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Featured researches published by P. Sarkar.


Biological Psychiatry | 2010

Maternal Prenatal Cortisol and Infant Cognitive Development: Moderation by Infant–Mother Attachment

Kristin Bergman; P. Sarkar; Vivette Glover; Thomas G. O'Connor

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 < .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.


Psychoneuroendocrinology | 2009

Association between maternal and amniotic fluid cortisol is moderated by maternal anxiety

Vivette Glover; Kristin Bergman; P. Sarkar; Thomas G. O’Connor

Maternal stress or anxiety during pregnancy can lead to neurodevelopmental and other problems in the child, and cortisol is one possible mediator. Animal models show that maternal prenatal stress can affect placental function, including regulation of placental 11beta-HSD2, the main barrier to the placental passage of cortisol. It is not known whether a parallel process exists in humans. The aim of the current study was to determine whether maternal anxiety increases the association between maternal plasma cortisol and amniotic fluid cortisol. The sample consisted of 262 women having amniocentesis, with normal pregnancies, who completed Spielberger State and Trait anxiety scales, from whom a plasma sample and an aliquot of amniotic fluid was obtained. The correlation between maternal and amniotic fluid cortisol was strongly dependent on both State and Trait maternal anxiety; in the most anxious State quartile r(62)=.59, p<.001 and in the least r(60)=.05, ns, a significant difference (p<.0015). The moderating effect of maternal anxiety on the association between maternal plasma and amniotic fluid cortisol remained when gestational age, maternal age, fetal sex, medication and time of collection were controlled for. There was no difference in amniotic fluid cortisol levels between the most and least anxious groups of mothers. However, the finding that there is a stronger correlation between maternal and fetal cortisol among more anxious pregnant women does suggests that the maternal emotional state can affect the function of the placenta.


Developmental Psychobiology | 2013

Prenatal cortisol exposure predicts infant cortisol response to acute stress

Thomas G. O'Connor; Kristin Bergman; P. Sarkar; Vivette Glover

Experimental animal findings suggest that early stress and glucocorticoid exposure may program the function of the hypothalamic-pituitary-adrenal (HPA) axis in the offspring. The extension of these findings to human development is not yet clear. A prospective longitudinal study was conducted on 125 mothers and their normally developing children. Amniotic fluid was obtained at, on average, 17.2 weeks gestation; infant behavior and cortisol response to a separation-reunion stress was assessed at 17 months. Amniotic fluid cortisol predicted infant cortisol response to separation-reunion stress: infants who were exposed to higher levels of cortisol in utero showed higher pre-stress cortisol values and blunted response to stress exposure. The association was independent of prenatal, obstetric, and socioeconomic factors and child-parent attachment. The findings provide some of the strongest data in humans that HPA axis functioning in the child may be predicted from prenatal cortisol exposure.


Journal of Neuroendocrinology | 2008

Maternal Antenatal Anxiety and Amniotic Fluid Cortisol and Testosterone: Possible Implications for Foetal Programming

P. Sarkar; Kristin Bergman; Thomas G. O’Connor; Vivette Glover

Both animal and human studies have shown that maternal stress or anxiety during pregnancy is associated with increased risk of disturbance in offspring neurodevelopment and behaviour. In animal models, increased foetal exposure to glucocorticoids has been found to be one mechanism for such foetal programming. Little is understood of the mediating mechanisms in humans, and one aim of our research programme is to investigate this further. This review presents a synopsis of some of our recent results. We aimed to test the hypothesis that maternal anxiety was associated with raised maternal cortisol, and that this in turn was related to increased foetal exposure to cortisol. We studied this by recruiting women at amniocentesis, obtained their Spielberger State Anxiety scores, and assessed maternal plasma cortisol and amniotic fluid cortisol. We also examined maternal plasma and amniotic fluid testosterone levels. Awaiting amniocentesis was in general anxiogenic, but with a wide range of anxiety scores. Maternal anxiety was significantly associated with plasma cortisol before 17 weeks, albeit of modest magnitude (r = 0.0.23), and not after 17 weeks of gestation. This is probably due to the known attenuation of the maternal hypothalamic‐pituitary‐adrenal axis with increasing gestation. We found a strong correlation between maternal plasma and amniotic fluid cortisol levels, which increased with gestation and became robust after 18 weeks. This correlation increased with maternal anxiety, suggesting a possible effect of maternal mood on placental function. There was a positive correlation between cortisol and testosterone in amniotic fluid, in both male and female foetuses independent of maternal anxiety, plasma testosterone, gestational age, and time of collection. Foetal stress may be associated with increased foetal exposure to testosterone. However, maternal anxiety did not predict amniotic fluid cortisol or testosterone level. Thus, the role of these hormones in mediating the effect of maternal mood on foetal development in humans remains to be demonstrated.


