Curt A. Sandman

picture of Curt A. Sandman

Professor Emeritus, Psychiatry & Human Behavior
School of Medicine

PH.D., Louisiana State University

Phone: (714) 940-1924
Fax: (714) 940-1939

University of California, Irvine
SUITE 1200
ORANGE, CA 92868
Research Interests
Current research is in the following areas: Perinatal stress as related to birth outcome
Academic Distinctions
Positions and Employment
1971-1974 Assistant Professor of Psychology, Ohio State University
1974-1978 Associate Professor of Psychology, Ohio State University
1978-1979 Professor of Psychology, Ohio State University
1979-2009 Director of Research, Program Psychologist, Fairview Developmental Center, Costa Mesa, CA
1979-2009 Professor-in-Residence, Psychobiology, University of California, Irvine (UCI)
1979-2009 Professor, Department of Psychiatry and Human Behavior, UCI
1984-2009 Vice-Chair, Department of Psychiatry and Human Behavior, UCI
2001-2007 Director, Applied Neurobehavioral Research Institute, State of California
2009-Present Professor Emeritus, Department of Psychiatry and Human Behavior, UCI

Partial List of Honors
1984 Stallone Foundation Award for studies in Autism
1986 MacArthur Foundation Network; Invited member
1991 IBM/Psychological Corporation THINKable award
1998 Nightingale Research Foundation Cambridge Faculty (Great Britain) award
1999 Decennial Award, Winter Neuropeptide Conference
1998 International Consensus Panel on Psychoactive Drugs; Chair, section on Opiate Blockers
1998 National Institutes of Mental Health, Chair, conference on dual diagnosis
1992 Fellow, International Society of Psychophysiology
1999 Fellow, International Neuropeptide Society
1990-2010 Study Sections and site visitor for NIA, NIMH, NIDA and
NICHD: Chair, BBBP6 Study Section, National Institutes of Health
2000 National Institute of Child Health and Development;Leader, Workshop on Fetal Behavioral Development
2003 American Association of Mental Retardation Distinguished Scientific Discovery Award for studies of biological basis of mental retardation
Research Abstract
In a series of studies in animal models, I have reported that in utero exposure of rats to peptide fragments permanently altered behavior and brain structure. Because these studies indicated that naturally occurring molecules had profound effects on the developing fetus, a series of studies during human pregnancy were initiated. During the past twenty-one years and continuing, I have been Principal Investigator for a series of NIH-funded studies that examined the effects of prenatal stress and activation of the HPA/placental axis on birth outcomes, the human fetus and the developing child. The findings from my projects that include over 800 women, contribute to the growing acceptance that maternal stress is a risk factor for poor outcomes in offspring. Studies from my group were among the earliest to confirm that a major stress peptide (CRH) was released from the placenta in increasing concentrations as pregnancy advanced toward term and played a significant role in parturition and in child developmental outcomes. Among the most significant findings are our recent reports that human fetal exposure to elevated signals of behavioral and biological maternal stress is associated with decreased cortical and subcortical volume in children at 6-9 years of age. The conclusion of our studies is that the human fetus plays an active role in its own development as it prepares for life after birth. Our studies are highly cited and make a major contribution to the Fetal Programming or Developmental Origins of Health and Disease (DOoHD) literature.

Buss, C., Davis, EP, Shahbaba, B, Pruessner, JC, Head, K, & Sandman, CA. Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems. Proceedings of the National Academy of Sciences, 2012, 109, E1312-1319.

Baram, TZ, Davis, EP, Obenaus, A, Sandman, CA, Small, S, Solodkin, A & Stern, H. Fragmentation and unpredictability of early-life xperience in mental disorders. American Journal of Psychiatry, 2012, 169, 907-915. PMID 22885631.

Sandman, CA & Davis, EP. Neurobehavioral risk is associated with gestational exposure to stress hormones. Expert Review of endocrinology & Metabolism, 2012, 7, 445-459.

Sandman, CA, Glynn, LM, & Davis EP. Is there a viability-vulnerability tradeoff? Sex differences in fetal programming. Journal of Psychosomatic Research, 2013, 75, 327-335.

Davis, EP., Sandman, CA., Buss, C., Wing, DA., & Head, K. Fetal glucocorticoid exposure is associated with preadolescent brain development. Biological Psychiatry, 2013, 74, 647-655.

