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Reference Materials

Perinatal Depression: Advancing Public Health Opportunities for Families Katherine L. Wisner, M.D., M.S Join to View
Antenatal screening for women at risk of post-natal depression. Austin, M-P. & Lumley, J. Join to View
Effect of direct fetal opiod analgesia on fetal hormonal and hemodynamic stress response to intrauterine needling. Fisk NM., et al. Join to View
Fetal exposure to maternal cortisol. Gitau R., et al. Join to View
Fetal HPA stress responses to invasive procedures are independent of maternal responses. Gitau, R., et al. Join to View
Früherkennung postpartaler Depression. Hebammenforum CL v. Ballestrem Join to View
Human fetal and maternal noradrenaline responses to invasive procedures. Giannakoulopoulos X., et al. Join to View
Postnatal depression. Cooper, P.J. & Murray, L. Join to View
The course and recurrence of postnatal depression: evidence for the specificity of the diagnostic concept. Cooper, P.J. & Murray L. Join to View
The development and validation of a predictive index for postnatal depression. Cooper, P.J., et al. Join to View
The treatment of postpartum depression: a comprehensive review. Boath, E. & Henshaw, C. Join to View
Exposure to Antenatal Depression and Childhood Maltreatment: Effects on Child Attributional Style O'Donnell, Katharine, Carmine Pariante, Pariante, & Pawlby, Susan Join to View

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Research Abstracts

Arch Womens Ment Health. 2009 Jun;12(3):135-41. Epub 2009 Apr 1.

Symptoms associated with the DSM IV diagnosis of depression in pregnancy and post partum.

Kammerer M, Marks MN, Pinard C, Taylor A, von Castelberg B, Künzli H, Glover V.

Institute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College London, Du Cane Road, London, W12 ONN, UK.

M.Kammerer@imperial.ac.uk

Pregnancy and the postpartum may affect symptoms of depression. However it has not yet been tested how the symptoms used for the DSM IV diagnosis of depression discriminate depressed from non depressed women perinatally. A modified version of the Structured Clinical Interview for DSM IV (SCID interview) was used that allowed assessment of all associated DSM IV symptoms of depression with depressed and non depressed women in pregnancy and the postpartum period. Loss of appetite was not associated with depression either ante or postnatally. The antenatal symptom pattern was different from the postnatal. The sensitivity of the symptoms ranged from 0.7% to 51.6%, and specificity from 61.3% to 99.1%. The best discriminating symptoms were motor retardation/agitation and concentration antenatally, and motor retardation/agitation, concentration and fatigue postnatally. Depression in pregnancy and postpartum depression show significantly different symptom profiles. Appetite is not suitable for the diagnosis of depression in the perinatal period.

Psychoneuroendocrinology. 2009 Sep;34(8):1184-8. Epub 2009 Apr 29.

Diurnal pattern of cortisol output in postnatal depression.

Taylor A, Glover V, Marks M, Kammerer M.

Institute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College London, Du Cane Road, London, W12 ONN, UK.

alyx.taylor@imperial.ac.uk

This study investigated the diurnal output of saliva cortisol in women with symptoms of depression postnatally. Twenty-one depressed and 30 non-depressed women at 7.5 weeks postpartum, and 21 non-perinatal controls, collected saliva at waking, 30 min, and 3 and 12h postwaking. Women who were not depressed postnatally showed a pattern of cortisol secretion over the day similar to non-perinatal controls. There was a significant difference in diurnal pattern between postnatally depressed and postnatally non-depressed women, due to a difference in the first two time points (waking and +30 min): compared to the other two groups who each had a significant increase in cortisol levels from waking to +30 min, the depressed women had significantly higher cortisol levels at waking and no increase at +30 min. The lack of a morning rise in the depressed women is similar to that reported for posttraumatic stress disorder and chronic fatigue syndrome and may reflect a response, in vulnerable women, to the marked cortisol withdrawal that occurs after delivery.

Dev Neurosci. 2009;31(4):285-92. Epub 2009 Jun 17.

Prenatal stress and neurodevelopment of the child: focus on the HPA axis and role of the placenta.

O'Donnell K, O'Connor TG, Glover V.

Institute of Reproductive and Developmental Biology, Imperial College London, London, UK.

Recent human studies have shown that a wide variety of prenatal stressors, from anxiety and partner relationship problems, to natural disasters, increase the risk for a diverse range of adverse neurodevelopmental outcomes in the child. These include impaired cognitive development and behavioral problems, autism and schizophrenia. However, many questions remain about the underlying processes. Much of the research, based on animal studies, has focussed on the maternal HPA axis, with mixed results. Maternal stress or anxiety during pregnancy has been found to be weakly associated with raised maternal cortisol, if at all. The placenta may be a more promising programming vector, because it controls fetal exposure to the maternal environment. Animal studies indicate that prenatal stress can affect the activity of the placental barrier enzyme 11-betaHSD2, which metabolises cortisol. We review the evidence for a similar mechanism in humans and how maternal stress may cause other changes in the placenta which affect fetal neurodevelopment.

Neurosci Biobehav Rev. 2009 Nov 13. [Epub ahead of print]

Prenatal stress and the programming of the HPA axis.

Glover V, O'Connor TG, O'Donnell K.

Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, United Kingdom.

