1017/S0954579417001353 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323 [article] Threat vigilance and socioeconomic disparities in metabolic health [Texte imprimé et/ou numérique] / Camelia E. HOSTINAR, Auteur ; Kharah M. ROSS, Auteur ; Meanne CHAN, Auteur ; Edith CHEN, Auteur ; Gregory E. MILLER, Auteur . - p.1721-1733. Langues : Anglais (eng) in Development and Psychopathology > 29-5 (December 2017) . - p.1721-1733 Index. décimale : PER Périodiques Résumé : A quarter of the global population meets diagnostic criteria for metabolic syndrome (MetS). MetS prevalence stratifies by socioeconomic status (SES), such that low SES is associated with higher MetS risk starting in childhood. Despite this trend, some low-SES children maintain good metabolic health across the life span, but the factors responsible for their resilience are not well understood. This study examined the role of threat vigilance as either a moderator or a mediator of the effects of low early life SES on adult metabolic risk. Three hundred twenty-five Canadians aged 15–55 participated (M = 36.4 years, SD = 10.7; 55.4% female). We coded parental occupational status between the ages of 0 and 5 to index early life SES. We used the International Diabetes Federation case definition for MetS based on waist circumference, blood pressure, triglyceride levels, HDL cholesterol, and glycosylated hemoglobin measures. Threat vigilance was assessed using the Weapons Identification Procedure, a visual discrimination paradigm that captures implicit perceptions of threat. Analyses supported the moderator hypothesis: low early life SES was associated with MetS diagnosis exclusively among those with high levels of threat vigilance. This suggests that low early life SES environments that heighten vigilance to threat might be particularly detrimental for metabolic health. Conversely, low threat vigilance may buffer against the metabolic risks associated with socioeconomic disadvantage. En ligne : http://dx.doi.org/10.1017/S0954579417001353 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323

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