Dépouillements

Future directions in prenatal stress research: Challenges and opportunities related to advancing our understanding of prenatal developmental origins of risk for psychopathology / C. DOYLE in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.721-724 Titre : Future directions in prenatal stress research: Challenges and opportunities related to advancing our understanding of prenatal developmental origins of risk for psychopathology Type de document : Texte imprimé et/ou numérique Auteurs : C. DOYLE, Auteur ; Dante CICCHETTI, Auteur Article en page(s) : p.721-724 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1017/s095457941800069x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Future directions in prenatal stress research: Challenges and opportunities related to advancing our understanding of prenatal developmental origins of risk for psychopathology [Texte imprimé et/ou numérique] / C. DOYLE, Auteur ; Dante CICCHETTI, Auteur . - p.721-724. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.721-724 Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1017/s095457941800069x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Prenatal depression, fetal neurobehavior, and infant temperament: Novel insights on early neurodevelopment from a socioeconomically disadvantaged Indian cohort / M. FERNANDES in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.725-742 Titre : Prenatal depression, fetal neurobehavior, and infant temperament: Novel insights on early neurodevelopment from a socioeconomically disadvantaged Indian cohort Type de document : Texte imprimé et/ou numérique Auteurs : M. FERNANDES, Auteur ; K. SRINIVASAN, Auteur ; G. MENEZES, Auteur ; P. G. RAMCHANDANI, Auteur Article en page(s) : p.725-742 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This article extends the research focusing on the early origins of psychopathology into the prenatal period, by exploring the association between maternal prenatal depression and offspring (fetal and infant) neurobehavior. The sample is recruited from a rural population in South India where women in the third trimester of pregnancy were assessed for depression and the heart rate responses of their fetuses to extrinsically applied vibroacoustic stimuli were studied. At 2 months postbirth, infant temperament and cortisol responsivity to immunization were assessed. The association between maternal prenatal depression and fetal responsivity to vibroacoustic stimulation, and infant responsivity to immunization, was U shaped with higher levels of responsivity noted in the offspring of mothers with very high and very low depression scores, and lower levels noted in the offspring of mothers with moderate depression scores. Maternal prenatal depression was not associated with infant temperament. The findings highlight the importance of environmental influences in the developmental origins of neurobehavior, suggesting that such differences, not evident at baseline, may emerge upon exposure to stressors. The study also emphasizes the need for further investigation in low- and middle-income contexts by providing preliminary evidence of the differing patterns of association observed between high- and low-income populations. En ligne : http://dx.doi.org/10.1017/s0954579418000615 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Prenatal depression, fetal neurobehavior, and infant temperament: Novel insights on early neurodevelopment from a socioeconomically disadvantaged Indian cohort [Texte imprimé et/ou numérique] / M. FERNANDES, Auteur ; K. SRINIVASAN, Auteur ; G. MENEZES, Auteur ; P. G. RAMCHANDANI, Auteur . - p.725-742. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.725-742 Index. décimale : PER Périodiques Résumé : This article extends the research focusing on the early origins of psychopathology into the prenatal period, by exploring the association between maternal prenatal depression and offspring (fetal and infant) neurobehavior. The sample is recruited from a rural population in South India where women in the third trimester of pregnancy were assessed for depression and the heart rate responses of their fetuses to extrinsically applied vibroacoustic stimuli were studied. At 2 months postbirth, infant temperament and cortisol responsivity to immunization were assessed. The association between maternal prenatal depression and fetal responsivity to vibroacoustic stimulation, and infant responsivity to immunization, was U shaped with higher levels of responsivity noted in the offspring of mothers with very high and very low depression scores, and lower levels noted in the offspring of mothers with moderate depression scores. Maternal prenatal depression was not associated with infant temperament. The findings highlight the importance of environmental influences in the developmental origins of neurobehavior, suggesting that such differences, not evident at baseline, may emerge upon exposure to stressors. The study also emphasizes the need for further investigation in low- and middle-income contexts by providing preliminary evidence of the differing patterns of association observed between high- and low-income populations. En ligne : http://dx.doi.org/10.1017/s0954579418000615 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Prenatal stress and the developing brain: Risks for neurodevelopmental disorders / B. R. H. VAN DEN BERGH in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.743-762 Titre : Prenatal stress and the developing brain: Risks for neurodevelopmental disorders Type de document : Texte imprimé et/ou numérique Auteurs : B. R. H. VAN DEN BERGH, Auteur ; R. DAHNKE, Auteur ; M. MENNES, Auteur Article en page(s) : p.743-762 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The prenatal period is increasingly considered as a crucial target for the primary prevention of neurodevelopmental and psychiatric disorders. Understanding their pathophysiological mechanisms remains a great challenge. Our review reveals new insights from prenatal brain development research, involving (epi)genetic research, neuroscience, recent imaging techniques, physical modeling, and computational simulation studies. Studies examining the effect of prenatal exposure to maternal distress on offspring brain development, using brain imaging techniques, reveal effects at birth and up into adulthood. Structural and functional changes are observed in several brain regions including the prefrontal, parietal, and temporal lobes, as well as the cerebellum, hippocampus, and amygdala. Furthermore, alterations are seen in functional connectivity of amygdalar-thalamus networks and in intrinsic brain networks, including default mode and attentional networks. The observed changes underlie offspring behavioral, cognitive, emotional development, and susceptibility to neurodevelopmental and psychiatric disorders. It is concluded that used brain measures have not yet been validated with regard to sensitivity, specificity, accuracy, or robustness in predicting neurodevelopmental and psychiatric disorders. Therefore, more prospective long-term longitudinal follow-up studies starting early in pregnancy should be carried out, in order to examine brain developmental measures as mediators in mediating the link between prenatal stress and offspring behavioral, cognitive, and emotional problems and susceptibility for disorders. En ligne : http://dx.doi.org/10.1017/s0954579418000342 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Prenatal stress and the developing brain: Risks for neurodevelopmental disorders [Texte imprimé et/ou numérique] / B. R. H. VAN DEN BERGH, Auteur ; R. DAHNKE, Auteur ; M. MENNES, Auteur . - p.743-762. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.743-762 Index. décimale : PER Périodiques Résumé : The prenatal period is increasingly considered as a crucial target for the primary prevention of neurodevelopmental and psychiatric disorders. Understanding their pathophysiological mechanisms remains a great challenge. Our review reveals new insights from prenatal brain development research, involving (epi)genetic research, neuroscience, recent imaging techniques, physical modeling, and computational simulation studies. Studies examining the effect of prenatal exposure to maternal distress on offspring brain development, using brain imaging techniques, reveal effects at birth and up into adulthood. Structural and functional changes are observed in several brain regions including the prefrontal, parietal, and temporal lobes, as well as the cerebellum, hippocampus, and amygdala. Furthermore, alterations are seen in functional connectivity of amygdalar-thalamus networks and in intrinsic brain networks, including default mode and attentional networks. The observed changes underlie offspring behavioral, cognitive, emotional development, and susceptibility to neurodevelopmental and psychiatric disorders. It is concluded that used brain measures have not yet been validated with regard to sensitivity, specificity, accuracy, or robustness in predicting neurodevelopmental and psychiatric disorders. Therefore, more prospective long-term longitudinal follow-up studies starting early in pregnancy should be carried out, in order to examine brain developmental measures as mediators in mediating the link between prenatal stress and offspring behavioral, cognitive, and emotional problems and susceptibility for disorders. En ligne : http://dx.doi.org/10.1017/s0954579418000342 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Prenatal neural origins of infant motor development: Associations between fetal brain and infant motor development / M. E. THOMASON in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.763-772 Titre : Prenatal neural origins of infant motor development: Associations between fetal brain and infant motor development Type de document : Texte imprimé et/ou numérique Auteurs : M. E. THOMASON, Auteur ; J. HECT, Auteur ; R. WALLER, Auteur ; J. H. MANNING, Auteur ; A. M. STACKS, Auteur ; Marjorie BEEGHLY, Auteur ; J. L. BOEVE, Auteur ; K. WONG, Auteur ; M. I. VAN DEN HEUVEL, Auteur ; E. HERNANDEZ-ANDRADE, Auteur ; S. S. HASSAN, Auteur ; R. ROMERO, Auteur Article en page(s) : p.763-772 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Functional circuits of the human brain emerge and change dramatically over the second half of gestation. It is possible that variation in neural functional system connectivity in utero predicts individual differences in infant behavioral development, but this possibility has yet to be examined. The current study examines the association between fetal sensorimotor brain system functional connectivity and infant postnatal motor ability. Resting-state functional connectivity data was obtained in 96 healthy human fetuses during the second and third trimesters of pregnancy. Infant motor ability was measured 7 months after birth using the Bayley Scales of Infant Development. Increased connectivity between the emerging motor network and regions of the prefrontal cortex, temporal lobes, posterior cingulate, and supplementary motor regions was observed in infants that showed more mature motor functions. In addition, females demonstrated stronger fetal-brain to infant-behavior associations. These observations extend prior longitudinal research back into prenatal brain development and raise exciting new ideas about the advent of risk and the ontogeny of early sex differences. En ligne : http://dx.doi.org/10.1017/s095457941800072x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Prenatal neural origins of infant motor development: Associations between fetal brain and infant motor development [Texte imprimé et/ou numérique] / M. E. THOMASON, Auteur ; J. HECT, Auteur ; R. WALLER, Auteur ; J. H. MANNING, Auteur ; A. M. STACKS, Auteur ; Marjorie BEEGHLY, Auteur ; J. L. BOEVE, Auteur ; K. WONG, Auteur ; M. I. VAN DEN HEUVEL, Auteur ; E. HERNANDEZ-ANDRADE, Auteur ; S. S. HASSAN, Auteur ; R. ROMERO, Auteur . - p.763-772. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.763-772 Index. décimale : PER Périodiques Résumé : Functional circuits of the human brain emerge and change dramatically over the second half of gestation. It is possible that variation in neural functional system connectivity in utero predicts individual differences in infant behavioral development, but this possibility has yet to be examined. The current study examines the association between fetal sensorimotor brain system functional connectivity and infant postnatal motor ability. Resting-state functional connectivity data was obtained in 96 healthy human fetuses during the second and third trimesters of pregnancy. Infant motor ability was measured 7 months after birth using the Bayley Scales of Infant Development. Increased connectivity between the emerging motor network and regions of the prefrontal cortex, temporal lobes, posterior cingulate, and supplementary motor regions was observed in infants that showed more mature motor functions. In addition, females demonstrated stronger fetal-brain to infant-behavior associations. These observations extend prior longitudinal research back into prenatal brain development and raise exciting new ideas about the advent of risk and the ontogeny of early sex differences. En ligne : http://dx.doi.org/10.1017/s095457941800072x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Major depressive disorder during pregnancy: Psychiatric medications have minimal effects on the fetus and infant yet development is compromised / H. C. GUSTAFSSON in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.773-785 Titre : Major depressive disorder during pregnancy: Psychiatric medications have minimal effects on the fetus and infant yet development is compromised Type de document : Texte imprimé et/ou numérique Auteurs : H. C. GUSTAFSSON, Auteur ; S. H. GOODMAN, Auteur ; T. FENG, Auteur ; J. CHOI, Auteur ; S. LEE, Auteur ; D. J. NEWPORT, Auteur ; B. KNIGHT, Auteur ; B. PINGETON, Auteur ; Z. N. STOWE, Auteur ; C. MONK, Auteur Article en page(s) : p.773-785 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Psychotropic medication use and psychiatric symptoms during pregnancy each are associated with adverse neurodevelopmental outcomes in offspring. Commonly, studies considering medication effects do not adequately assess symptoms, nor evaluate children when the effects are believed to occur, the fetal period. This study examined maternal serotonin reuptake inhibitor and polypharmacy use in relation to serial assessments of five indices of fetal neurobehavior and Bayley Scales of Infant Development at 12 months in N = 161 socioeconomically advantaged, non-Hispanic White women with a shared risk phenotype, diagnosed major depressive disorder. On average fetuses showed the expected development over gestation. In contrast, infant average Bayley psychomotor and mental development scores were low (M = 84.10 and M = 89.92, range of normal limits 85-114) with rates of delay more than 2-3 times what would be expected based on this measure's normative data. Controlling for prenatal and postnatal depressive symptoms, prenatal medication effects on neurobehavioral development were largely undetected in the fetus and infant. Mental health care directed primarily at symptoms may not address the additional psychosocial needs of women parenting infants. Speculatively, prenatal serotonin reuptake inhibitor exposure may act as a plasticity rather than risk factor, potentially enhancing receptivity to a nonoptimal postnatal environment in some mother-infant dyads. En ligne : http://dx.doi.org/10.1017/s0954579418000639 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Major depressive disorder during pregnancy: Psychiatric medications have minimal effects on the fetus and infant yet development is compromised [Texte imprimé et/ou numérique] / H. C. GUSTAFSSON, Auteur ; S. H. GOODMAN, Auteur ; T. FENG, Auteur ; J. CHOI, Auteur ; S. LEE, Auteur ; D. J. NEWPORT, Auteur ; B. KNIGHT, Auteur ; B. PINGETON, Auteur ; Z. N. STOWE, Auteur ; C. MONK, Auteur . - p.773-785. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.773-785 Index. décimale : PER Périodiques Résumé : Psychotropic medication use and psychiatric symptoms during pregnancy each are associated with adverse neurodevelopmental outcomes in offspring. Commonly, studies considering medication effects do not adequately assess symptoms, nor evaluate children when the effects are believed to occur, the fetal period. This study examined maternal serotonin reuptake inhibitor and polypharmacy use in relation to serial assessments of five indices of fetal neurobehavior and Bayley Scales of Infant Development at 12 months in N = 161 socioeconomically advantaged, non-Hispanic White women with a shared risk phenotype, diagnosed major depressive disorder. On average fetuses showed the expected development over gestation. In contrast, infant average Bayley psychomotor and mental development scores were low (M = 84.10 and M = 89.92, range of normal limits 85-114) with rates of delay more than 2-3 times what would be expected based on this measure's normative data. Controlling for prenatal and postnatal depressive symptoms, prenatal medication effects on neurobehavioral development were largely undetected in the fetus and infant. Mental health care directed primarily at symptoms may not address the additional psychosocial needs of women parenting infants. Speculatively, prenatal serotonin reuptake inhibitor exposure may act as a plasticity rather than risk factor, potentially enhancing receptivity to a nonoptimal postnatal environment in some mother-infant dyads. En ligne : http://dx.doi.org/10.1017/s0954579418000639 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression? / E. P. 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 et/ou numérique Auteurs : E. P. DAVIS, Auteur ; B. L. HANKIN, Auteur ; D. A. SWALES, Auteur ; M. C. 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 et/ou numérique] / E. P. DAVIS, Auteur ; B. L. HANKIN, Auteur ; D. A. SWALES, Auteur ; M. C. 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

Incorporating epigenetic mechanisms to advance fetal programming theories / E. CONRADT in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.807-824 Titre : Incorporating epigenetic mechanisms to advance fetal programming theories Type de document : Texte imprimé et/ou numérique Auteurs : E. CONRADT, Auteur ; Daniel E. ADKINS, Auteur ; S. E. CROWELL, Auteur ; K. L. RABY, Auteur ; L. M. DIAMOND, Auteur ; B. ELLIS, Auteur Article en page(s) : p.807-824 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match-mismatch model (an evolutionary-developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field. En ligne : http://dx.doi.org/10.1017/s0954579418000469 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Incorporating epigenetic mechanisms to advance fetal programming theories [Texte imprimé et/ou numérique] / E. CONRADT, Auteur ; Daniel E. ADKINS, Auteur ; S. E. CROWELL, Auteur ; K. L. RABY, Auteur ; L. M. DIAMOND, Auteur ; B. ELLIS, Auteur . - p.807-824. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.807-824 Index. décimale : PER Périodiques Résumé : Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match-mismatch model (an evolutionary-developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field. En ligne : http://dx.doi.org/10.1017/s0954579418000469 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Prenatal programming of postnatal plasticity revisited-And extended / S. HARTMAN in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.825-842 Titre : Prenatal programming of postnatal plasticity revisited-And extended Type de document : Texte imprimé et/ou numérique Auteurs : S. HARTMAN, Auteur ; J. BELSKY, Auteur Article en page(s) : p.825-842 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Two sets of evidence reviewed herein, one indicating that prenatal stress is associated with elevated behavioral and physiological dysregulation and the other that such phenotypic functioning is itself associated with heightened susceptibility to positive and negative environmental influences postnatally, raises the intriguing hypothesis first advanced by Pluess and Belsky (2011) that prenatal stress fosters, promotes, or "programs" postnatal developmental plasticity. Here we review further evidence consistent with this proposition, including new experimental research systematically manipulating both prenatal stress and postnatal rearing. Collectively this work would seem to explain why prenatal stress has so consistently been linked to problematic development: stresses encountered prenatally are likely to continue postnatally, thereby adversely affecting the development of children programmed (by prenatal stress) to be especially susceptible to environmental effects. Less investigated are the potential benefits prenatal stress may promote, due to increased plasticity, when the postnatal environment proves to be favorable. Future directions of research pertaining to potential mechanisms instantiating postnatal plasticity and moderators of such prenatal-programming effects are outlined. En ligne : http://dx.doi.org/10.1017/s0954579418000548 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Prenatal programming of postnatal plasticity revisited-And extended [Texte imprimé et/ou numérique] / S. HARTMAN, Auteur ; J. BELSKY, Auteur . - p.825-842. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.825-842 Index. décimale : PER Périodiques Résumé : Two sets of evidence reviewed herein, one indicating that prenatal stress is associated with elevated behavioral and physiological dysregulation and the other that such phenotypic functioning is itself associated with heightened susceptibility to positive and negative environmental influences postnatally, raises the intriguing hypothesis first advanced by Pluess and Belsky (2011) that prenatal stress fosters, promotes, or "programs" postnatal developmental plasticity. Here we review further evidence consistent with this proposition, including new experimental research systematically manipulating both prenatal stress and postnatal rearing. Collectively this work would seem to explain why prenatal stress has so consistently been linked to problematic development: stresses encountered prenatally are likely to continue postnatally, thereby adversely affecting the development of children programmed (by prenatal stress) to be especially susceptible to environmental effects. Less investigated are the potential benefits prenatal stress may promote, due to increased plasticity, when the postnatal environment proves to be favorable. Future directions of research pertaining to potential mechanisms instantiating postnatal plasticity and moderators of such prenatal-programming effects are outlined. En ligne : http://dx.doi.org/10.1017/s0954579418000548 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Prenatal maternal stress, fetal programming, and mechanisms underlying later psychopathology-A global perspective / V. GLOVER in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.843-854 Titre : Prenatal maternal stress, fetal programming, and mechanisms underlying later psychopathology-A global perspective Type de document : Texte imprimé et/ou numérique Auteurs : V. GLOVER, Auteur ; Kieran J. O'DONNELL, Auteur ; T. G. O'CONNOR, Auteur ; J. FISHER, Auteur Article en page(s) : p.843-854 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : There is clear evidence that the mother's stress, anxiety, or depression during pregnancy can alter the development of her fetus and her child, with an increased risk for later psychopathology. We are starting to understand some of the underlying mechanisms including the role of the placenta, gene-environment interactions, epigenetics, and specific systems including the hypothalamic-pituitary-adrenal axis and cytokines. In this review we also consider how these effects may be different, and potentially exacerbated, in different parts of the world. There can be many reasons for elevated prenatal stress, as in communities at war. There may be raised pregnancy-specific anxiety with high levels of maternal and infant death. There can be raised interpersonal violence (in Afghanistan 90.2% of women thought that "wife beating" was justified compared with 2.0% in Argentina). There may be interactions with nutritional deficiencies or with extremes of temperature. Prenatal stress alters the microbiome, and this can differ in different countries. Genetic differences in different ethnic groups may make some more vulnerable or more resilient to the effects of prenatal stress on child neurodevelopment. Most research on these questions has been in predominantly Caucasian samples from high-income countries. It is now time to understand more about prenatal stress and psychopathology, and the role of both social and biological differences, in the rest of the world. En ligne : http://dx.doi.org/10.1017/s095457941800038x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Prenatal maternal stress, fetal programming, and mechanisms underlying later psychopathology-A global perspective [Texte imprimé et/ou numérique] / V. GLOVER, Auteur ; Kieran J. O'DONNELL, Auteur ; T. G. O'CONNOR, Auteur ; J. FISHER, Auteur . - p.843-854. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.843-854 Index. décimale : PER Périodiques Résumé : There is clear evidence that the mother's stress, anxiety, or depression during pregnancy can alter the development of her fetus and her child, with an increased risk for later psychopathology. We are starting to understand some of the underlying mechanisms including the role of the placenta, gene-environment interactions, epigenetics, and specific systems including the hypothalamic-pituitary-adrenal axis and cytokines. In this review we also consider how these effects may be different, and potentially exacerbated, in different parts of the world. There can be many reasons for elevated prenatal stress, as in communities at war. There may be raised pregnancy-specific anxiety with high levels of maternal and infant death. There can be raised interpersonal violence (in Afghanistan 90.2% of women thought that "wife beating" was justified compared with 2.0% in Argentina). There may be interactions with nutritional deficiencies or with extremes of temperature. Prenatal stress alters the microbiome, and this can differ in different countries. Genetic differences in different ethnic groups may make some more vulnerable or more resilient to the effects of prenatal stress on child neurodevelopment. Most research on these questions has been in predominantly Caucasian samples from high-income countries. It is now time to understand more about prenatal stress and psychopathology, and the role of both social and biological differences, in the rest of the world. En ligne : http://dx.doi.org/10.1017/s095457941800038x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Predicting child temperament and behavior from the fetus / Janet A. DIPIETRO in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.855-870 Titre : Predicting child temperament and behavior from the fetus Type de document : Texte imprimé et/ou numérique Auteurs : Janet A. DIPIETRO, Auteur ; K. M. VOEGTLINE, Auteur ; H. A. PATER, Auteur ; K. A. COSTIGAN, Auteur Article en page(s) : p.855-870 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : There remains little debate that the period before birth sets the stage for subsequent development, yet scant evidence exists showing continuity from characteristics of the individual fetus to characteristics of the child. This report examines, in two studies, whether baseline and evoked fetal neurobehavioral functioning are predictive of features of child temperament and behavior as reported by mothers when offspring were between 7 and 14 years old (M = 10.1 years). Study 1 utilizes data generated from 333 maternal-fetal pairs collected during an undisturbed condition during the second half of gestation in relation to the child temperament dimensions of behavioral inhibition and exuberance. Associations at 32 weeks gestation were detected between all features of fetal neurobehavior and behavioral inhibition. In adjusted models, slower fetal heart rate and less fetal movement were associated with significant unique variance in predicting higher levels of childhood behavioral inhibition. No associations were detected for exuberance. Study 2 focuses on the association of evoked fetal reactivity and recovery to induced maternal arousal with subsequent child behavioral difficulties in a subset of the full sample (n = 130). Greater recovery in fetal heart rate following maternal stimulation was predictive of fewer behavioral difficulties and more prosocial behavior in childhood. Results from both studies provide support for gestational origins of core individual differences that portend childhood outcomes with foundational reactivity and regulatory components. En ligne : http://dx.doi.org/10.1017/s0954579418000482 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Predicting child temperament and behavior from the fetus [Texte imprimé et/ou numérique] / Janet A. DIPIETRO, Auteur ; K. M. VOEGTLINE, Auteur ; H. A. PATER, Auteur ; K. A. COSTIGAN, Auteur . - p.855-870. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.855-870 Index. décimale : PER Périodiques Résumé : There remains little debate that the period before birth sets the stage for subsequent development, yet scant evidence exists showing continuity from characteristics of the individual fetus to characteristics of the child. This report examines, in two studies, whether baseline and evoked fetal neurobehavioral functioning are predictive of features of child temperament and behavior as reported by mothers when offspring were between 7 and 14 years old (M = 10.1 years). Study 1 utilizes data generated from 333 maternal-fetal pairs collected during an undisturbed condition during the second half of gestation in relation to the child temperament dimensions of behavioral inhibition and exuberance. Associations at 32 weeks gestation were detected between all features of fetal neurobehavior and behavioral inhibition. In adjusted models, slower fetal heart rate and less fetal movement were associated with significant unique variance in predicting higher levels of childhood behavioral inhibition. No associations were detected for exuberance. Study 2 focuses on the association of evoked fetal reactivity and recovery to induced maternal arousal with subsequent child behavioral difficulties in a subset of the full sample (n = 130). Greater recovery in fetal heart rate following maternal stimulation was predictive of fewer behavioral difficulties and more prosocial behavior in childhood. Results from both studies provide support for gestational origins of core individual differences that portend childhood outcomes with foundational reactivity and regulatory components. En ligne : http://dx.doi.org/10.1017/s0954579418000482 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

The influence of prenatal experience on behavioral and social development: The benefits and limitations of an animal model / R. LICKLITER in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.871-880 Titre : The influence of prenatal experience on behavioral and social development: The benefits and limitations of an animal model Type de document : Texte imprimé et/ou numérique Auteurs : R. LICKLITER, Auteur Article en page(s) : p.871-880 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prenatal experience is both a formative and a regulatory force in the process of development. As a result, birth is not an adequate starting point for explanations of behavioral development. However, surprisingly little is currently known regarding the role of prenatal experience in the emergence and facilitation of perceptual, cognitive, or social development. Our lack of knowledge in this area is due in part to the very restricted experimental manipulations possible with human fetuses. A comparative approach utilizing animal models provides an essential step in addressing this gap in our knowledge and providing testable predictions for studies with human fetuses, infants, and children. Further, animal-based comparative research serves to minimize the amount of exploratory research undertaken with human subjects and hone in on issues and research directions worthy of further research investment. In this article, I review selected animal-based research exploring how developmental influences during the prenatal period can guide and constrain subsequent behavioral and social development. I then discuss the importance of linking the prenatal environment to postnatal outcomes in terms of how psychologists conceptualize "innate" biases, preferences, and skills in the study of human development. En ligne : http://dx.doi.org/10.1017/s0954579418000640 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] The influence of prenatal experience on behavioral and social development: The benefits and limitations of an animal model [Texte imprimé et/ou numérique] / R. LICKLITER, Auteur . - p.871-880. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.871-880 Index. décimale : PER Périodiques Résumé : Prenatal experience is both a formative and a regulatory force in the process of development. As a result, birth is not an adequate starting point for explanations of behavioral development. However, surprisingly little is currently known regarding the role of prenatal experience in the emergence and facilitation of perceptual, cognitive, or social development. Our lack of knowledge in this area is due in part to the very restricted experimental manipulations possible with human fetuses. A comparative approach utilizing animal models provides an essential step in addressing this gap in our knowledge and providing testable predictions for studies with human fetuses, infants, and children. Further, animal-based comparative research serves to minimize the amount of exploratory research undertaken with human subjects and hone in on issues and research directions worthy of further research investment. In this article, I review selected animal-based research exploring how developmental influences during the prenatal period can guide and constrain subsequent behavioral and social development. I then discuss the importance of linking the prenatal environment to postnatal outcomes in terms of how psychologists conceptualize "innate" biases, preferences, and skills in the study of human development. En ligne : http://dx.doi.org/10.1017/s0954579418000640 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

An epigenetic pathway approach to investigating associations between prenatal exposure to maternal mood disorder and newborn neurobehavior / E. CONRADT in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.881-890 Titre : An epigenetic pathway approach to investigating associations between prenatal exposure to maternal mood disorder and newborn neurobehavior Type de document : Texte imprimé et/ou numérique Auteurs : E. CONRADT, Auteur ; Daniel E. ADKINS, Auteur ; S. E. CROWELL, Auteur ; C. MONK, Auteur ; M. S. KOBOR, Auteur Article en page(s) : p.881-890 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Following recent advances in behavioral and psychiatric epigenetics, researchers are increasingly using epigenetic methods to study prenatal exposure to maternal mood disorder and its effects on fetal and newborn neurobehavior. Despite notable progress, various methodological limitations continue to obscure our understanding of the epigenetic mechanisms underpinning prenatal exposure to maternal mood disorder on newborn neurobehavioral development. Here we detail this problem, discussing limitations of the currently dominant analytical approaches (i.e., candidate epigenetic and epigenome-wide association studies), then present a solution that retains many benefits of existing methods while minimizing their shortcomings: epigenetic pathway analysis. We argue that the application of pathway-based epigenetic approaches that target DNA methylation at transcription factor binding sites could substantially deepen our mechanistic understanding of how prenatal exposures influence newborn neurobehavior. En ligne : http://dx.doi.org/10.1017/s0954579418000688 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] An epigenetic pathway approach to investigating associations between prenatal exposure to maternal mood disorder and newborn neurobehavior [Texte imprimé et/ou numérique] / E. CONRADT, Auteur ; Daniel E. ADKINS, Auteur ; S. E. CROWELL, Auteur ; C. MONK, Auteur ; M. S. KOBOR, Auteur . - p.881-890. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.881-890 Index. décimale : PER Périodiques Résumé : Following recent advances in behavioral and psychiatric epigenetics, researchers are increasingly using epigenetic methods to study prenatal exposure to maternal mood disorder and its effects on fetal and newborn neurobehavior. Despite notable progress, various methodological limitations continue to obscure our understanding of the epigenetic mechanisms underpinning prenatal exposure to maternal mood disorder on newborn neurobehavioral development. Here we detail this problem, discussing limitations of the currently dominant analytical approaches (i.e., candidate epigenetic and epigenome-wide association studies), then present a solution that retains many benefits of existing methods while minimizing their shortcomings: epigenetic pathway analysis. We argue that the application of pathway-based epigenetic approaches that target DNA methylation at transcription factor binding sites could substantially deepen our mechanistic understanding of how prenatal exposures influence newborn neurobehavior. En ligne : http://dx.doi.org/10.1017/s0954579418000688 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

The early care environment and DNA methylome variation in childhood / E. GARG in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.891-903 Titre : The early care environment and DNA methylome variation in childhood Type de document : Texte imprimé et/ou numérique Auteurs : E. GARG, Auteur ; L. CHEN, Auteur ; T. T. T. NGUYEN, Auteur ; I. POKHVISNEVA, Auteur ; L. M. CHEN, Auteur ; E. UNTERNAEHRER, Auteur ; J. L. MACISAAC, Auteur ; L. M. MCEWEN, Auteur ; S. M. MAH, Auteur ; H. GAUDREAU, Auteur ; R. LEVITAN, Auteur ; E. MOSS, Auteur ; M. B. SOKOLOWSKI, Auteur ; J. L. KENNEDY, Auteur ; M. S. STEINER, Auteur ; M. J. MEANEY, Auteur ; J. D. HOLBROOK, Auteur ; P. P. SILVEIRA, Auteur ; N. KARNANI, Auteur ; M. S. KOBOR, Auteur ; Kieran J. O'DONNELL, Auteur Article en page(s) : p.891-903 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prenatal adversity shapes child neurodevelopment and risk for later mental health problems. The quality of the early care environment can buffer some of the negative effects of prenatal adversity on child development. Retrospective studies, in adult samples, highlight epigenetic modifications as sentinel markers of the quality of the early care environment; however, comparable data from pediatric cohorts are lacking. Participants were drawn from the Maternal Adversity Vulnerability and Neurodevelopment (MAVAN) study, a longitudinal cohort with measures of infant attachment, infant development, and child mental health. Children provided buccal epithelial samples (mean age = 6.99, SD = 1.33 years, n = 226), which were used for analyses of genome-wide DNA methylation and genetic variation. We used a series of linear models to describe the association between infant attachment and (a) measures of child outcome and (b) DNA methylation across the genome. Paired genetic data was used to determine the genetic contribution to DNA methylation at attachment-associated sites. Infant attachment style was associated with infant cognitive development (Mental Development Index) and behavior (Behavior Rating Scale) assessed with the Bayley Scales of Infant Development at 36 months. Infant attachment style moderated the effects of prenatal adversity on Behavior Rating Scale scores at 36 months. Infant attachment was also significantly associated with a principal component that accounted for 11.9% of the variation in genome-wide DNA methylation. These effects were most apparent when comparing children with a secure versus a disorganized attachment style and most pronounced in females. The availability of paired genetic data revealed that DNA methylation at approximately half of all infant attachment-associated sites was best explained by considering both infant attachment and child genetic variation. This study provides further evidence that infant attachment can buffer some of the negative effects of early adversity on measures of infant behavior. We also highlight the interplay between infant attachment and child genotype in shaping variation in DNA methylation. Such findings provide preliminary evidence for a molecular signature of infant attachment and may help inform attachment-focused early intervention programs. En ligne : http://dx.doi.org/10.1017/s0954579418000627 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] The early care environment and DNA methylome variation in childhood [Texte imprimé et/ou numérique] / E. GARG, Auteur ; L. CHEN, Auteur ; T. T. T. NGUYEN, Auteur ; I. POKHVISNEVA, Auteur ; L. M. CHEN, Auteur ; E. UNTERNAEHRER, Auteur ; J. L. MACISAAC, Auteur ; L. M. MCEWEN, Auteur ; S. M. MAH, Auteur ; H. GAUDREAU, Auteur ; R. LEVITAN, Auteur ; E. MOSS, Auteur ; M. B. SOKOLOWSKI, Auteur ; J. L. KENNEDY, Auteur ; M. S. STEINER, Auteur ; M. J. MEANEY, Auteur ; J. D. HOLBROOK, Auteur ; P. P. SILVEIRA, Auteur ; N. KARNANI, Auteur ; M. S. KOBOR, Auteur ; Kieran J. O'DONNELL, Auteur . - p.891-903. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.891-903 Index. décimale : PER Périodiques Résumé : Prenatal adversity shapes child neurodevelopment and risk for later mental health problems. The quality of the early care environment can buffer some of the negative effects of prenatal adversity on child development. Retrospective studies, in adult samples, highlight epigenetic modifications as sentinel markers of the quality of the early care environment; however, comparable data from pediatric cohorts are lacking. Participants were drawn from the Maternal Adversity Vulnerability and Neurodevelopment (MAVAN) study, a longitudinal cohort with measures of infant attachment, infant development, and child mental health. Children provided buccal epithelial samples (mean age = 6.99, SD = 1.33 years, n = 226), which were used for analyses of genome-wide DNA methylation and genetic variation. We used a series of linear models to describe the association between infant attachment and (a) measures of child outcome and (b) DNA methylation across the genome. Paired genetic data was used to determine the genetic contribution to DNA methylation at attachment-associated sites. Infant attachment style was associated with infant cognitive development (Mental Development Index) and behavior (Behavior Rating Scale) assessed with the Bayley Scales of Infant Development at 36 months. Infant attachment style moderated the effects of prenatal adversity on Behavior Rating Scale scores at 36 months. Infant attachment was also significantly associated with a principal component that accounted for 11.9% of the variation in genome-wide DNA methylation. These effects were most apparent when comparing children with a secure versus a disorganized attachment style and most pronounced in females. The availability of paired genetic data revealed that DNA methylation at approximately half of all infant attachment-associated sites was best explained by considering both infant attachment and child genetic variation. This study provides further evidence that infant attachment can buffer some of the negative effects of early adversity on measures of infant behavior. We also highlight the interplay between infant attachment and child genotype in shaping variation in DNA methylation. Such findings provide preliminary evidence for a molecular signature of infant attachment and may help inform attachment-focused early intervention programs. En ligne : http://dx.doi.org/10.1017/s0954579418000627 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Maternal programming: Application of a developmental psychopathology perspective / L. M. GLYNN in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.905-919 Titre : Maternal programming: Application of a developmental psychopathology perspective Type de document : Texte imprimé et/ou numérique Auteurs : L. M. GLYNN, Auteur ; M. A. HOWLAND, Auteur ; M. FOX, Auteur Article en page(s) : p.905-919 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The fetal phase of life has long been recognized as a sensitive period of development. Here we posit that pregnancy represents a simultaneous sensitive period for the adult female with broad and persisting consequences for her health and development, including risk for psychopathology. In this review, we examine the transition to motherhood through the lens of developmental psychopathology. Specifically, we summarize the typical and atypical changes in brain and behavior that characterize the perinatal period. We highlight how the exceptional neuroplasticity exhibited by women during this life phase may account for increased vulnerability for psychopathology. Further, we discuss several modes of signaling that are available to the fetus to affect maternal phenotypes (hormones, motor activity, and gene transfer) and also illustrate how evolutionary perspectives can help explain how and why fetal functions may contribute to maternal psychopathology. The developmental psychopathology perspective has spurred advances in understanding risk and resilience for mental health in many domains. As such, it is surprising that this major epoch in the female life span has yet to benefit fully from similar applications. En ligne : http://dx.doi.org/10.1017/s0954579418000524 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Maternal programming: Application of a developmental psychopathology perspective [Texte imprimé et/ou numérique] / L. M. GLYNN, Auteur ; M. A. HOWLAND, Auteur ; M. FOX, Auteur . - p.905-919. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.905-919 Index. décimale : PER Périodiques Résumé : The fetal phase of life has long been recognized as a sensitive period of development. Here we posit that pregnancy represents a simultaneous sensitive period for the adult female with broad and persisting consequences for her health and development, including risk for psychopathology. In this review, we examine the transition to motherhood through the lens of developmental psychopathology. Specifically, we summarize the typical and atypical changes in brain and behavior that characterize the perinatal period. We highlight how the exceptional neuroplasticity exhibited by women during this life phase may account for increased vulnerability for psychopathology. Further, we discuss several modes of signaling that are available to the fetus to affect maternal phenotypes (hormones, motor activity, and gene transfer) and also illustrate how evolutionary perspectives can help explain how and why fetal functions may contribute to maternal psychopathology. The developmental psychopathology perspective has spurred advances in understanding risk and resilience for mental health in many domains. As such, it is surprising that this major epoch in the female life span has yet to benefit fully from similar applications. En ligne : http://dx.doi.org/10.1017/s0954579418000524 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Social buffering of the maternal and infant HPA axes: Mediation and moderation in the intergenerational transmission of adverse childhood experiences / J. C. THOMAS in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.921-939 Titre : Social buffering of the maternal and infant HPA axes: Mediation and moderation in the intergenerational transmission of adverse childhood experiences Type de document : Texte imprimé et/ou numérique Auteurs : J. C. THOMAS, Auteur ; N. LETOURNEAU, Auteur ; Tavis S. CAMPBELL, Auteur ; G. F. GIESBRECHT, Auteur Article en page(s) : p.921-939 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Supportive social relationships can reduce both psychological and physiological responses to stressful experiences. Recently, studies have also assessed the potential for social relationships to buffer the intergenerational transmission of stress. The majority of these studies, however, have focussed on social learning as a mechanism responsible for the intergenerational transmission of stress. Evidence of biological mechanisms is lacking. The objective of the current study was, therefore, to determine whether the association between maternal adverse childhood experiences (ACEs) and infant hypothalamic-pituitary-adrenal (HPA) axis function is mediated by maternal HPA axis function during pregnancy and moderated by social support. Data were from 243 mother-infant dyads enrolled in a prospective longitudinal cohort (the Alberta Pregnancy Outcomes and Nutrition Study). Maternal history of ACEs was retrospectively assessed while maternal perceived social support and salivary cortisol were assessed prospectively at 6-22 weeks gestation (Time 1) and 27-37 weeks gestation (Time 2), and infant cortisol reactivity to a laboratory stressor and maternal perceived social support were assessed at 5-10 months postnatal (Time 3). Results revealed that maternal HPA axis function during pregnancy mediated the effects of maternal ACEs on infant HPA axis reactivity, suggesting that the maternal HPA axis is a mechanism by which maternal early life stress is transmitted to offspring. Furthermore, social support in the prenatal and postnatal periods moderated the cascade from maternal ACEs to infant HPA axis reactivity. Specifically, prenatal social support moderated the association between ACEs and maternal HPA axis function during pregnancy, and postnatal social support moderated the association between maternal HPA axis function and infant cortisol reactivity. These findings highlight the social sensitivity of the HPA axis and suggest the utility of social relationships as an intervention target to reduce the effects of maternal early life stress on infant outcomes. En ligne : http://dx.doi.org/10.1017/s0954579418000512 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Social buffering of the maternal and infant HPA axes: Mediation and moderation in the intergenerational transmission of adverse childhood experiences [Texte imprimé et/ou numérique] / J. C. THOMAS, Auteur ; N. LETOURNEAU, Auteur ; Tavis S. CAMPBELL, Auteur ; G. F. GIESBRECHT, Auteur . - p.921-939. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.921-939 Index. décimale : PER Périodiques Résumé : Supportive social relationships can reduce both psychological and physiological responses to stressful experiences. Recently, studies have also assessed the potential for social relationships to buffer the intergenerational transmission of stress. The majority of these studies, however, have focussed on social learning as a mechanism responsible for the intergenerational transmission of stress. Evidence of biological mechanisms is lacking. The objective of the current study was, therefore, to determine whether the association between maternal adverse childhood experiences (ACEs) and infant hypothalamic-pituitary-adrenal (HPA) axis function is mediated by maternal HPA axis function during pregnancy and moderated by social support. Data were from 243 mother-infant dyads enrolled in a prospective longitudinal cohort (the Alberta Pregnancy Outcomes and Nutrition Study). Maternal history of ACEs was retrospectively assessed while maternal perceived social support and salivary cortisol were assessed prospectively at 6-22 weeks gestation (Time 1) and 27-37 weeks gestation (Time 2), and infant cortisol reactivity to a laboratory stressor and maternal perceived social support were assessed at 5-10 months postnatal (Time 3). Results revealed that maternal HPA axis function during pregnancy mediated the effects of maternal ACEs on infant HPA axis reactivity, suggesting that the maternal HPA axis is a mechanism by which maternal early life stress is transmitted to offspring. Furthermore, social support in the prenatal and postnatal periods moderated the cascade from maternal ACEs to infant HPA axis reactivity. Specifically, prenatal social support moderated the association between ACEs and maternal HPA axis function during pregnancy, and postnatal social support moderated the association between maternal HPA axis function and infant cortisol reactivity. These findings highlight the social sensitivity of the HPA axis and suggest the utility of social relationships as an intervention target to reduce the effects of maternal early life stress on infant outcomes. En ligne : http://dx.doi.org/10.1017/s0954579418000512 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Prenatal CRH: An integrating signal of fetal distress / Curt A. SANDMAN in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.941-952 Titre : Prenatal CRH: An integrating signal of fetal distress Type de document : Texte imprimé et/ou numérique Auteurs : Curt A. SANDMAN, Auteur Article en page(s) : p.941-952 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Corticotropin-releasing hormone (CRH) is distributed throughout the brain and in peripheral sites but primarily is localized in the paraventricular nucleus of the hypothalamus. It is a "master" stress hormone that is responsible for the synthesis of proopiomelanocortin (POMC) in the anterior pituitary gland. Behaviorally active peptide hormones, including adrenocorticotropin hormone (ACTH) and B-endorphin, are liberated from POMC by enzymes to activate critical processes during stress. CRH is not detectable in the circulation even during extreme stress. However, during human pregnancy, the human placenta expresses the gene for CRH (pCRH) resulting in detectable levels in maternal plasma that increases 20- to 40-fold over the course of gestation. Placental CRH is identical to CRH of hypothalamic origin in size, structure, immunoreactivity, and bioactivity. However, unlike the negative feedback between adrenal cortisol and hypothalamic CRH, cortisol stimulates the synthesis and release of pCRH. The bidirectional release of pCRH into maternal and fetal compartments is associated with regulating the timing of delivery, remodeling the fetal nervous system, and influencing developmental trajectories. Fetal exposure to pCRH during early and late gestation is associated with unique patterns of cortical thinning in school-age children. Placental CRH is elevated in response to physical and behavioral stress and may be an integrative marker of early adversity. En ligne : http://dx.doi.org/10.1017/s0954579418000664 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Prenatal CRH: An integrating signal of fetal distress [Texte imprimé et/ou numérique] / Curt A. SANDMAN, Auteur . - p.941-952. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.941-952 Index. décimale : PER Périodiques Résumé : Corticotropin-releasing hormone (CRH) is distributed throughout the brain and in peripheral sites but primarily is localized in the paraventricular nucleus of the hypothalamus. It is a "master" stress hormone that is responsible for the synthesis of proopiomelanocortin (POMC) in the anterior pituitary gland. Behaviorally active peptide hormones, including adrenocorticotropin hormone (ACTH) and B-endorphin, are liberated from POMC by enzymes to activate critical processes during stress. CRH is not detectable in the circulation even during extreme stress. However, during human pregnancy, the human placenta expresses the gene for CRH (pCRH) resulting in detectable levels in maternal plasma that increases 20- to 40-fold over the course of gestation. Placental CRH is identical to CRH of hypothalamic origin in size, structure, immunoreactivity, and bioactivity. However, unlike the negative feedback between adrenal cortisol and hypothalamic CRH, cortisol stimulates the synthesis and release of pCRH. The bidirectional release of pCRH into maternal and fetal compartments is associated with regulating the timing of delivery, remodeling the fetal nervous system, and influencing developmental trajectories. Fetal exposure to pCRH during early and late gestation is associated with unique patterns of cortical thinning in school-age children. Placental CRH is elevated in response to physical and behavioral stress and may be an integrative marker of early adversity. En ligne : http://dx.doi.org/10.1017/s0954579418000664 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Children's stress regulation mediates the association between prenatal maternal mood and child executive functions for boys, but not girls / R. NEUENSCHWANDER in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.953-969 Titre : Children's stress regulation mediates the association between prenatal maternal mood and child executive functions for boys, but not girls Type de document : Texte imprimé et/ou numérique Auteurs : R. NEUENSCHWANDER, Auteur ; K. HOOKENSON, Auteur ; U. BRAIN, Auteur ; R. E. GRUNAU, Auteur ; A. M. DEVLIN, Auteur ; J. WEINBERG, Auteur ; A. DIAMOND, Auteur ; T. F. OBERLANDER, Auteur Article en page(s) : p.953-969 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prenatal exposure to maternal mood disturbances shapes children's cognitive development reflected in the critical construct of executive functions (EFs). Little is known, however, about underlying mechanisms. By examining cortisol responses in both everyday and lab challenge settings, we tested whether the child/offspring hypothalamic-pituitary-adrenal axis mediates effects of prenatal maternal mood on child EFs at age 6. In 107 Canadian children born to women with a wide range of anxious and depressive symptoms during pregnancy, we found that in boys but not girls, depressed and/or anxious prenatal maternal mood is associated with heightened diurnal cortisol levels in everyday settings, as well as heightened cortisol reactivity to a lab challenge and that this heightened reactivity was associated with poorer EFs. Among boys we also observed that cortisol reactivity but not diurnal cortisol mediated the association between depressed and/or anxious prenatal maternal mood and EFs. Depressed and/or anxious prenatal maternal mood was related to child EFs for both girls and boys. To our knowledge, this is the first study to demonstrate a mediating role for child stress regulation in the association between prenatal maternal stress-related mood disturbances and child EFs, providing evidence of a mechanism contributing to fetal programming of cognition. En ligne : http://dx.doi.org/10.1017/s095457941800041x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Children's stress regulation mediates the association between prenatal maternal mood and child executive functions for boys, but not girls [Texte imprimé et/ou numérique] / R. NEUENSCHWANDER, Auteur ; K. HOOKENSON, Auteur ; U. BRAIN, Auteur ; R. E. GRUNAU, Auteur ; A. M. DEVLIN, Auteur ; J. WEINBERG, Auteur ; A. DIAMOND, Auteur ; T. F. OBERLANDER, Auteur . - p.953-969. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.953-969 Index. décimale : PER Périodiques Résumé : Prenatal exposure to maternal mood disturbances shapes children's cognitive development reflected in the critical construct of executive functions (EFs). Little is known, however, about underlying mechanisms. By examining cortisol responses in both everyday and lab challenge settings, we tested whether the child/offspring hypothalamic-pituitary-adrenal axis mediates effects of prenatal maternal mood on child EFs at age 6. In 107 Canadian children born to women with a wide range of anxious and depressive symptoms during pregnancy, we found that in boys but not girls, depressed and/or anxious prenatal maternal mood is associated with heightened diurnal cortisol levels in everyday settings, as well as heightened cortisol reactivity to a lab challenge and that this heightened reactivity was associated with poorer EFs. Among boys we also observed that cortisol reactivity but not diurnal cortisol mediated the association between depressed and/or anxious prenatal maternal mood and EFs. Depressed and/or anxious prenatal maternal mood was related to child EFs for both girls and boys. To our knowledge, this is the first study to demonstrate a mediating role for child stress regulation in the association between prenatal maternal stress-related mood disturbances and child EFs, providing evidence of a mechanism contributing to fetal programming of cognition. En ligne : http://dx.doi.org/10.1017/s095457941800041x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Cortisol, cortisone, and BDNF in amniotic fluid in the second trimester of pregnancy: Effect of early life and current maternal stress and socioeconomic status / M. DEUSCHLE in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.971-980 Titre : Cortisol, cortisone, and BDNF in amniotic fluid in the second trimester of pregnancy: Effect of early life and current maternal stress and socioeconomic status Type de document : Texte imprimé et/ou numérique Auteurs : M. DEUSCHLE, Auteur ; F. HENDLMEIER, Auteur ; S. WITT, Auteur ; M. RIETSCHEL, Auteur ; M. GILLES, Auteur ; A. SANCHEZ-GUIJO, Auteur ; L. FANANAS, Auteur ; S. HENTZE, Auteur ; S. A. WUDY, Auteur ; R. HELLWEG, Auteur Article en page(s) : p.971-980 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The prenatal environment shapes the offspring's phenotype; moreover, transgenerational stress and stress during pregnancy may play a role. Brain-derived neurotrophic factor (BDNF) and glucocorticoids influence neurodevelopment during pregnancy, and there is evidence that BDNF in amniotic fluid is mainly of fetal origin, while the source of glucocorticoids is maternal. We tested the hypothesis that maternal early life stress, psychiatric diagnoses, anxiety, perceived stress, and socioeconomic status influence BDNF and glucocorticoid concentrations in amniotic fluid in the second trimester. We studied 79 pregnant women who underwent amniocentesis in the early second trimester and analyzed BDNF, cortisol, and cortisone concentrations in amniotic fluid. The endocrine data were related to maternal early life adversities (Childhood Trauma Questionaire), perceived stress (Perceived Stress Scale), anxiety, socioeconomic status (family income), and the presence of psychiatric diseases. We found BDNF in amniotic fluid to be positively related to maternal early adversity (Childhood Trauma Questionaire). Low family income (socioeconomic status) was related to high amniotic fluid glucocorticoid concentrations. Neither glucocorticoid concentrations nor hydroxy steroid dehydrogenase (HSD2) activity could be related to BDNF concentrations in amniotic fluid. Early maternal adverse events may be reflected in the fetal BDNF regulation, and it should be tested whether this relates to differences in neurodevelopment. En ligne : http://dx.doi.org/10.1017/s0954579418000147 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Cortisol, cortisone, and BDNF in amniotic fluid in the second trimester of pregnancy: Effect of early life and current maternal stress and socioeconomic status [Texte imprimé et/ou numérique] / M. DEUSCHLE, Auteur ; F. HENDLMEIER, Auteur ; S. WITT, Auteur ; M. RIETSCHEL, Auteur ; M. GILLES, Auteur ; A. SANCHEZ-GUIJO, Auteur ; L. FANANAS, Auteur ; S. HENTZE, Auteur ; S. A. WUDY, Auteur ; R. HELLWEG, Auteur . - p.971-980. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.971-980 Index. décimale : PER Périodiques Résumé : The prenatal environment shapes the offspring's phenotype; moreover, transgenerational stress and stress during pregnancy may play a role. Brain-derived neurotrophic factor (BDNF) and glucocorticoids influence neurodevelopment during pregnancy, and there is evidence that BDNF in amniotic fluid is mainly of fetal origin, while the source of glucocorticoids is maternal. We tested the hypothesis that maternal early life stress, psychiatric diagnoses, anxiety, perceived stress, and socioeconomic status influence BDNF and glucocorticoid concentrations in amniotic fluid in the second trimester. We studied 79 pregnant women who underwent amniocentesis in the early second trimester and analyzed BDNF, cortisol, and cortisone concentrations in amniotic fluid. The endocrine data were related to maternal early life adversities (Childhood Trauma Questionaire), perceived stress (Perceived Stress Scale), anxiety, socioeconomic status (family income), and the presence of psychiatric diseases. We found BDNF in amniotic fluid to be positively related to maternal early adversity (Childhood Trauma Questionaire). Low family income (socioeconomic status) was related to high amniotic fluid glucocorticoid concentrations. Neither glucocorticoid concentrations nor hydroxy steroid dehydrogenase (HSD2) activity could be related to BDNF concentrations in amniotic fluid. Early maternal adverse events may be reflected in the fetal BDNF regulation, and it should be tested whether this relates to differences in neurodevelopment. En ligne : http://dx.doi.org/10.1017/s0954579418000147 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Testosterone-cortisol dissociation in children exposed to prenatal maternal stress, and relationship with aggression: Project Ice Storm / T. V. NGUYEN in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.981-994 Titre : Testosterone-cortisol dissociation in children exposed to prenatal maternal stress, and relationship with aggression: Project Ice Storm Type de document : Texte imprimé et/ou numérique Auteurs : T. V. NGUYEN, Auteur ; S. L. JONES, Auteur ; G. ELGBEILI, Auteur ; P. MONNIER, Auteur ; C. YU, Auteur ; D. P. LAPLANTE, Auteur ; S. KING, Auteur Article en page(s) : p.981-994 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prenatal maternal stress (PNMS) has been associated with postnatal behavioral alterations that may be partly explained by interactions between the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes. Yet it remains unclear whether PNMS leads to enduring HPA-HPG alterations in the offspring, and whether HPA-HPG interactions can impact behavior during development, in particular levels of aggression in childhood. Here we investigated the relationship between a marker for HPG axis function (baseline testosterone) and a marker for HPA axis response (cortisol area under the curve) in 11(1/2)-year-olds whose mothers were exposed to the 1998 Quebec ice storm during pregnancy (n = 59 children; 31 boys, 28 girls). We examined (a) whether the degree of objective or subjective PNMS regulates the testosterone-cortisol relationship at age 11(1/2), and (b) whether this testosterone-cortisol relationship is associated with differences in aggressive behavior. We found that, at lower levels of subjective PNMS, baseline testosterone and cortisol reactivity were positively correlated; in contrast, there was no relationship between these hormones at higher levels of subjective PNMS. Cortisol response moderated the relationship between testosterone and aggression. These results support the notion PNMS may explain variance in fetal HPA-HPG interactions, and that these interactions may be associated with aggressive behavior in late childhood. En ligne : http://dx.doi.org/10.1017/s0954579418000652 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Testosterone-cortisol dissociation in children exposed to prenatal maternal stress, and relationship with aggression: Project Ice Storm [Texte imprimé et/ou numérique] / T. V. NGUYEN, Auteur ; S. L. JONES, Auteur ; G. ELGBEILI, Auteur ; P. MONNIER, Auteur ; C. YU, Auteur ; D. P. LAPLANTE, Auteur ; S. KING, Auteur . - p.981-994. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.981-994 Index. décimale : PER Périodiques Résumé : Prenatal maternal stress (PNMS) has been associated with postnatal behavioral alterations that may be partly explained by interactions between the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-gonadal (HPG) axes. Yet it remains unclear whether PNMS leads to enduring HPA-HPG alterations in the offspring, and whether HPA-HPG interactions can impact behavior during development, in particular levels of aggression in childhood. Here we investigated the relationship between a marker for HPG axis function (baseline testosterone) and a marker for HPA axis response (cortisol area under the curve) in 11(1/2)-year-olds whose mothers were exposed to the 1998 Quebec ice storm during pregnancy (n = 59 children; 31 boys, 28 girls). We examined (a) whether the degree of objective or subjective PNMS regulates the testosterone-cortisol relationship at age 11(1/2), and (b) whether this testosterone-cortisol relationship is associated with differences in aggressive behavior. We found that, at lower levels of subjective PNMS, baseline testosterone and cortisol reactivity were positively correlated; in contrast, there was no relationship between these hormones at higher levels of subjective PNMS. Cortisol response moderated the relationship between testosterone and aggression. These results support the notion PNMS may explain variance in fetal HPA-HPG interactions, and that these interactions may be associated with aggressive behavior in late childhood. En ligne : http://dx.doi.org/10.1017/s0954579418000652 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

