gerry giesbrecht, phd, r psych department of paediatrics ... · gerry giesbrecht, phd, r psych ....
TRANSCRIPT
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Gerry Giesbrecht, PhD, R Psych Department of Paediatrics, University of Calgary Alberta Children’s Hospital Research Institute
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Overview of Today’s Talk
Why exposure timing is an important topic in developmental science.
How change in maternal stress
physiology during pregnancy could explain time effects.
Cortisol remains a potent stress signal throughout pregnancy.
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The Effects of Exposures Depend on Timing
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Source: Class et al. (2011). Psychosomatic Medicine, 73, 234-241.
Birth outcomes as a function of GA and stress exposure
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Source: Davis & Sandman (2010). Child Development, 81, 131-148.
Cognitive development as a function of GA and cortisol
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Conclusion
Early exposure is worse than later exposure.
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Period of hypo-responsivity
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What Causes Timing Effects?
Changes in Biological Vulnerability
Fetal Development
Changes in Maternal Stress Physiology
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Attenuation of Perceived Stress
Source: Glynn et al. (2004) Journal of Psychosomatic Research, 56, 47-52.
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Attenuation of Heart Rate Response to Stress
Source: Entringer et al. (2010). Stress, 13, 258-268.
Note: No cortisol response in either group.
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Lack of Cortisol Response to Cold Stress
Source: Kammerer et al. (2002) BMC Pregnancy and Childbirth, 2:8.
GA = 37 weeks
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Lack of Cortisol Response to CRH in Late Gestation
Source: Schulte et al. (1990) Clinical Endocrinology, 33, 99-106
39 weeks GA
4-5 weeks post-partum
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Summary
HPA axis resists acute changes Could dose reduction explain the timing effects?
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Giesbrecht et al., (2012). Psychoneuroendocrinology, 37, 270-279
Does the HPA axis become insensitive to psychological stimulation?
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Evidence of cortisol reactivity in late gestation
Source: De Weerth et al. (2007) Acta Obstetricia et Gynecologica, 86, 1181-1192.
33 weeks GA
3.4 nmol/l
3.2 nmol/l
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Evidence of cortisol reactivity in late gestation
Source: Schulte et al. (1990) Clinical Endocrinology, 33, 99-106
39 weeks GA
4-5 weeks post-partum
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Overview of Assessments: Pregnancy, Mood, and Cortisol Study
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Study Protocol
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0.2
0.22
0.24
0.26
0.28
0.3
0.32
0.34
0.36
0.38
2
2.2
2.4
2.6
2.8
3
3.2
3.4
3.6
3.8
4
1st 2nd 3rd
Cor
tisol
ug/
dL
Psyc
holg
ical
Dis
tres
s
Trimester
Distress
Cortisol
Average Cortisol and Distress Trajectories over Pregnancy
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Association Model Interpretation Momentary (level 1) Effects Estimate SE p WAKING Levels -1.64 .026 <.001 Waking level = 0.19 µg/dL CAR .32 .049 <.001 38% increase TIME -.12 .006 <.001 11.3% decrease/hour TIME2 .002 .0007 .001 0.2% increase/hour2
PSYCHOLOGICAL DISTRESS .024 .008 .006 Maximum effect = 31% increase Gestation Age (level 2) Effects For Waking Levels For CAR For Time For Time2 For Psychological Distress
Cortisol and Psychological Distress Covary over Time
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Association Model Moderator Model Momentary (level 1) Effects Estimate SE p Estimate SE p WAKING Levels -1.64 .026 <.001 -1.62 .025 <.001 CAR .32 .049 <.001 .32 .047 <.001 TIME -.12 .006 <.001 -.12 .005 <.001 TIME2 .002 .0007 .001 .002 .0007 .004 PSYCHOLOGICAL DISTRESS .024 .008 .006 .024 .006 <.001 Gestation Age (level 2) Effects For Waking Levels .027 .002 <.001 For CAR -.006 .005 .17 For Time .001 .0005 .02 For Time2 -.0002 .00007 .02 For Psychological Distress .0009 .0006 .13
Covariation between Cortisol and Psychological Distress is not Attenuated by Advancing Gestation
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Conclusion
HPA axis remains responsive to psychological stimulation.
Attenuation of maternal stress response is not a plausible explanation for the effects of exposure timing.
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Acknowledgments
Collaborators Bonnie Kaplan Tavis Campbell Nicole Letourneau & the APrON study Team
Trainees & Assistants Codie Rouleau Diego Padilla Ontanon Tiffany Haig Julia Poole Amy Hampson