Journal of Child Psychology and Psychiatry | 2008

Quality of child-parent attachment moderates the impact of antenatal stress on child fearfulness.

Kristin Bergman; P. Sarkar; Vivette Glover; Thomas G. O’Connor

BACKGROUND Animal studies have shown that prenatal stress has persisting effects on several aspects of offspring development; more recent studies show that this effect may be eliminated by positive postnatal rearing. Human studies of prenatal anxiety/stress are now also beginning to document links between antenatal stress/anxiety and behavioural and cognitive development of the child; however, there is no human evidence as to whether the early caregiving environment moderates the effect of antenatal anxiety/stress on child outcomes. METHODS Antenatal and postnatal measures of stress were collected on 123 women who were recruited from an antenatal clinic. Laboratory-based assessment of the childrens cognitive development and fearfulness were assessed when the children were aged 17 months. In addition, child-parent attachment quality was assessed using the Strange Situation. RESULTS Attachment classification moderated the link between antenatal stress and observed fearfulness. The effect of antenatal stress on fearfulness was most accentuated in children with an Insecure/Resistant attachment classification; the significant antenatal stress x attachment classification interaction held after controlling for postnatal stress and obstetric, social and demographic factors. Attachment did not moderate the effects of antenatal anxiety on cognitive development. DISCUSSION These findings provide the first human evidence that postnatal parenting may moderate the adverse effects of antenatal stress. These results raise developmental questions about the timing and effect of interventions to reduce the adverse effects of antenatal stress exposure.


Hormones and Behavior | 2010

In utero cortisol and testosterone exposure and fear reactivity in infancy

Kristin Bergman; Vivette Glover; P. Sarkar; Dave H. Abbott; Thomas G. O'Connor

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.


Clinical Endocrinology | 2007

Amniotic fluid testosterone: relationship with cortisol and gestational age

P. Sarkar; Kristin Bergman; Nicholas M. Fisk; Thomas G. O'Connor; Vivette Glover

Introduction  Foetal exposure to testosterone is increasingly implicated in the programming of future reproductive and nonreproductive behaviour. Some outcomes associated with prenatal exposure to testosterone may be predicted from exposure to prenatal stress, suggesting a link between them. The peak serum levels of testosterone in the foetus are thought to be around 14–18 weeks’ gestation, and we explored testosterone levels at different gestations. Although best investigated in foetal plasma, this is now difficult because of the decline in frequency of foetal blood sampling; in this study, we used amniotic fluid as a biomarker to investigate foetal exposure.


Clinical Endocrinology | 2007

Ontogeny of foetal exposure to maternal cortisol using midtrimester amniotic fluid as a biomarker

P. Sarkar; Kristin Bergman; Nicholas M. Fisk; Thomas G. O'Connor; Vivette Glover

Objective  There is increasing evidence that antenatal stress has long‐lasting effects on child development, but there is less accord on the mechanisms and the gestational window of susceptibility. One possible mechanism is by foetal exposure to maternal cortisol. To explore this, we investigated the relationship between cortisol in maternal plasma and amniotic fluid, and any moderating influence of gestational age.


Journal of the American Academy of Child and Adolescent Psychiatry | 2007

Maternal Stress During Pregnancy Predicts Cognitive Ability and Fearfulness in Infancy

Kristin Bergman; P. Sarkar; Thomas G. O'Connor; Neena Modi; Vivette Glover


Prenatal Diagnosis | 2006

Maternal anxiety at amniocentesis and plasma cortisol

P. Sarkar; Kristin Bergman; Nicholas M. Fisk; Vivette Glover

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Thomas G. O'Connor

University of Rochester Medical Center

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Thomas G. O’Connor

University of Rochester Medical Center

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Neena Modi

Imperial College London

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Dave H. Abbott

University of Wisconsin-Madison

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