Sex Differences in Infant Cortisol Reactivity Following Prenatal Intimate Partner Violence Exposure

• In Event: Poster Session 03
  In Poster Session: PS 03 Topic - Biological Processes: Psychophysiology

Abstract

Hypothalamic-pituitary-adrenal (HPA) axis plays a significant role in the development of numerous childhood psychological disorders (see Lupien et al., 2009 for review). Early life stress, including stress occurring during the prenatal period, can alter HPA function and increase the likelihood of later child psychopathology (Brennan et. al., 2008; Grant et al., 2009; Martinez-Torteya et al., 2017). Specifically, recent research has demonstrated an association between prenatal exposure to intimate partner violence (IPV) and infant cortisol reactivity (Levendosky et al., 2016); however, it remains unclear if the relationship between prenatal IPV and cortisol reactivity is affected by infant sex. Previous studies of prenatal exposure to teratogens and other life stress, other than IPV, suggest sex specific HPA functioning (Eiden et al., 2009; 2015; Hollanders et al., 2017; Schuetze et al., 2008). For boys, prenatal exposure to adverse circumstances predicts cortisol reactivity, while girls appear comparatively unaffected (e.g., Eiden et. al., 2009; 2015; Schuetze et al., 2008). Thus, we hypothesized that exposure to high levels of IPV would positively predict cortisol response for boys only. Methods. Mother-infant dyads (n = 182, infant males = 74, age = 11.83 months) were recruited from 3 major midwestern metropolitan areas. After consenting, mothers and infants completed an assessment battery including an infant stress task and a retrospective measure of both prenatal and postnatal IPV. To control for maternal stress (in addition to IPV), a cumulative risk measure was created. Infant saliva, assayed for cortisol, was collected at baseline, 5, 20, and 40 minutes following the stress task and cortisol reactivity was indexed by area under the curve with respect to increase. Results. Regression analyses indicated a significant interaction (see Table 1). Contrary to our hypotheses, prenatal IPV positively predicted girls’ cortisol responses, but negatively predicted boys’ responses. That is, girls who experienced high levels of prenatal IPV had greater cortisol reactivity to a laboratory stressor while boys showed a blunted response. (See Figure 1). Discussion. Our findings were contradictory to prior research. This might be explained by the uniqueness of IPV as a form of prenatal stress relative to teratogen exposure examined in previous research. That is, IPV represents a physical and psychological form of stress, while teratogens constitute a pharmacological stressor. In this light, it may be that the type of prenatal stress uniquely affects infant HPA axes. Additionally, as cortisol reactivity is known to vary in intensity over early development (Davis & Granger, 2009), and previous studies recruited infants who were 7 and 9 months old, it may be that the different pattern of cortisol reactivity present in our 12 month old infants is a result of age specific HPA functioning. Future research should consider how specific forms of prenatal stress may interact with both infant age and infant sex to produce unique patterns of cortisol reactivity across the early years of a child’s life.

Authors

• William David Eckerle, Michigan State University
  Presenting Author

• Joseph S. Lonstein, Michigan State University
  Non-Presenting Author

• Amy K. Nuttall, Michigan State University
  Non-Presenting Author

• G. Anne Bogat, Michigan State University
  Non-Presenting Author

• Alytia Akiko Levendosky, Michigan State University
  Non-Presenting Author