There are several independent prospective studies showing that a wide variety of forms of prenatal stress can have long-term effects on the behavioural and cognitive outcome for the child. Animal studies have shown that prenatal stress, as well as affecting behaviour, can also reprogram the function of the HPA axis in the offspring. However, the effects on the HPA axis are very variable depending on the nature of the stress, its timing in gestation, the genetic strain of the animal, the sex and age of the offspring and whether basal or stimulated HPA axis responses are studied. There are also several recent studies showing long-term effects of prenatal stress on basal cortisol levels, or cortisol responses to stress, in humans. The designs of these studies differ considerably, many are small, and the effects on outcome are also varied. There is little evidence, so far, that altered function of the HPA axis in the child mediates the behavioural or cognitive alterations observed to be associated with prenatal stress. Copyright © 2009 Elsevier Ltd. All rights reserved.

Horm Behav. 2010 Mar;57(3):306-12. Epub 2010 Jan 6.

In utero cortisol and testosterone exposure and fear reactivity in infancy.

Bergman K, Glover V, Sarkar P, Abbott DH, O'Connor TG.

Institute of Reproductive and Developmental Biology, Imperial College London, London, UK.

Fetal programming is emerging as a major conceptual model for understanding developmental origins of health and disease, including behavioral outcomes. As part of a larger study of prenatal stress and child development, we examined the association between prenatal hormone exposure and fear reactivity, a temperament dimension that is a predictor of long-term behavioral adjustment. Amniotic fluid was collected from a sample of women undergoing clinically indicated amniocentesis for later analysis of cortisol and testosterone. Children with normal birth outcomes were recalled for follow-up assessment at 17 months, at which time we administered an observational assessment of temperament (lab-TAB; n=108). Information on pregnancy and obstetric outcome was included as covariates. Results indicated that there was a significant association between prenatal testosterone and observed fear reactivity in boys (r(53)=0.34, p=0.01); no significant effect was found in girls (r(54)=-0.07, ns); the effect remained when obstetric, psychosocial, and parental anxiety were controlled for. There was not a significant association between fetal cortisol exposure and fear reactivity. The prediction from in utero testosterone exposure to fear reactivity in boys extends prior research on prenatal testosterone and may represent an association with a general predisposition to greater arousal and reactivity. Copyright 2010 Elsevier Inc. All rights reserved. Arch Womens Ment Health. 2010 Jan 26. [Epub ahead of print]

Anxiety, depression and saliva cortisol in women with a medical disorder during pregnancy.

King NM, Chambers J, O'Donnell K, Jayaweera SR, Williamson C, Glover VA.

Kammerer M, Marks MN, Pinard C, Taylor A, von Castelberg B, Künzli H, Glover V.

Institute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College London, Hammersmith Campus, Du Cane Road, London, W12 ONN, UK

nicole.king07@imperial.ac.uk

Anxiety and depression during pregnancy increase the risk for an adverse pregnancy outcome and neurodevelopmental problems in the child. The aim of this study was to investigate anxiety and depression in women with a medical disorder of pregnancy compared with control antenatal women, and any association with saliva cortisol. One hundred and twenty pregnant women (60 with a known medical disorder and 60 without, mean gestation 32 weeks) completed five self-rating questionnaires (Spielberger State and Trait Anxiety, Edinburgh Postnatal Depression Scale (EPDS), the Adult Wellbeing Scale and a Life Events Questionnaire). Diurnal saliva samples were obtained from 39 women with a medical disorder and 50 controls for cortisol analysis. The medical disorders group were significantly more anxious and depressed than the controls (mean (SD)) state anxiety 40.0 (11.5) vs. 31.6 (8.8), p = 0.00; trait anxiety 39.4 (9.5) vs. 35.2 (9.2), p = 0.02; adult wellbeing 15.9 (7.5) vs. 12.3 (7.5) p = 0.01; and EPDS 9.6 (5.4) vs. 5.9 (4.8), p = 0.00). There was no difference in the life events scores between the groups. The subgroup of women suffering from hyperemesis gravidarum had particularly high EPDS scores, (16.2 (3), n = 5, p = 0.00) compared with controls. There were no significant differences in the cortisol levels between the groups. Some women with a medical disorder during pregnancy showed considerably elevated levels of anxiety and depression. Health professionals need to be aware that these women need extra psychological support. Biol Psychiatry. 2010 Jun 1;67(11):1026-32. Epub 2010 Feb 25.

Maternal prenatal cortisol and infant cognitive development: moderation by infant-mother attachment.

Bergman K, Sarkar P, Glover V, O'Connor TG.

Institute of Reproductive and Developmental Biology, Imperial College London, London, United Kingdom.

BACKGROUND: Experimental animal studies suggest that early glucocorticoid exposure may have lasting effects on the neurodevelopment of the offspring; animal studies also suggest that this effect may be eliminated by positive postnatal rearing. The relevance of these findings to humans is not known. METHODS: We prospectively followed 125 mothers and their normally developing children from pregnancy through 17 months postnatal. Amniotic fluid was obtained at, on average, 17.2 weeks gestation; infants were assessed at an average age of 17 months with the Bayley Scales of Infant Development, and ratings of infant-mother attachment classification were made from the standard Ainsworth Strange Situation assessment. RESULTS: Prenatal cortisol exposure, indexed by amniotic fluid levels, negatively predicted cognitive ability in the infant, independent of prenatal, obstetric, and socioeconomic factors. This association was moderated by child-mother attachment: in children with an insecure attachment, the correlation was [r(54) = -.47, p 'less than' .001]; in contrast, the association was nonexistent in children who had a secure attachment [r(70) = -.05, ns]. CONCLUSIONS: These findings mimic experimental animal findings and provide the first direct human evidence that increased cortisol in utero is associated with impaired cognitive development, and that its impact is dependent on the quality of the mother-infant relationship. Copyright 2010 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.