Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective / Vivette GLOVER in Journal of Child Psychology and Psychiatry, 52-4 (April 2011)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 52-4 (April 2011) . - p.356-367 Titre : Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective Type de document : Texte imprimé et/ou numérique Auteurs : Vivette GLOVER, Auteur Année de publication : 2011 Article en page(s) : p.356-367 Langues : Anglais (eng) Mots-clés : Prenatal  stress  anxiety  evolution  child development  psychopathology Index. décimale : PER Périodiques Résumé : If a mother is stressed or anxious while pregnant her child is more likely to show a range of symptoms such as those of attention deficit hyperactivity disorder, conduct disorder, aggression or anxiety. While there remains some debate about what proportion of these effects are due to the prenatal or the postnatal environment, and the role of genetics, there is good evidence that prenatal stress exposure can increase the risk for later psychopathology. Why should this be? In our evolutionary history it is possible that some increase in these characteristics in some individuals was adaptive in a stressful environment, and that this type of fetal programming prepared the child or group for the environment in which they were going to find themselves. Anxiety may have been associated with increased vigilance, distractible attention with more perception of danger, impulsivity with more exploration, conduct disorder with a willingness to break rules, and aggression with the ability to fight intruders or predators. This adaptation for a future dangerous environment may explain why stress and anxiety, rather than depression, seem to have these programming effects; why there is a dose–response relationship with prenatal stress from moderate to severe and it is not only toxic stress that has consequences; why not all children are affected and why individual children are affected in different ways; and why the outcomes affected can depend on the sex of the offspring. An evolutionary perspective may give a different understanding of children in our society with these symptoms, and suggest new directions for research. For example, there is some evidence that the type of cognitive deficits observed after prenatal stress have specific characteristics; these may be those which were adaptive in a past environment. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02371.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=119 [article] Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective [Texte imprimé et/ou numérique] / Vivette GLOVER, Auteur . - 2011 . - p.356-367. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 52-4 (April 2011) . - p.356-367 Mots-clés : Prenatal  stress  anxiety  evolution  child development  psychopathology Index. décimale : PER Périodiques Résumé : If a mother is stressed or anxious while pregnant her child is more likely to show a range of symptoms such as those of attention deficit hyperactivity disorder, conduct disorder, aggression or anxiety. While there remains some debate about what proportion of these effects are due to the prenatal or the postnatal environment, and the role of genetics, there is good evidence that prenatal stress exposure can increase the risk for later psychopathology. Why should this be? In our evolutionary history it is possible that some increase in these characteristics in some individuals was adaptive in a stressful environment, and that this type of fetal programming prepared the child or group for the environment in which they were going to find themselves. Anxiety may have been associated with increased vigilance, distractible attention with more perception of danger, impulsivity with more exploration, conduct disorder with a willingness to break rules, and aggression with the ability to fight intruders or predators. This adaptation for a future dangerous environment may explain why stress and anxiety, rather than depression, seem to have these programming effects; why there is a dose–response relationship with prenatal stress from moderate to severe and it is not only toxic stress that has consequences; why not all children are affected and why individual children are affected in different ways; and why the outcomes affected can depend on the sex of the offspring. An evolutionary perspective may give a different understanding of children in our society with these symptoms, and suggest new directions for research. For example, there is some evidence that the type of cognitive deficits observed after prenatal stress have specific characteristics; these may be those which were adaptive in a past environment. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02371.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=119

