Critical Reflection

72 Abstracts / Psychoneuroendocrinology 83S (2017) 1–89

Symposium 19: The impact of prenatal and postnatal stress in childhood on hypothalamic-pituitary-adrenal function, proinflammatory markers, and mental health in adolescence and adulthood Time: Saturday, 09/Sep/2017: 10:30 am–12:00 pm Session Chair: Mark A. Ellenbogen

A 10-year longitudinal study of cumulative stress in childhood, the cortisol response at awakening, and depressive symptoms in the offspring of parents with bipolar disorder

Mark A. Ellenbogen 1,∗, Claire-Dominique Walker 2, Sheilagh Hodgins 3

1 Centre for Research in Human Development, Concordia University, Canada 2 Douglas Mental Health University Institute and McGill University, Canada 3 Department of Psychiatry, Université de Montréal, Canada E-mail address: [email protected] (M.A. Ellenbogen).

Background: The offspring of parents with bipolar disorder (OBD), relative to control offspring, are at high risk for developing affective disorders and have elevated daytime cortisol levels. It is possible that these changes to the hypothalamic-pituitary-adrenal (HPA) axis in the OBD occur in response to prenatal and postnatal stress and adversity in the environment. According to the cumu- lative stress hypothesis, stress-sensitive physiological systems are altered by exposure to multiple adversities, irrespective of the type. We tested whether cumulative stress exposure in childhood medi- ates the relationship between risk status (having a parent with bipolar disorder) and the cortisol response following awakening (CAR) in young adulthood. We also tested whether an elevated CAR response in the OBD was related to the development of depressive symptoms.

Methods: The sample (19.3 ± 3.4 years) consisted of 58 OBD and 60 offspring of parents with no affective disorder (controls). Cumu- lative stress was measured as an index of exposure to obstetric complications and other stress-related risk factors in parents.

Results: Bootstrapping analyses revealed that the cumulative stress in childhood significantly mediated the relationship between risk status and an elevated CAR in young adulthood (CI: 0.02–0.22). A sequential multiple mediation model demonstrated significant pathways from risk status to cumulative stress, from cumulative stress to an elevated CAR, and from an elevated CAR to depressive symptoms in young adulthood (CI: 0.01–0.18).

Conclusions: These findings highlight the role of cumulative stress as a putative mechanism leading to the development of affec- tive disorders through HPA dysfunction.

http://dx.doi.org/10.1016/j.psyneuen.2017.07.432

Prenatal maternal stress predicts cortisol stress response and child behavior problems at ages 4 and 13: Project Ice Storm

Suzanne King 1,2,∗, Erin Yong Ping 3, Guillaume Elgbeili 2, David P. Laplante 2

1 McGill University, Canada 2 Douglas Mental Health University Institute, Canada 3 Concordia University, Canada E-mail address: [email protected] (S. King).

Background: Studying associations between prenatal maternal stress (PNMS) and the hypothalamic-pituitary-adrenal (HPA) axis in humans is problematic given ethical constraints against assign- ing stressors to pregnant women. Yet, it is important to increase understanding of the fetal origins of HPA axis development in children, and subsequent links to mental health. Natural disasters provide varying degrees of hardship to the population, often in quasi-random ways.

Method: In June 1998 we recruited women who were pregnant during the January 1998 Quebec Ice Storm and assessed their objec- tive exposure and their subjective distress (PTSD symptoms). When their children were 4 years old (n = 34) we sampled salivary cortisol before and after vaccination, and at age 13 (n = 45) before and after the Trier Social Stress Test. Mothers rated their children’s behavior problems with the Child Behavior Checklist (CBCL).

Results: At age 4, objective and subjective PNMS interacted to explain variance in cortisol: the lowest cortisol response was in children of mothers who were either over-reactors or under- reactors to their objective exposure. Lower cortisol and higher subjective PNMS explained greater internalizing (R2 = .30) and externalizing (R2 = .34) problems. At age 13, greater objective exposure predicted higher acute cortisol response. More severe externalizing problems were associated with more severe subjec- tive PNMS and lower acute cortisol response (R2 = .21); associations were not significant for internalizing problems.

Conclusions: Different aspects of PNMS predict child HPA axis in different ways at different ages, and failure to mount an HPA axis response predicts more severe behavior problems in childhood and adolescence.

http://dx.doi.org/10.1016/j.psyneuen.2017.07.433

Interaction of childhood maltreatment and polymorphisms of the FKBP5 gene on the cortisol response to stress in adolescents

Raegan Mazurka 1,∗, Katherine E. Wynne-Edwards 2, Kate L. Harkness 1

1 Queen’s University, Canada 2 University of Calgary, Canada E-mail address: [email protected] (R. Mazurka).

Background: Childhood maltreatment is associated with increased risk for psychopathology as well as differences in the neurobiological stress response. An additional factor associated with neuroendocrine functioning and increased psychopathology risk is polymorphisms within the FKBP5 gene. In this preliminary investigation, we examined the gene-environment interaction of childhood maltreatment and variation in the FKBP5 gene on the cortisol response to the Trier Social Stress Test.

Methods: Our sample consisted of 90 depressed and non- depressed adolescents (11–21 years). We assessed HPA axis function by measuring salivary cortisol over the Trier Social Stress