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PNMC 21 October 2009

Stress and Anxiety in Pregnancy and Child Development T homas G. O’Connor University of Rochester Medical Center. PNMC 21 October 2009. Theoretical and Public Health Context.

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PNMC 21 October 2009

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  1. Stress and Anxiety in Pregnancy and Child DevelopmentThomas G. O’ConnorUniversity of Rochester Medical Center PNMC 21 October 2009

  2. Theoretical and Public Health Context • The developmental programming/developmental origins of adult disease model has influenced cardiovascular research, and it may be relevant to psychological, immunological, and other phenotypes • If a developmental programming model concerning prenatal stress were applicable, then there would be important implications for prevention and public health • Prenatal stress/anxiety is a compelling research paradigm: • a) there are animal and humans models that require translation • b) a developmental perspective is required • c) consideration of inter-acting biological systems is needed • d) findings have obvious potential for intervention

  3. Stress/anxiety in pregnancy is associated with elevated cortisol in the mom [this is unlikely the only meaningful biological correlate/effect] Cortisol is transmitted to the fetus, either directly or indirectly, and notwithstanding placental function Cortisol exposure during this [“sensitive”] period has a direct effect on fetal brain and mediates the link between prenatal stress/anxiety and infant outcomes Early exposure may “program” certain systems, suggesting long-term effects on behavior (e.g., fear), immune system, and stress physiology Postnatal factors may moderate the effects of prenatal exposure A Prenatal Stress Hypothesis and Model

  4. Stress/anxiety in pregnancy is associated with elevated cortisol in the mom Cortisol is transmitted to the fetus, either directly or indirectly, and notwithstanding placental function Cortisol exposure during this [“sensitive”] period has a direct effect on fetal brain Early exposure may “program” certain systems, suggesting long-term effects on behavior (e.g., fear), immune system, and stress physiology Postnatal factors may moderate the effects of prenatal exposure Translating from Animal to Human Work AnimalHuman Yes ? Yes Yes Yes ? Yes maybe Yes ?

  5. Imperial College Study(March of Dimes funded; Glover, O’Connor, Bergman, Sarkar) • Key features: • Recruited from amniocentesis clinic because amniotic fluid is a fairly direct index of fetal exposure to prenatal hormones • Only mothers with normal pregnancies and babies were included • Children assessed at age 17 months: detailed assessments of childrearing, HPA axis, cognitive ability, temperament

  6. 1. Stress/anxiety in pregnancy is associated with elevated cortisol in the mom State Anxiety is weakly associated with maternal cortisol (ln) in pregnancy r(254)=0.18, p<0.01 Source: Glover et al.; Data from Imperial College Study

  7. 2. Cortisol is transmitted to the fetus

  8. Maternal plasma and amniotic fluid cortisol (ln) are moderately positively correlated (r(267)=0.32, p<0.001) Correlation between maternal plasma and amniotic fluid cortisol (ln) according to gestation Source: Sarkar et al., 2007; Glover et al., in press

  9. 3. Cortisol exposure during this [“sensitive”] period has a direct effect on fetal brain

  10. Human evidence suggests that there is something particular about prenatal stress exposure NB: r’s -.39 and -.05, respectively Source: Bergman et al., 2007

  11. Prenatal Exposure to Cortisol Predicts Lower Cognitive Ability at ~17 Months Source: Bergman et al., in press

  12. What about postnatal rearing?

  13. Post-natal Childrearing Assessment (~17 months) • Quality of child-parent attachment is assessed using the Strange Situation • Standardized assessment of child behavior during 7 3-minute episodes in which there are separations and reunions with the parent • Attachment research has incorporated HPA-axis related findings, with some positive results • The Strange Situation is used as both a relationship assessment and as a context for assessing child HPA axis functioning

  14. Association between Prenatal Exposure to Cortisol and Lower Cognitive Ability is Moderated by Early Rearing Source: Bergman et al., in press

  15. ALSPAC Study(NIMH funded; O’Connor, Glover, Golding) • Longitudinal prospective follow-up of ~6500 15 year-olds on whom prenatal stress/anxiety and detailed developmental data were collected from pregnancy • Age 15 assessments include in-person psychiatric assessments, diurnal cortisol (n=1,000), and DNA

  16. Prenatal stress is associated with elevated cortisol at age 10 ½ years Source: O’Connor et al., Biological Psychiatry, 2005

  17. Prenatal Anxiety Predicts Behavioural/Emotional Problems 47 months 81 months boys girls NB: Controlling for prenatal, obstetric, and psychosocial risks plus postnatal anxiety and depression Source: O’Connor et al., 2002 Brit J Psychiatry, 2003 J Child Psychology & Psychiatry

  18. Rochester Studies(NIMH funded: O’Connor, Glover et al.) • NIMH-funded study of n=200 women from pregnancy to infant age 16 months • Sampling from OB clinic serving population at high psychosocial risk • Prenatal assessments, as above, plus infant assessments at 2, 6, & 16 months involving behavior, saliva and blood samples • Two distinct but interrelated components of adaptive immune function, the humoral (antibody) and T-cell mediated responses

  19. Review of General Findings on Human Research on Prenatal Anxiety/Stress and Child Outcomes • Reliable associations between maternal (and not paternal) prenatal Anxiety/Stress and: • Pregnancy complications • Obstetric outcomes • Cognitive development • Behavioral/emotional problems • Indicators of neurodevelopment (e.g., atypical laterality, dermatoglyphic asymmetry of finger ridge counts; autism & schizophrenia?) • Persistence of effect beyond middle childhood and controlling for postnatal anxiety/stress But, • Mechanisms of action are unclear • Studies have ignored postnatal rearing conditions • Risk phenotype remains somewhat ambiguous • Genetic factors have not been formally considered • Maternal nutritional is status under-examined

  20. Limitations of the model and method • There is an over-reliance on HPA axis and cortisol in particular as a candidate mechanism: • lack of attention to obvious confounders, including other systems & hormones, nutrition, and genetics • persisting methodological variability in HPA assessment • Some uncertainty about the risk phenotype • There are limits to what kinds of maternal and child/fetal data can be collected, e.g., re: placenta, prenatal exposure • Questions about individual differences, timing, duration and severity of exposure are unresolved • Long-term follow-up assessments are still rare • Intervention designs are rarer still

  21. General Conclusions • The observation that child-parent attachment moderates the effect of prenatal cortisol exposure • replicates animal data in this paradigm • provides one of the few human examples that early caregiving quality alters biological risk vulnerability • Intervention studies are needed not only to enact the implications of human research but also to provide confirming causal evidence

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