Antenatal maternal stress and long-term effects on child neurodevelopment: how and why? / Nicole M. TALGE in Journal of Child Psychology and Psychiatry, 48-3/4 (March/April 2007)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 48-3/4 (March/April 2007) . - p.245–261 Titre : Antenatal maternal stress and long-term effects on child neurodevelopment: how and why? Type de document : Texte imprimé et/ou numérique Auteurs : Nicole M. TALGE, Auteur ; Charles NEAL, Auteur ; Vivette GLOVER, Auteur Année de publication : 2007 Article en page(s) : p.245–261 Langues : Anglais (eng) Mots-clés : Antenatal prenatal stress anxiety child-neurodevelopment attention-deficit/hyperactivity HPA-axis cortisol Index. décimale : PER Périodiques Résumé : We review a significant body of evidence from independent prospective studies that if a mother is stressed while pregnant, her child is substantially more likely to have emotional or cognitive problems, including an increased risk of attentional deficit/hyperactivity, anxiety, and language delay. These findings are independent of effects due to maternal postnatal depression and anxiety. We still do not know what forms of anxiety or stress are most detrimental, but research suggests that the relationship with the partner can be important in this respect. The magnitude of these effects is clinically significant, as the attributable load of emotional/behavioral problems due to antenatal stress and/or anxiety is approximately 15%. Animal models suggest that activity of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis and its hormonal end-product cortisol are involved in these effects in both mother and offspring. The fetal environment can be altered if stress in the mother changes her hormonal profile, and in humans, there is a strong correlation between maternal and fetal cortisol levels. However, many problems remain in understanding the mechanisms involved in this interaction. For example, maternal cortisol responses to stress decline over the course of pregnancy, and earlier in pregnancy, the link between maternal and fetal cortisol is less robust. It is possible that the effects of maternal anxiety and stress on the developing fetus and child are moderated by other factors such as a maternal diet (e.g., protein load). It is suggested that extra vigilance or anxiety, readily distracted attention, or a hyper-responsive HPA axis may have been adaptive in a stressful environment during evolution, but exists today at the cost of vulnerability to neurodevelopmental disorders. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2006.01714.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=948 [article] Antenatal maternal stress and long-term effects on child neurodevelopment: how and why? [Texte imprimé et/ou numérique] / Nicole M. TALGE, Auteur ; Charles NEAL, Auteur ; Vivette GLOVER, Auteur . - 2007 . - p.245–261. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 48-3/4 (March/April 2007) . - p.245–261 Mots-clés : Antenatal prenatal stress anxiety child-neurodevelopment attention-deficit/hyperactivity HPA-axis cortisol Index. décimale : PER Périodiques Résumé : We review a significant body of evidence from independent prospective studies that if a mother is stressed while pregnant, her child is substantially more likely to have emotional or cognitive problems, including an increased risk of attentional deficit/hyperactivity, anxiety, and language delay. These findings are independent of effects due to maternal postnatal depression and anxiety. We still do not know what forms of anxiety or stress are most detrimental, but research suggests that the relationship with the partner can be important in this respect. The magnitude of these effects is clinically significant, as the attributable load of emotional/behavioral problems due to antenatal stress and/or anxiety is approximately 15%. Animal models suggest that activity of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis and its hormonal end-product cortisol are involved in these effects in both mother and offspring. The fetal environment can be altered if stress in the mother changes her hormonal profile, and in humans, there is a strong correlation between maternal and fetal cortisol levels. However, many problems remain in understanding the mechanisms involved in this interaction. For example, maternal cortisol responses to stress decline over the course of pregnancy, and earlier in pregnancy, the link between maternal and fetal cortisol is less robust. It is possible that the effects of maternal anxiety and stress on the developing fetus and child are moderated by other factors such as a maternal diet (e.g., protein load). It is suggested that extra vigilance or anxiety, readily distracted attention, or a hyper-responsive HPA axis may have been adaptive in a stressful environment during evolution, but exists today at the cost of vulnerability to neurodevelopmental disorders. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2006.01714.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=948

Evidence for sex differences in fetal programming of physiological stress reactivity in infancy / Florin TIBU in Development and Psychopathology, 26-4 (Part 1) (November 2014)  

