90. Second Generation Effects of Trauma: Evidence for Developmental Programming

90. Second Generation Effects of Trauma: Evidence for Developmental Programming

Biological Psychiatry Thursday Abstracts prenatal psychological distress by the 3rd trimester (β 5 .25, p 5 .010). Conclusions: The interaction betw...

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Biological Psychiatry

Thursday Abstracts

prenatal psychological distress by the 3rd trimester (β 5 .25, p 5 .010). Conclusions: The interaction between psychological distress and sleep quality during pregnancy is not necessarily fixed. By using a woman’s personal history to inform her prenatal care, she can receive more targeted interventions. Supported By: R01 NIMH Keywords: ACE, trauma, sleep, depression, pregnancy

90. Second Generation Effects of Trauma: Evidence for Developmental Programming Rachel Yehuda1, Linda M Bierer2, Heather N Bader2, Nikolaos P Daskalakis3, Torsten Klengel4, and Elisabeth Binder5 Mount Sinai School of Medicine/JJP VA, 2James J. Peters Veterans Administration Medical Center Bronx/Icahn School of Medicine at Mount Sinai, 3Mount Sinai School of Medicine, 4Harvard University, 5Max-Planck Institute of Psychiatry 1

Background: Developmental programming is known to mediate some effects of trauma exposure in childhood, and may be critical to the appearance of intergenerational trauma effects. The data shown will support the idea that effects of a preconception trauma on offspring functional and molecular biology may differ based on parental gender and age at the time of exposure. Methods: Two studies were conducted in Holocaust offspring and Jewish controls. In the first, 24-hr urinary cortisol and 11β-hydroxysteroid dehydrogenase-2 (11β-HSD2) activity were determined using GCMS; for the second, lymphocyte FKBP5 methylation was assessed by pyrosequencing. Results: Reduced cortisol excretion (p 5 .046) and elevated 11β-HSD-2 activity (p 5 .008) were observed in offspring compared to controls, particularly among those whose mothers had been children during World War II (p 5 .029). In the second study, FKBP5 methylation at intron 7, site 6 was higher among females than males (F(1,93) 5 14.76 p,.0005), and lower in Holocaust offspring than controls (F (1,93) 5 4.655, p 5 .034, controlling for gender). There was a significant effect of age of maternal exposure (F(3,70) 5 5.776, p 5 .001, controlling for gender and age of paternal exposure) that was based on reduced methylation in offspring with maternal exposure in childhood (p 5 .005). There were no significant associations of FKBP5 methylation with age of paternal exposure. Conclusions: These data demonstrate specific associations between preconception parental trauma and offspring neuroendocrine and molecular glucocorticoid regulation, and point to childhood maternal exposure as a critical determinant of intergenerational transmission. The results complement observations from previous work and are consistent with the influence of glucocorticoid programming. Supported By: NIMH (1RC1MH088101-01) “Identification of an Epigenetic Risk Marker for PTSD”; NIMH (R01 MH 6467501) “Biology of Risk and PTSD in Holocaust Survivor Offspring”

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Keywords: intergenerational, Trauma Exposure, developmental programming, DNA methylation, FKBP5

91. Maternal Early Life Adversity: Impact on Offspring Stress Responsiveness Cynthia Epperson, Kathleen Morrison, Liisa V. Hantsoo, Grace Ewing, Jessica Podcasy, Mary D. Sammel, and Tracy L. Bale University of Pennsylvania Background: One mechanism by which maternal childhood adversity may impact offspring development is through programming of the maternal and infant hypothalamic pituitary adrenal axis (HPA-A). Methods: Maternal psychophysiologic response to a mild stressor was assessed twice during pregnancy (n 5 90) and once at 6 weeks postpartum. One-third of women reported experiencing at least two adverse childhood experiences before the age of 18 and were considered the High ACE Group, while those with zero or one ACE formed the Low ACE Group. Finally mother-infant pairs underwent a separation stressor and the infants a restraint and noise stressor at 6 months of age. Salivary cortisol was collected across each procedure from both mothers and infants according to previously published methods. Cortisol levels were log transformed and repeated measures mixed-model ANOVA was performed to evaluate ACE category and time as predictors of cortisol change-from-baseline, controlling for race as a confounder. Results: ACE category predicted log-transformed cortisol change-from-baseline (P , 0.05), with High ACE women, on average, experiencing a 50% lower cortisol response to the infant separation paradigm than did low ACE women. Infants of High ACE mothers also demonstrated lower cortisol response to restraint and noise stress (with no difference by sex). Maternal stress response during pregnancy will be discussed in relationship to infant response postpartum. Conclusions: Maternal early life stress contributes to altered cortisol response to an ecologically relevant postpartum stressor, namely separation from the offspring, that is then mirrored in the offspring during their stress exposure. To date, findings are similar in male and female infants. Supported By: R01 MH099910 Keywords: Early Life Stress, Pregnancy, offspring, HPA Function, prenatal maternal stress

92. Sex Differences in Resting State Functional Connectivity (rs-FC) of Limbic Circuits in PTSD Liat Helpman1, Zhu Xi2, Benjamin Suarez-Jimenez3, Amit Lazarov3, and Yuval Neria3 Columbia University Medical Center, 2NYSPI and Columbia University, 3Columbia University 1

Background: Women are at twofold risk of posttraumatic stress disorder (PTSD) following trauma than men. Studies of sex differences have been mostly epidemiological, few examining neural mechanisms despite literature identifying

Biological Psychiatry May 15, 2017; 81:S1–S139 www.sobp.org/journal