Glynn LM & Sandman CA. Evaluation of the association between placental corticotrophin-releasing hormone and postpartum depressive symptoms. Psychosomatic Medicine, 2014, 76(5):355-362.

Sandman, CA, Head, K., Muftuler, LT., Su, L., Buss, C., & Davis, EP. Shape of the basal ganglia in preadolescent children is associated with cognitive performance. NeuroImage, 2014, 99, 93-102.

Kim, D-J, Davis, EP, Sandman, CA, Sporns, O., O'Donnell, BF, Buss, C., & Hetrick, WP. Longer gestation is associated with more efficient brain networks in preadolescent children. NeuroImage, 2014, 100, 619-627.

Sandman CA, Glynn LM, & Davis EP. Neurobehavioral consequences of fetal exposure to gestational stress. In: Kisilevsky BS, Reissland N, Eds. Fetal Development: Research on Brain and Behavior, Environmental Influences and Emerging Technologies. 2016, pp 229-265. Springer, New York, NY: ISBN: 978-3-319-22023-9

Sandman, CA, Class, QA, Glynn, LM & Davis, EP. Neurobehavioral disorders and Developmental Origins of Health and Disease. In CS Rosenfeld (Ed) The Epigenome and Developmental Origins of Health and Disease. Academic Press/Elsevier, Waltham, MA, 2015. pp 235-266 ISBN: 978-0-12-801383-0 doi:10.1016/B978-0-12-801383-0.12001-8

Sandman, CA. Mysteries of the human fetus revealed. Child Development, 2015, SEP 80(3), 124-137.

Sandman, CA. Prenatal Development. In (Miller, H, Ed) The SAGE Encyclopedia of Theory in Psychology. in press.

Sandman, CA. Fetal exposure to placental corticotropic-releasing hormone (pCRH) programs developmental trajectories. Peptides, 2015, 72, 145-153

Sandman, CA, Buss, C, Head, K, & Davis, EP. Fetal exposure to maternal depressive symptoms is associated with cortical thickness in late childhood. Biological Psychiatry, 2015, 77, 234-334 NIHMS613398.

Kim, D-J, Davis, EP, Sandman, CA , Sporns, O., O'Donnell, BF, Buss, C, & Hetrick, WP. Children's intellectual ability is associated with structural network integrity. NeuroImage, 2016, 124, 550-556.

Fox, M., Sandman, CA, Davis, EP. &Glynn, LM. Intra-individual consistency in endocrine profiles across successive pregnancies. Journal of Clinical Endocrinology and Metabolism, in press doi: 10.1210/jc.2015-2620

319. Howland, MA, Sandman, CA, Glynn, LM, Crippen, C & Davis, EP. Fetal exposure to placental corticotropin-releasing hormone is associated with child self-reported Internalizing Symptoms. Psychoneuroendocrinology, 2016, 67, 10-17.

Schoemaker, D., Buss, C, Head, K, Sandman, CA, Davis, EP, Chakravarty, MM, Gauthier, S, Pruessner, JC. Hippocampus and amygdala volumes from magnetic resonance images in children: Assessing accuracy of FreeSurfer and FSL against manual segmentation. NeuroImage, 2016, 129, 1-14
R01/HD65823 Davis (PI) 2010-2015 NIH/NICHD; Role: Co-Investigator Vulnerability to Prenatal Glucocorticoids Programs Infant Development Primary aim is to determine the influence of administration of betamethasone in women at risk for preterm delivery on placental CRH, gestational age at birth and infant outcomes.
P50/MH096889 2013-2018 NIMH Role: Project 2 Principal Investigator Influence of Fragmented early life exposures on emotional and cognitive vulnerabilities Primary aim of this Conte Center is to examine the influence of fetal exposure to inconsistent or fragmented maternal signals on emotional and cognitive development in animal and human models.
RECENTLY COMPLETED R01/HD051852 Sandman (PI) 07/06-06/12 NIH/NICHD; Role: PI Fetal Programming of Early Development Primary aim of this study is to examine the developmental outcomes of children who were exposed to prenatal biological and psychosocial stress. Emotional regulation, cognition, anatomy of brain structures, and HPA axis regulation are measured in children who have an extensive history of prenatal stress exposure.
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