Public ISBD [article]  inDevelopment and Psychopathology > 26-4 (Part 1) (November 2014) . - p.879-888 Titre : Evidence for sex differences in fetal programming of physiological stress reactivity in infancy Type de document : Texte imprimé et/ou numérique Auteurs : Florin TIBU, Auteur ; Jonathan HILL, Auteur ; Helen SHARP, Auteur ; Kate MARSHALL, Auteur ; Vivette GLOVER, Auteur ; Andrew PICKLES, Auteur Année de publication : 2014 Article en page(s) : p.879-888 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Associations between low birth weight and prenatal anxiety and later psychopathology may arise from programming effects likely to be adaptive under some, but not other, environmental exposures and modified by sex differences. If physiological reactivity, which also confers vulnerability or resilience in an environment-dependent manner, is associated with birth weight and prenatal anxiety, it will be a candidate to mediate the links with psychopathology. From a general population sample of 1,233 first-time mothers recruited at 20 weeks gestation, a sample of 316 stratified by adversity was assessed at 32 weeks and when their infants were aged 29 weeks (N = 271). Prenatal anxiety was assessed by self-report, birth weight from medical records, and vagal reactivity from respiratory sinus arrhythmia during four nonstressful and one stressful (still-face) procedure. Lower birth weight for gestational age predicted higher vagal reactivity only in girls (interaction term, p = .016), and prenatal maternal anxiety predicted lower vagal reactivity only in boys (interaction term, p = .014). These findings are consistent with sex differences in fetal programming, whereby prenatal risks are associated with increased stress reactivity in females but decreased reactivity in males, with distinctive advantages and penalties for each sex. En ligne : http://dx.doi.org/10.1017/S0954579414000194 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=242 [article] Evidence for sex differences in fetal programming of physiological stress reactivity in infancy [Texte imprimé et/ou numérique] / Florin TIBU, Auteur ; Jonathan HILL, Auteur ; Helen SHARP, Auteur ; Kate MARSHALL, Auteur ; Vivette GLOVER, Auteur ; Andrew PICKLES, Auteur . - 2014 . - p.879-888. Langues : Anglais (eng) in Development and Psychopathology > 26-4 (Part 1) (November 2014) . - p.879-888 Index. décimale : PER Périodiques Résumé : Associations between low birth weight and prenatal anxiety and later psychopathology may arise from programming effects likely to be adaptive under some, but not other, environmental exposures and modified by sex differences. If physiological reactivity, which also confers vulnerability or resilience in an environment-dependent manner, is associated with birth weight and prenatal anxiety, it will be a candidate to mediate the links with psychopathology. From a general population sample of 1,233 first-time mothers recruited at 20 weeks gestation, a sample of 316 stratified by adversity was assessed at 32 weeks and when their infants were aged 29 weeks (N = 271). Prenatal anxiety was assessed by self-report, birth weight from medical records, and vagal reactivity from respiratory sinus arrhythmia during four nonstressful and one stressful (still-face) procedure. Lower birth weight for gestational age predicted higher vagal reactivity only in girls (interaction term, p = .016), and prenatal maternal anxiety predicted lower vagal reactivity only in boys (interaction term, p = .014). These findings are consistent with sex differences in fetal programming, whereby prenatal risks are associated with increased stress reactivity in females but decreased reactivity in males, with distinctive advantages and penalties for each sex. En ligne : http://dx.doi.org/10.1017/S0954579414000194 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=242

Maternal prenatal anxiety and child brain-derived neurotrophic factor (BDNF) genotype: Effects on internalizing symptoms from 4 to 15 years of age / Kieran J. O'DONNELL in Development and Psychopathology, 26-4 (Part 2) (November 2014)  

