An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression? / Elysia Poggi DAVIS in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.787-806 Titre : An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression? Type de document : texte imprimé Auteurs : Elysia Poggi DAVIS, Auteur ; Benjamin L. HANKIN, Auteur ; Danielle A. SWALES, Auteur ; M. Camille HOFFMAN, Auteur Article en page(s) : p.787-806 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Maternal depression is one of the most common prenatal complications, and prenatal maternal depression predicts many child psychopathologies. Here, we apply the fetal programming hypothesis as an organizational framework to address the possibility that fetal exposure to maternal depressive symptoms during pregnancy affects fetal development of vulnerabilities and risk mechanisms, which enhance risk for subsequent psychopathology. We consider four candidate pathways through which maternal prenatal depression may affect the propensity of offspring to develop later psychopathology across the life span: brain development, physiological stress regulation (hypothalamic-pituitary-adrenocortical axis), negative emotionality, and cognitive (effortful) control. The majority of past research has been correlational, so potential causal conclusions have been limited. We describe an ongoing experimental test of the fetal programming influence of prenatal maternal depressive symptoms using a randomized controlled trial design. In this randomized controlled trial, interpersonal psychotherapy is compared to enhanced usual care among distressed pregnant women to evaluate whether reducing prenatal maternal depressive symptoms has a salutary impact on child ontogenetic vulnerabilities and thereby reduces offspring's risk for emergence of later psychopathology. En ligne : http://dx.doi.org/10.1017/s0954579418000470 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression? [texte imprimé] / Elysia Poggi DAVIS, Auteur ; Benjamin L. HANKIN, Auteur ; Danielle A. SWALES, Auteur ; M. Camille HOFFMAN, Auteur . - p.787-806. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.787-806 Index. décimale : PER Périodiques Résumé : Maternal depression is one of the most common prenatal complications, and prenatal maternal depression predicts many child psychopathologies. Here, we apply the fetal programming hypothesis as an organizational framework to address the possibility that fetal exposure to maternal depressive symptoms during pregnancy affects fetal development of vulnerabilities and risk mechanisms, which enhance risk for subsequent psychopathology. We consider four candidate pathways through which maternal prenatal depression may affect the propensity of offspring to develop later psychopathology across the life span: brain development, physiological stress regulation (hypothalamic-pituitary-adrenocortical axis), negative emotionality, and cognitive (effortful) control. The majority of past research has been correlational, so potential causal conclusions have been limited. We describe an ongoing experimental test of the fetal programming influence of prenatal maternal depressive symptoms using a randomized controlled trial design. In this randomized controlled trial, interpersonal psychotherapy is compared to enhanced usual care among distressed pregnant women to evaluate whether reducing prenatal maternal depressive symptoms has a salutary impact on child ontogenetic vulnerabilities and thereby reduces offspring's risk for emergence of later psychopathology. En ligne : http://dx.doi.org/10.1017/s0954579418000470 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Exposure to prenatal maternal distress and infant white matter neurodevelopment / Catherine H. DEMERS in Development and Psychopathology, 33-5 (December 2021)  

Public ISBD [article]  inDevelopment and Psychopathology > 33-5 (December 2021) . - p.1526-1538 Titre : Exposure to prenatal maternal distress and infant white matter neurodevelopment Type de document : texte imprimé Auteurs : Catherine H. DEMERS, Auteur ; Maria M. BAGONIS, Auteur ; Khalid AL-ALI, Auteur ; Sarah E. GARCIA, Auteur ; Martin A. STYNER, Auteur ; John H. GILMORE, Auteur ; M. Camille HOFFMAN, Auteur ; Benjamin L. HANKIN, Auteur ; Elysia Poggi DAVIS, Auteur Article en page(s) : p.1526-1538 Langues : Anglais (eng) Mots-clés : pregnancy  white matter microstructure  magnetic resonance imaging (MRI)  diffusion tensor imaging (DTI)  anxiety Index. décimale : PER Périodiques Résumé : The prenatal period represents a critical time for brain growth and development. These rapid neurological advances render the fetus susceptible to various influences with life-long implications for mental health. Maternal distress signals are a dominant early life influence, contributing to birth outcomes and risk for offspring psychopathology. This prospective longitudinal study evaluated the association between prenatal maternal distress and infant white matter microstructure. Participants included a racially and socioeconomically diverse sample of 85 mother–infant dyads. Prenatal distress was assessed at 17 and 29 weeks’ gestational age (GA). Infant structural data were collected via diffusion tensor imaging (DTI) at 42–45 weeks’ postconceptional age. Findings demonstrated that higher prenatal maternal distress at 29 weeks’ GA was associated with increased fractional anisotropy, b = .283, t(64) = 2.319, p = .024, and with increased axial diffusivity, b = .254, t(64) = 2.067, p = .043, within the right anterior cingulate white matter tract. No other significant associations were found with prenatal distress exposure and tract fractional anisotropy or axial diffusivity at 29 weeks’ GA, or earlier in gestation. En ligne : http://dx.doi.org/10.1017/S0954579421000742 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457 [article] Exposure to prenatal maternal distress and infant white matter neurodevelopment [texte imprimé] / Catherine H. DEMERS, Auteur ; Maria M. BAGONIS, Auteur ; Khalid AL-ALI, Auteur ; Sarah E. GARCIA, Auteur ; Martin A. STYNER, Auteur ; John H. GILMORE, Auteur ; M. Camille HOFFMAN, Auteur ; Benjamin L. HANKIN, Auteur ; Elysia Poggi DAVIS, Auteur . - p.1526-1538. Langues : Anglais (eng) in Development and Psychopathology > 33-5 (December 2021) . - p.1526-1538 Mots-clés : pregnancy  white matter microstructure  magnetic resonance imaging (MRI)  diffusion tensor imaging (DTI)  anxiety Index. décimale : PER Périodiques Résumé : The prenatal period represents a critical time for brain growth and development. These rapid neurological advances render the fetus susceptible to various influences with life-long implications for mental health. Maternal distress signals are a dominant early life influence, contributing to birth outcomes and risk for offspring psychopathology. This prospective longitudinal study evaluated the association between prenatal maternal distress and infant white matter microstructure. Participants included a racially and socioeconomically diverse sample of 85 mother–infant dyads. Prenatal distress was assessed at 17 and 29 weeks’ gestational age (GA). Infant structural data were collected via diffusion tensor imaging (DTI) at 42–45 weeks’ postconceptional age. Findings demonstrated that higher prenatal maternal distress at 29 weeks’ GA was associated with increased fractional anisotropy, b = .283, t(64) = 2.319, p = .024, and with increased axial diffusivity, b = .254, t(64) = 2.067, p = .043, within the right anterior cingulate white matter tract. No other significant associations were found with prenatal distress exposure and tract fractional anisotropy or axial diffusivity at 29 weeks’ GA, or earlier in gestation. En ligne : http://dx.doi.org/10.1017/S0954579421000742 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457

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