The role of prenatal maternal stress in the development of childhood anxiety symptomatology: The QF2011 Queensland Flood Study / M. A. MCLEAN in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.995-1007 Titre : The role of prenatal maternal stress in the development of childhood anxiety symptomatology: The QF2011 Queensland Flood Study Type de document : Texte imprimé et/ou numérique Auteurs : M. A. MCLEAN, Auteur ; Vanessa E. COBHAM, Auteur ; G. SIMCOCK, Auteur ; G. ELGBEILI, Auteur ; S. KILDEA, Auteur ; S. KING, Auteur Article en page(s) : p.995-1007 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : It is possible that findings suggesting a link between prenatal maternal stress (PNMS) and anxiety symptoms in offspring are confounded by postnatal and/or shared mother-child heritability effects. Following exposure to a natural disaster, the Queensland Flood Study investigated the unique and additive effects of various types of disaster-related PNMS (objective hardship, cognitive appraisal, and subjective distress) on childhood anxiety symptomatology (internalizing and/or anxiety symptom measures). Timing of flood exposure during pregnancy and child sex were examined as potential moderators. After controlling for maternal psychosocial factors, greater objective hardship as a result of the floods was significantly associated with greater anxiety symptoms (N = 114) and marginally associated with greater internalizing behaviors (N = 115). Earlier timing of the flood in pregnancy was associated with greater anxiety symptoms. No such associations were found between any PNMS measure and teacher-rated child internalizing behaviors (N = 90). Sex and timing did not moderate associations. Our findings suggest that, in isolation, increased maternal hardship due to exposure to an independent stressor, during pregnancy, may have a programming effect on childhood anxiety symptoms. En ligne : http://dx.doi.org/10.1017/s0954579418000408 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] The role of prenatal maternal stress in the development of childhood anxiety symptomatology: The QF2011 Queensland Flood Study [Texte imprimé et/ou numérique] / M. A. MCLEAN, Auteur ; Vanessa E. COBHAM, Auteur ; G. SIMCOCK, Auteur ; G. ELGBEILI, Auteur ; S. KILDEA, Auteur ; S. KING, Auteur . - p.995-1007. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.995-1007 Index. décimale : PER Périodiques Résumé : It is possible that findings suggesting a link between prenatal maternal stress (PNMS) and anxiety symptoms in offspring are confounded by postnatal and/or shared mother-child heritability effects. Following exposure to a natural disaster, the Queensland Flood Study investigated the unique and additive effects of various types of disaster-related PNMS (objective hardship, cognitive appraisal, and subjective distress) on childhood anxiety symptomatology (internalizing and/or anxiety symptom measures). Timing of flood exposure during pregnancy and child sex were examined as potential moderators. After controlling for maternal psychosocial factors, greater objective hardship as a result of the floods was significantly associated with greater anxiety symptoms (N = 114) and marginally associated with greater internalizing behaviors (N = 115). Earlier timing of the flood in pregnancy was associated with greater anxiety symptoms. No such associations were found between any PNMS measure and teacher-rated child internalizing behaviors (N = 90). Sex and timing did not moderate associations. Our findings suggest that, in isolation, increased maternal hardship due to exposure to an independent stressor, during pregnancy, may have a programming effect on childhood anxiety symptoms. En ligne : http://dx.doi.org/10.1017/s0954579418000408 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Prenatal intimate partner violence exposure predicts infant biobehavioral regulation: Moderation by the brain-derived neurotrophic factor (BDNF) gene / C. MARTINEZ-TORTEYA in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1009-1021 Titre : Prenatal intimate partner violence exposure predicts infant biobehavioral regulation: Moderation by the brain-derived neurotrophic factor (BDNF) gene Type de document : Texte imprimé et/ou numérique Auteurs : C. MARTINEZ-TORTEYA, Auteur ; C. J. FIGGE, Auteur ; M. A. GILCHRIST, Auteur ; M. MUZIK, Auteur ; A. P. KING, Auteur ; M. SORENSON, Auteur Article en page(s) : p.1009-1021 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The ability to regulate stress is a critical developmental milestone of early childhood that involves a set of interconnected behavioral and physiological processes and is influenced by genetic and environmental stimuli. Prenatal exposure to traumatic stress and trauma, including intimate partner violence (IPV), increases risk for offspring biobehavioral regulation problems during childhood and adolescence. Although individual differences in susceptibility to prenatal stress have been largely unexplored, a handful of studies suggest children with specific genetic characteristics are most vulnerable to prenatal stress. We evaluated the brain-derived neurotrophic factor Val66Met gene (BDNF) as a moderator of the effect of prenatal IPV exposure on infant temperamental and cortisol regulation in response to a psychosocial challenge. Ninety-nine mother-infant dyads recruited from the community were assessed when infants (51% female) were 11 to 14 months. Maternal reports of IPV during pregnancy and infant temperament were obtained, and infant saliva was collected for genotyping and to assess cortisol reactivity (before and after the Strange Situation Task). Significant genetic moderation effects were found. Among infants with the BDNF Met allele, prenatal IPV predicted worse temperamental regulation and mobilization of the cortisol response, while controlling for infant postnatal exposure to IPV, other maternal traumatic experiences, and infant sex. However, prenatal IPV exposure was not associated with temperamental or cortisol outcomes among infant carriers of the Val/Val genotype. Findings are discussed in relation to prenatal programming and biological susceptibility to stress. En ligne : http://dx.doi.org/10.1017/s0954579418000329 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Prenatal intimate partner violence exposure predicts infant biobehavioral regulation: Moderation by the brain-derived neurotrophic factor (BDNF) gene [Texte imprimé et/ou numérique] / C. MARTINEZ-TORTEYA, Auteur ; C. J. FIGGE, Auteur ; M. A. GILCHRIST, Auteur ; M. MUZIK, Auteur ; A. P. KING, Auteur ; M. SORENSON, Auteur . - p.1009-1021. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1009-1021 Index. décimale : PER Périodiques Résumé : The ability to regulate stress is a critical developmental milestone of early childhood that involves a set of interconnected behavioral and physiological processes and is influenced by genetic and environmental stimuli. Prenatal exposure to traumatic stress and trauma, including intimate partner violence (IPV), increases risk for offspring biobehavioral regulation problems during childhood and adolescence. Although individual differences in susceptibility to prenatal stress have been largely unexplored, a handful of studies suggest children with specific genetic characteristics are most vulnerable to prenatal stress. We evaluated the brain-derived neurotrophic factor Val66Met gene (BDNF) as a moderator of the effect of prenatal IPV exposure on infant temperamental and cortisol regulation in response to a psychosocial challenge. Ninety-nine mother-infant dyads recruited from the community were assessed when infants (51% female) were 11 to 14 months. Maternal reports of IPV during pregnancy and infant temperament were obtained, and infant saliva was collected for genotyping and to assess cortisol reactivity (before and after the Strange Situation Task). Significant genetic moderation effects were found. Among infants with the BDNF Met allele, prenatal IPV predicted worse temperamental regulation and mobilization of the cortisol response, while controlling for infant postnatal exposure to IPV, other maternal traumatic experiences, and infant sex. However, prenatal IPV exposure was not associated with temperamental or cortisol outcomes among infant carriers of the Val/Val genotype. Findings are discussed in relation to prenatal programming and biological susceptibility to stress. En ligne : http://dx.doi.org/10.1017/s0954579418000329 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Testing the programming of temperament and psychopathology in two independent samples of children with prenatal substance exposure / B. LIN in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1023-1040 Titre : Testing the programming of temperament and psychopathology in two independent samples of children with prenatal substance exposure Type de document : Texte imprimé et/ou numérique Auteurs : B. LIN, Auteur ; B. D. OSTLUND, Auteur ; E. CONRADT, Auteur ; Linda L. LAGASSE, Auteur ; B. M. LESTER, Auteur Article en page(s) : p.1023-1040 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prenatal programming models have rarely been applied to research on children with prenatal substance exposure, despite evidence suggesting that prenatal drug exposure is a form of stress that impacts neurodevelopmental outcomes and risk for psychopathology. Utilizing data from two longitudinal multisite studies comprising children prenatally exposed to substances as well as a nonexposed comparison group (Maternal Lifestyle Study, n = 1,388; Infant Development, Environment, and Lifestyle study, n = 412), we tested whether early phenotypic indicators of hypothesized programming effects, indexed by growth parameters at birth and infant temperament, served as a link between prenatal substance exposure and internalizing and externalizing behavior at age 5. Latent profile analysis indicated that individual differences in reactivity and regulation for infants prenatally exposed to substances was best characterized by four temperament profiles. These profiles were virtually identical across two independent samples, and demonstrated unique associations with adjustment difficulties nearly 5 years later. Results of path analysis using structural equation modeling also showed that increased prenatal substance exposure was linked to poorer growth parameters at birth, profiles of temperamental reactivity in infancy, and internalizing and externalizing behavior at age 5. This pathway was partially replicated across samples. This study was among the first to link known individual-level correlates of prenatal substance exposure into a specific pathway to childhood problem behavior. Implications for the developmental origins of a child's susceptibility to psychopathology as a result of intrauterine substance exposure are discussed. En ligne : http://dx.doi.org/10.1017/s0954579418000391 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Testing the programming of temperament and psychopathology in two independent samples of children with prenatal substance exposure [Texte imprimé et/ou numérique] / B. LIN, Auteur ; B. D. OSTLUND, Auteur ; E. CONRADT, Auteur ; Linda L. LAGASSE, Auteur ; B. M. LESTER, Auteur . - p.1023-1040. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1023-1040 Index. décimale : PER Périodiques Résumé : Prenatal programming models have rarely been applied to research on children with prenatal substance exposure, despite evidence suggesting that prenatal drug exposure is a form of stress that impacts neurodevelopmental outcomes and risk for psychopathology. Utilizing data from two longitudinal multisite studies comprising children prenatally exposed to substances as well as a nonexposed comparison group (Maternal Lifestyle Study, n = 1,388; Infant Development, Environment, and Lifestyle study, n = 412), we tested whether early phenotypic indicators of hypothesized programming effects, indexed by growth parameters at birth and infant temperament, served as a link between prenatal substance exposure and internalizing and externalizing behavior at age 5. Latent profile analysis indicated that individual differences in reactivity and regulation for infants prenatally exposed to substances was best characterized by four temperament profiles. These profiles were virtually identical across two independent samples, and demonstrated unique associations with adjustment difficulties nearly 5 years later. Results of path analysis using structural equation modeling also showed that increased prenatal substance exposure was linked to poorer growth parameters at birth, profiles of temperamental reactivity in infancy, and internalizing and externalizing behavior at age 5. This pathway was partially replicated across samples. This study was among the first to link known individual-level correlates of prenatal substance exposure into a specific pathway to childhood problem behavior. Implications for the developmental origins of a child's susceptibility to psychopathology as a result of intrauterine substance exposure are discussed. En ligne : http://dx.doi.org/10.1017/s0954579418000391 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Prenatal stress and models explaining risk for psychopathology revisited: Generic vulnerability and divergent pathways / A. C. HUIZINK in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1041-1062 Titre : Prenatal stress and models explaining risk for psychopathology revisited: Generic vulnerability and divergent pathways Type de document : Texte imprimé et/ou numérique Auteurs : A. C. HUIZINK, Auteur ; S. R. DE ROOIJ, Auteur Article en page(s) : p.1041-1062 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The present review revisits three hypothesized models that potentially could explain how prenatal maternal stress influences fetal development, birth outcomes, and subsequent developmental psychopathology. These models were mostly based on animal models, and new evidence for these models from human studies is evaluated. Furthermore, divergent trajectories from prenatal exposure to adversities to offspring affected outcomes are reviewed, including the comparison of studies on prenatal maternal stress with research on maternal substance use and maternal malnutrition during pregnancy. Finally, new directions in research on the mechanism underlying prenatal stress effects on human offspring is summarized. While it is concluded that there is abundant evidence for the negative associations between prenatal maternal stress and offspring behavioral, brain, and psychopathological outcomes in humans, there is no consistent evidence for specific mechanisms or specific outcomes in relation to stress exposure in utero. Rather, principles of multifinality and equifinality best describe the consequences for the offspring, suggesting a generic vulnerability and different pathways from prenatal adversities to developmental psychopathology, which complicates the search for underlying mechanisms. New and promising directions for research are provided to get a better understanding of how prenatal stress gets under the skin to affect fetal development. En ligne : http://dx.doi.org/10.1017/s0954579418000354 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Prenatal stress and models explaining risk for psychopathology revisited: Generic vulnerability and divergent pathways [Texte imprimé et/ou numérique] / A. C. HUIZINK, Auteur ; S. R. DE ROOIJ, Auteur . - p.1041-1062. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1041-1062 Index. décimale : PER Périodiques Résumé : The present review revisits three hypothesized models that potentially could explain how prenatal maternal stress influences fetal development, birth outcomes, and subsequent developmental psychopathology. These models were mostly based on animal models, and new evidence for these models from human studies is evaluated. Furthermore, divergent trajectories from prenatal exposure to adversities to offspring affected outcomes are reviewed, including the comparison of studies on prenatal maternal stress with research on maternal substance use and maternal malnutrition during pregnancy. Finally, new directions in research on the mechanism underlying prenatal stress effects on human offspring is summarized. While it is concluded that there is abundant evidence for the negative associations between prenatal maternal stress and offspring behavioral, brain, and psychopathological outcomes in humans, there is no consistent evidence for specific mechanisms or specific outcomes in relation to stress exposure in utero. Rather, principles of multifinality and equifinality best describe the consequences for the offspring, suggesting a generic vulnerability and different pathways from prenatal adversities to developmental psychopathology, which complicates the search for underlying mechanisms. New and promising directions for research are provided to get a better understanding of how prenatal stress gets under the skin to affect fetal development. En ligne : http://dx.doi.org/10.1017/s0954579418000354 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Atypical fetal development: Fetal alcohol syndrome, nutritional deprivation, teratogens, and risk for neurodevelopmental disorders and psychopathology / Michael K. GEORGIEFF in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1063-1086 Titre : Atypical fetal development: Fetal alcohol syndrome, nutritional deprivation, teratogens, and risk for neurodevelopmental disorders and psychopathology Type de document : Texte imprimé et/ou numérique Auteurs : Michael K. GEORGIEFF, Auteur ; P. V. TRAN, Auteur ; E. S. CARLSON, Auteur Article en page(s) : p.1063-1086 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Accumulating evidence indicates that the fetal environment plays an important role in brain development and sets the brain on a trajectory across the life span. An abnormal fetal environment results when factors that should be present during a critical period of development are absent or when factors that should not be in the developing brain are present. While these factors may acutely disrupt brain function, the real cost to society resides in the long-term effects, which include important mental health issues. We review the effects of three factors, fetal alcohol exposure, teratogen exposure, and nutrient deficiencies, on the developing brain and the consequent risk for developmental psychopathology. Each is reviewed with respect to the evidence found in epidemiological and clinical studies in humans as well as preclinical molecular and cellular studies that explicate mechanisms of action. En ligne : http://dx.doi.org/10.1017/s0954579418000500 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Atypical fetal development: Fetal alcohol syndrome, nutritional deprivation, teratogens, and risk for neurodevelopmental disorders and psychopathology [Texte imprimé et/ou numérique] / Michael K. GEORGIEFF, Auteur ; P. V. TRAN, Auteur ; E. S. CARLSON, Auteur . - p.1063-1086. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1063-1086 Index. décimale : PER Périodiques Résumé : Accumulating evidence indicates that the fetal environment plays an important role in brain development and sets the brain on a trajectory across the life span. An abnormal fetal environment results when factors that should be present during a critical period of development are absent or when factors that should not be in the developing brain are present. While these factors may acutely disrupt brain function, the real cost to society resides in the long-term effects, which include important mental health issues. We review the effects of three factors, fetal alcohol exposure, teratogen exposure, and nutrient deficiencies, on the developing brain and the consequent risk for developmental psychopathology. Each is reviewed with respect to the evidence found in epidemiological and clinical studies in humans as well as preclinical molecular and cellular studies that explicate mechanisms of action. En ligne : http://dx.doi.org/10.1017/s0954579418000500 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Impact of maternal prenatal smoking on fetal to infant neurobehavioral development / L. R. STROUD in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1087-1105 Titre : Impact of maternal prenatal smoking on fetal to infant neurobehavioral development Type de document : Texte imprimé et/ou numérique Auteurs : L. R. STROUD, Auteur ; M. MCCALLUM, Auteur ; A. L. SALISBURY, Auteur Article en page(s) : p.1087-1105 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Despite recent emphasis on the profound importance of the fetal environment in "programming" postnatal development, measurement of offspring development typically begins after birth. Using a novel coding strategy combining direct fetal observation via ultrasound and actocardiography, we investigated the impact of maternal smoking during pregnancy (MSDP) on fetal neurobehavior; we also investigated links between fetal and infant neurobehavior. Participants were 90 pregnant mothers and their infants (52 MSDP-exposed; 51% minorities; ages 18-40). Fetal neurobehavior at baseline and in response to vibro-acoustic stimulus was assessed via ultrasound and actocardiography at M = 35 weeks gestation and coded via the Fetal Neurobehavioral Assessment System (FENS). After delivery, the NICU Network Neurobehavioral Scale was administered up to seven times over the first postnatal month. MSDP was associated with increased fetal activity and fetal limb movements. Fetal activity, complex body movements, and cardiac-somatic coupling were associated with infants' ability to attend to stimuli and to self-regulate over the first postnatal month. Furthermore, differential associations emerged by MSDP group between fetal activity, complex body movements, quality of movement, and coupling, and infant attention and self-regulation. The present study adds to a growing literature establishing the validity of fetal neurobehavioral measures in elucidating fetal programming pathways. En ligne : http://dx.doi.org/10.1017/s0954579418000676 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Impact of maternal prenatal smoking on fetal to infant neurobehavioral development [Texte imprimé et/ou numérique] / L. R. STROUD, Auteur ; M. MCCALLUM, Auteur ; A. L. SALISBURY, Auteur . - p.1087-1105. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1087-1105 Index. décimale : PER Périodiques Résumé : Despite recent emphasis on the profound importance of the fetal environment in "programming" postnatal development, measurement of offspring development typically begins after birth. Using a novel coding strategy combining direct fetal observation via ultrasound and actocardiography, we investigated the impact of maternal smoking during pregnancy (MSDP) on fetal neurobehavior; we also investigated links between fetal and infant neurobehavior. Participants were 90 pregnant mothers and their infants (52 MSDP-exposed; 51% minorities; ages 18-40). Fetal neurobehavior at baseline and in response to vibro-acoustic stimulus was assessed via ultrasound and actocardiography at M = 35 weeks gestation and coded via the Fetal Neurobehavioral Assessment System (FENS). After delivery, the NICU Network Neurobehavioral Scale was administered up to seven times over the first postnatal month. MSDP was associated with increased fetal activity and fetal limb movements. Fetal activity, complex body movements, and cardiac-somatic coupling were associated with infants' ability to attend to stimuli and to self-regulate over the first postnatal month. Furthermore, differential associations emerged by MSDP group between fetal activity, complex body movements, quality of movement, and coupling, and infant attention and self-regulation. The present study adds to a growing literature establishing the validity of fetal neurobehavioral measures in elucidating fetal programming pathways. En ligne : http://dx.doi.org/10.1017/s0954579418000676 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Identifying the contribution of prenatal risk factors to offspring development and psychopathology: What designs to use and a critique of literature on maternal smoking and stress in pregnancy / F. RICE in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1107-1128 Titre : Identifying the contribution of prenatal risk factors to offspring development and psychopathology: What designs to use and a critique of literature on maternal smoking and stress in pregnancy Type de document : Texte imprimé et/ou numérique Auteurs : F. RICE, Auteur ; K. LANGLEY, Auteur ; C. WOODFORD, Auteur ; George DAVEY SMITH, Auteur ; A. THAPAR, Auteur Article en page(s) : p.1107-1128 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Identifying prenatal environmental factors that have genuinely causal effects on psychopathology is an important research priority, but it is crucial to select an appropriate research design. In this review we explain why and what sorts of designs are preferable and focus on genetically informed/sensitive designs. In the field of developmental psychopathology, causal inferences about prenatal risks have not always been based on evidence generated from appropriate designs. We focus on reported links between maternal smoking during pregnancy and offspring attention-deficit/hyperactivity disorder or conduct problems. Undertaking a systematic review of findings from genetically informed designs and "triangulating" evidence from studies with different patterns of bias, we conclude that at present findings suggest it is unlikely that there is a substantial causal effect of maternal smoking in pregnancy on either attention-deficit/hyperactivity disorder or conduct problems. In contrast, for offspring birth weight (which serves as a positive control) findings strongly support a negative causal effect of maternal smoking in pregnancy. For maternal pregnancy stress, too few studies use genetically sensitive designs to draw firm conclusions, but continuity with postnatal stress seems important. We highlight the importance of moving beyond observational designs, for systematic evaluation of the breadth of available evidence and choosing innovative designs. We conclude that a broader set of prenatal risk factors should be examined, including those relevant in low- and middle-income contexts. Future directions include a greater use of molecular genetically informed designs such as Mendelian randomization to test causal hypotheses about prenatal exposure and offspring outcome. En ligne : http://dx.doi.org/10.1017/s0954579418000421 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Identifying the contribution of prenatal risk factors to offspring development and psychopathology: What designs to use and a critique of literature on maternal smoking and stress in pregnancy [Texte imprimé et/ou numérique] / F. RICE, Auteur ; K. LANGLEY, Auteur ; C. WOODFORD, Auteur ; George DAVEY SMITH, Auteur ; A. THAPAR, Auteur . - p.1107-1128. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1107-1128 Index. décimale : PER Périodiques Résumé : Identifying prenatal environmental factors that have genuinely causal effects on psychopathology is an important research priority, but it is crucial to select an appropriate research design. In this review we explain why and what sorts of designs are preferable and focus on genetically informed/sensitive designs. In the field of developmental psychopathology, causal inferences about prenatal risks have not always been based on evidence generated from appropriate designs. We focus on reported links between maternal smoking during pregnancy and offspring attention-deficit/hyperactivity disorder or conduct problems. Undertaking a systematic review of findings from genetically informed designs and "triangulating" evidence from studies with different patterns of bias, we conclude that at present findings suggest it is unlikely that there is a substantial causal effect of maternal smoking in pregnancy on either attention-deficit/hyperactivity disorder or conduct problems. In contrast, for offspring birth weight (which serves as a positive control) findings strongly support a negative causal effect of maternal smoking in pregnancy. For maternal pregnancy stress, too few studies use genetically sensitive designs to draw firm conclusions, but continuity with postnatal stress seems important. We highlight the importance of moving beyond observational designs, for systematic evaluation of the breadth of available evidence and choosing innovative designs. We conclude that a broader set of prenatal risk factors should be examined, including those relevant in low- and middle-income contexts. Future directions include a greater use of molecular genetically informed designs such as Mendelian randomization to test causal hypotheses about prenatal exposure and offspring outcome. En ligne : http://dx.doi.org/10.1017/s0954579418000421 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Prenatal stress and the development of psychopathology: Lifestyle behaviors as a fundamental part of the puzzle / C. DE WEERTH in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1129-1144 Titre : Prenatal stress and the development of psychopathology: Lifestyle behaviors as a fundamental part of the puzzle Type de document : Texte imprimé et/ou numérique Auteurs : C. DE WEERTH, Auteur Article en page(s) : p.1129-1144 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Maternal psychological stress, depression, and anxiety during pregnancy (prenatal stress; PNS) are thought to impact fetal development with long-term effects on offspring outcome. These effects would include physical and mental health, including psychopathology. Maternal sleep, diet, and exercise during pregnancy are lifestyle behaviors that are understudied and often solely included in PNS studies as confounders. However, there are indications that these lifestyle behaviors may actually constitute essential mediators between PNS and fetal programming processes. The goal of this theoretical review was to investigate this idea by looking at the evidence for associations between PNS and sleep, diet, and exercise, and by piecing together the information on potential underlying mechanisms and causal pathways through which these factors may affect the offspring. The analysis of the literature led to the conclusion that sleep, diet, and exercise during pregnancy, may have fundamental roles as mediators between PNS and maternal pregnancy physiology. By integrating these lifestyle behaviors into models of prenatal programming of development, a qualitatively higher and more comprehensive understanding of the prenatal origins of psychopathology can be obtained. The review finalizes by discussing some of the present challenges facing the field of PNS and offspring programming, and offering solutions for future research. En ligne : http://dx.doi.org/10.1017/s0954579418000494 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Prenatal stress and the development of psychopathology: Lifestyle behaviors as a fundamental part of the puzzle [Texte imprimé et/ou numérique] / C. DE WEERTH, Auteur . - p.1129-1144. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1129-1144 Index. décimale : PER Périodiques Résumé : Maternal psychological stress, depression, and anxiety during pregnancy (prenatal stress; PNS) are thought to impact fetal development with long-term effects on offspring outcome. These effects would include physical and mental health, including psychopathology. Maternal sleep, diet, and exercise during pregnancy are lifestyle behaviors that are understudied and often solely included in PNS studies as confounders. However, there are indications that these lifestyle behaviors may actually constitute essential mediators between PNS and fetal programming processes. The goal of this theoretical review was to investigate this idea by looking at the evidence for associations between PNS and sleep, diet, and exercise, and by piecing together the information on potential underlying mechanisms and causal pathways through which these factors may affect the offspring. The analysis of the literature led to the conclusion that sleep, diet, and exercise during pregnancy, may have fundamental roles as mediators between PNS and maternal pregnancy physiology. By integrating these lifestyle behaviors into models of prenatal programming of development, a qualitatively higher and more comprehensive understanding of the prenatal origins of psychopathology can be obtained. The review finalizes by discussing some of the present challenges facing the field of PNS and offspring programming, and offering solutions for future research. En ligne : http://dx.doi.org/10.1017/s0954579418000494 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Inflammation-related epigenetic risk and child and adolescent mental health: A prospective study from pregnancy to middle adolescence / Edward D. BARKER in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1145-1156 Titre : Inflammation-related epigenetic risk and child and adolescent mental health: A prospective study from pregnancy to middle adolescence Type de document : Texte imprimé et/ou numérique Auteurs : Edward D. BARKER, Auteur ; Charlotte A. M. CECIL, Auteur ; E. WALTON, Auteur ; L. C. HOUTEPEN, Auteur ; T. G. O'CONNOR, Auteur ; A. DANESE, Auteur ; Sara R. JAFFEE, Auteur ; S. K. G. JENSEN, Auteur ; C. PARIANTE, Auteur ; W. MCARDLE, Auteur ; T. R. GAUNT, Auteur ; C. L. RELTON, Auteur ; S. ROBERTS, Auteur Article en page(s) : p.1145-1156 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : In 785 mother-child (50% male) pairs from a longitudinal epidemiological birth cohort, we investigated associations between inflammation-related epigenetic polygenic risk scores (i-ePGS), environmental exposures, cognitive function, and child and adolescent internalizing and externalizing problems. We examined prenatal and postnatal effects. For externalizing problems, one prenatal effect was found: i-ePGS at birth associated with higher externalizing problems (ages 7-15) indirectly through lower cognitive function (age 7). For internalizing problems, we identified two effects. For a prenatal effect, i-ePGS at birth associated with higher internalizing symptoms via continuity in i-ePGS at age 7. For a postnatal effect, higher postnatal adversity exposure (birth through age 7) associated with higher internalizing problems (ages 7-15) via higher i-ePGS (age 7). Hence, externalizing problems were related mainly to prenatal effects involving lower cognitive function, whereas internalizing problems appeared related to both prenatal and postnatal effects. The present study supports a link between i-ePGS and child and adolescent mental health. En ligne : http://dx.doi.org/10.1017/s0954579418000330 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Inflammation-related epigenetic risk and child and adolescent mental health: A prospective study from pregnancy to middle adolescence [Texte imprimé et/ou numérique] / Edward D. BARKER, Auteur ; Charlotte A. M. CECIL, Auteur ; E. WALTON, Auteur ; L. C. HOUTEPEN, Auteur ; T. G. O'CONNOR, Auteur ; A. DANESE, Auteur ; Sara R. JAFFEE, Auteur ; S. K. G. JENSEN, Auteur ; C. PARIANTE, Auteur ; W. MCARDLE, Auteur ; T. R. GAUNT, Auteur ; C. L. RELTON, Auteur ; S. ROBERTS, Auteur . - p.1145-1156. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1145-1156 Index. décimale : PER Périodiques Résumé : In 785 mother-child (50% male) pairs from a longitudinal epidemiological birth cohort, we investigated associations between inflammation-related epigenetic polygenic risk scores (i-ePGS), environmental exposures, cognitive function, and child and adolescent internalizing and externalizing problems. We examined prenatal and postnatal effects. For externalizing problems, one prenatal effect was found: i-ePGS at birth associated with higher externalizing problems (ages 7-15) indirectly through lower cognitive function (age 7). For internalizing problems, we identified two effects. For a prenatal effect, i-ePGS at birth associated with higher internalizing symptoms via continuity in i-ePGS at age 7. For a postnatal effect, higher postnatal adversity exposure (birth through age 7) associated with higher internalizing problems (ages 7-15) via higher i-ePGS (age 7). Hence, externalizing problems were related mainly to prenatal effects involving lower cognitive function, whereas internalizing problems appeared related to both prenatal and postnatal effects. The present study supports a link between i-ePGS and child and adolescent mental health. En ligne : http://dx.doi.org/10.1017/s0954579418000330 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Prenatal inflammation and risk for schizophrenia: A role for immune proteins in neurodevelopment / D. M. ALLSWEDE in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1157-1178 Titre : Prenatal inflammation and risk for schizophrenia: A role for immune proteins in neurodevelopment Type de document : Texte imprimé et/ou numérique Auteurs : D. M. ALLSWEDE, Auteur ; Tyrone D. CANNON, Auteur Article en page(s) : p.1157-1178 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prenatal inflammation is an established risk factor for schizophrenia. However, the specific inflammatory pathways that mediate this association remain unclear. Potential candidate systems include inflammatory markers produced by microglia, such as cytokines and complement. Accumulating evidence suggests that these markers play a role in typical neurodevelopmental processes, such as synapse formation and interneuron migration. Rodent models demonstrate that altered marker levels during the prenatal period can cause lasting deficits in these systems, leading to cognitive deficits that resemble schizophrenia. This review assesses the potential role of prenatal cytokine and complement elevations on the etiology of schizophrenia. The current neurobiological understanding of the development of schizophrenia is reviewed to identify candidate cellular mechanisms that may be influenced by prenatal inflammation. We discuss the functions that cytokines and complement may play in prenatal neurodevelopment, review evidence that links exposure to these factors with risk for schizophrenia, and consider how these markers may interact with genetic vulnerabilities to influence the neurodevelopment of schizophrenia. We consider how prenatal inflammatory exposure may influence childhood and adolescent developmental risk trajectories for schizophrenia. Finally, we identify areas of further research needed to support the development of anti-inflammatory treatments to prevent the development of schizophrenia in at-risk neonates. En ligne : http://dx.doi.org/10.1017/s0954579418000317 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Prenatal inflammation and risk for schizophrenia: A role for immune proteins in neurodevelopment [Texte imprimé et/ou numérique] / D. M. ALLSWEDE, Auteur ; Tyrone D. CANNON, Auteur . - p.1157-1178. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1157-1178 Index. décimale : PER Périodiques Résumé : Prenatal inflammation is an established risk factor for schizophrenia. However, the specific inflammatory pathways that mediate this association remain unclear. Potential candidate systems include inflammatory markers produced by microglia, such as cytokines and complement. Accumulating evidence suggests that these markers play a role in typical neurodevelopmental processes, such as synapse formation and interneuron migration. Rodent models demonstrate that altered marker levels during the prenatal period can cause lasting deficits in these systems, leading to cognitive deficits that resemble schizophrenia. This review assesses the potential role of prenatal cytokine and complement elevations on the etiology of schizophrenia. The current neurobiological understanding of the development of schizophrenia is reviewed to identify candidate cellular mechanisms that may be influenced by prenatal inflammation. We discuss the functions that cytokines and complement may play in prenatal neurodevelopment, review evidence that links exposure to these factors with risk for schizophrenia, and consider how these markers may interact with genetic vulnerabilities to influence the neurodevelopment of schizophrenia. We consider how prenatal inflammatory exposure may influence childhood and adolescent developmental risk trajectories for schizophrenia. Finally, we identify areas of further research needed to support the development of anti-inflammatory treatments to prevent the development of schizophrenia in at-risk neonates. En ligne : http://dx.doi.org/10.1017/s0954579418000317 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Opening windows of opportunities: Evidence for interventions to prevent or treat depression in pregnant women being associated with changes in offspring's developmental trajectories of psychopathology risk / S. H. GOODMAN in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1179-1196 Titre : Opening windows of opportunities: Evidence for interventions to prevent or treat depression in pregnant women being associated with changes in offspring's developmental trajectories of psychopathology risk Type de document : Texte imprimé et/ou numérique Auteurs : S. H. GOODMAN, Auteur ; K. A. CULLUM, Auteur ; S. DIMIDJIAN, Auteur ; L. M. RIVER, Auteur ; C. Y. KIM, Auteur Article en page(s) : p.1179-1196 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Although animal models and correlational studies support a model of fetal programming as a mechanism in the transmission of risk for psychopathology from parents to children, the experimental studies that are required to empirically test the model with the human prenatal dyad are scarce. With a systematic review and meta-analysis of the literature, we critically examined the evidence regarding the neurobiological and behavioral changes in infants as a function of randomized clinical trials to prevent or reduce maternal depression during pregnancy, treating randomized clinical trials as experiments testing the fetal programming model. Based on 25 articles that met inclusion criteria, we found support for interventions designed to change maternal prenatal mood being associated with changes in offspring functioning, but with a very small effect size. Effect sizes ranged broadly, and were higher for younger children. The findings enhance understanding of putative mechanisms in the transmission of risk from women's prenatal depression to infants' vulnerabilities to, and early signs of, the development of psychopathology. We note limitations of the literature and suggest solutions to advance understanding of how preventing or treating depression in pregnant women might disrupt the transmission of risk to the infants. En ligne : http://dx.doi.org/10.1017/s0954579418000536 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Opening windows of opportunities: Evidence for interventions to prevent or treat depression in pregnant women being associated with changes in offspring's developmental trajectories of psychopathology risk [Texte imprimé et/ou numérique] / S. H. GOODMAN, Auteur ; K. A. CULLUM, Auteur ; S. DIMIDJIAN, Auteur ; L. M. RIVER, Auteur ; C. Y. KIM, Auteur . - p.1179-1196. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1179-1196 Index. décimale : PER Périodiques Résumé : Although animal models and correlational studies support a model of fetal programming as a mechanism in the transmission of risk for psychopathology from parents to children, the experimental studies that are required to empirically test the model with the human prenatal dyad are scarce. With a systematic review and meta-analysis of the literature, we critically examined the evidence regarding the neurobiological and behavioral changes in infants as a function of randomized clinical trials to prevent or reduce maternal depression during pregnancy, treating randomized clinical trials as experiments testing the fetal programming model. Based on 25 articles that met inclusion criteria, we found support for interventions designed to change maternal prenatal mood being associated with changes in offspring functioning, but with a very small effect size. Effect sizes ranged broadly, and were higher for younger children. The findings enhance understanding of putative mechanisms in the transmission of risk from women's prenatal depression to infants' vulnerabilities to, and early signs of, the development of psychopathology. We note limitations of the literature and suggest solutions to advance understanding of how preventing or treating depression in pregnant women might disrupt the transmission of risk to the infants. En ligne : http://dx.doi.org/10.1017/s0954579418000536 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367