Public ISBD [article]  inDevelopment and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1255-1266 Titre : Maternal prenatal anxiety and child brain-derived neurotrophic factor (BDNF) genotype: Effects on internalizing symptoms from 4 to 15 years of age Type de document : Texte imprimé et/ou numérique Auteurs : Kieran J. O'DONNELL, Auteur ; Vivette GLOVER, Auteur ; Joanna D. HOLBROOK, Auteur ; Thomas G. O'CONNOR, Auteur Année de publication : 2014 Article en page(s) : p.1255-1266 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Multiple behavioral and health outcomes, including internalizing symptoms, may be predicted from prenatal maternal anxiety, depression, or stress. However, not all children are affected, and those that are can be affected in different ways. Here we test the hypothesis that the effects of prenatal anxiety are moderated by genetic variation in the child's brain-derived neurotrophic factor (BDNF) gene, using the Avon Longitudinal Study of Parents and Children population cohort. Internalizing symptoms were assessed from 4 to 13 years of age using the Strengths and Difficulties Questionnaire (n = 8,584); a clinical interview with the adolescents was conducted at age 15 years (n = 4,704). Obstetric and psychosocial risk and postnatal maternal symptoms were included as covariates. Results show that prenatal maternal anxiety predicted internalizing symptoms, including with the diagnostic assessment at 15 years. There was a main effect of two BDNF polymorphisms (rs6265 [val66met] and rs11030104) on internalizing symptoms up to age 13. There was also genetic moderation of the prenatal anxiety effect by different BDNF polymorphisms (rs11030121 and rs7124442), although significant effects were limited to preadolescence. The findings suggest a role for BDNF gene–environment interactions in individual vulnerability to the effects of prenatal anxiety on child internalizing symptoms. En ligne : http://dx.doi.org/10.1017/S095457941400100X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=245 [article] Maternal prenatal anxiety and child brain-derived neurotrophic factor (BDNF) genotype: Effects on internalizing symptoms from 4 to 15 years of age [Texte imprimé et/ou numérique] / Kieran J. O'DONNELL, Auteur ; Vivette GLOVER, Auteur ; Joanna D. HOLBROOK, Auteur ; Thomas G. O'CONNOR, Auteur . - 2014 . - p.1255-1266. Langues : Anglais (eng) in Development and Psychopathology > 26-4 (Part 2) (November 2014) . - p.1255-1266 Index. décimale : PER Périodiques Résumé : Multiple behavioral and health outcomes, including internalizing symptoms, may be predicted from prenatal maternal anxiety, depression, or stress. However, not all children are affected, and those that are can be affected in different ways. Here we test the hypothesis that the effects of prenatal anxiety are moderated by genetic variation in the child's brain-derived neurotrophic factor (BDNF) gene, using the Avon Longitudinal Study of Parents and Children population cohort. Internalizing symptoms were assessed from 4 to 13 years of age using the Strengths and Difficulties Questionnaire (n = 8,584); a clinical interview with the adolescents was conducted at age 15 years (n = 4,704). Obstetric and psychosocial risk and postnatal maternal symptoms were included as covariates. Results show that prenatal maternal anxiety predicted internalizing symptoms, including with the diagnostic assessment at 15 years. There was a main effect of two BDNF polymorphisms (rs6265 [val66met] and rs11030104) on internalizing symptoms up to age 13. There was also genetic moderation of the prenatal anxiety effect by different BDNF polymorphisms (rs11030121 and rs7124442), although significant effects were limited to preadolescence. The findings suggest a role for BDNF gene–environment interactions in individual vulnerability to the effects of prenatal anxiety on child internalizing symptoms. En ligne : http://dx.doi.org/10.1017/S095457941400100X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=245

No relationship between prenatal androgen exposure and autistic traits: convergent evidence from studies of children with congenital adrenal hyperplasia and of amniotic testosterone concentrations in typically developing children / Karson T. F. KUNG in Journal of Child Psychology and Psychiatry, 57-12 (December 2016)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 57-12 (December 2016) . - p.1455-1462 Titre : No relationship between prenatal androgen exposure and autistic traits: convergent evidence from studies of children with congenital adrenal hyperplasia and of amniotic testosterone concentrations in typically developing children Type de document : Texte imprimé et/ou numérique Auteurs : Karson T. F. KUNG, Auteur ; Debra SPENCER, Auteur ; Vickie PASTERSKI, Auteur ; Sharon NEUFELD, Auteur ; Vivette GLOVER, Auteur ; Thomas G. O'CONNOR, Auteur ; Peter C. HINDMARSH, Auteur ; Ieuan A. HUGHES, Auteur ; Carlo L. ACERINI, Auteur ; Melissa HINES, Auteur Article en page(s) : p.1455-1462 Langues : Anglais (eng) Mots-clés : Congenital adrenal hyperplasia  fetal testosterone  prenatal testosterone exposure  autism  autistic traits  extreme male brain Index. décimale : PER Périodiques Résumé : Background There is a marked male preponderance in autism spectrum conditions. The extreme male brain theory and the fetal androgen theory of autism suggest that elevated prenatal testosterone exposure is a key contributor to autistic traits. The current paper reports findings from two separate studies that test this hypothesis. Methods A parent-report questionnaire, the Childhood Autism Spectrum Test (CAST), was employed to measure autistic traits in both studies. The first study examined autistic traits in young children with congenital adrenal hyperplasia (CAH), a condition causing unusually high concentrations of testosterone prenatally in girls. Eighty one children with CAH (43 girls) and 72 unaffected relatives (41 girls), aged 4–11 years, were assessed. The second study examined autistic traits in relation to amniotic testosterone in 92 typically developing children (48 girls), aged 3–5 years. Results Findings from neither study supported the association between prenatal androgen (testosterone) exposure and autistic traits. Specifically, young girls with and without CAH did not differ significantly in CAST scores and amniotic testosterone concentrations were not significantly associated with CAST scores in boys, girls, or the whole sample. Conclusions These studies do not support a relationship between prenatal testosterone exposure and autistic traits. These findings augment prior research suggesting no consistent relationship between early androgen exposure and autistic traits. En ligne : http://dx.doi.org/10.1111/jcpp.12602 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=298 [article] No relationship between prenatal androgen exposure and autistic traits: convergent evidence from studies of children with congenital adrenal hyperplasia and of amniotic testosterone concentrations in typically developing children [Texte imprimé et/ou numérique] / Karson T. F. KUNG, Auteur ; Debra SPENCER, Auteur ; Vickie PASTERSKI, Auteur ; Sharon NEUFELD, Auteur ; Vivette GLOVER, Auteur ; Thomas G. O'CONNOR, Auteur ; Peter C. HINDMARSH, Auteur ; Ieuan A. HUGHES, Auteur ; Carlo L. ACERINI, Auteur ; Melissa HINES, Auteur . - p.1455-1462. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 57-12 (December 2016) . - p.1455-1462 Mots-clés : Congenital adrenal hyperplasia  fetal testosterone  prenatal testosterone exposure  autism  autistic traits  extreme male brain Index. décimale : PER Périodiques Résumé : Background There is a marked male preponderance in autism spectrum conditions. The extreme male brain theory and the fetal androgen theory of autism suggest that elevated prenatal testosterone exposure is a key contributor to autistic traits. The current paper reports findings from two separate studies that test this hypothesis. Methods A parent-report questionnaire, the Childhood Autism Spectrum Test (CAST), was employed to measure autistic traits in both studies. The first study examined autistic traits in young children with congenital adrenal hyperplasia (CAH), a condition causing unusually high concentrations of testosterone prenatally in girls. Eighty one children with CAH (43 girls) and 72 unaffected relatives (41 girls), aged 4–11 years, were assessed. The second study examined autistic traits in relation to amniotic testosterone in 92 typically developing children (48 girls), aged 3–5 years. Results Findings from neither study supported the association between prenatal androgen (testosterone) exposure and autistic traits. Specifically, young girls with and without CAH did not differ significantly in CAST scores and amniotic testosterone concentrations were not significantly associated with CAST scores in boys, girls, or the whole sample. Conclusions These studies do not support a relationship between prenatal testosterone exposure and autistic traits. These findings augment prior research suggesting no consistent relationship between early androgen exposure and autistic traits. En ligne : http://dx.doi.org/10.1111/jcpp.12602 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=298

Quality of child–parent attachment moderates the impact of antenatal stress on child fearfulness / K. BERGMAN in Journal of Child Psychology and Psychiatry, 49-10 (October 2008)  

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The persisting effect of maternal mood in pregnancy on childhood psychopathology / Kieran J. O'DONNELL in Development and Psychopathology, 26-2 (May 2014)  

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