Search
Program Calendar
Browse By Day
Browse By Time
Browse By Panel
Browse By Session Type
Browse By Topic Area
Search Tips
Virtual Exhibit Hall
Personal Schedule
Sign In
X (Twitter)
There is compelling evidence that children exposed to high levels of prenatal stress are at high risk for a host of adverse health outcomes (Kim, Bale, Epperson, 2015; Stein, Pearson, Goodman, Rapa, Rahman, McCallum, et al., 2014). Prenatal maternal stress (PNMS) increases fetal exposure to stress biomarkers (e.g., cortisol and pro-inflammatory cytokines) and may alter the development of critical biological systems (e.g., the endocrine, immune, and nervous systems) (Beijers, Buitelaar, de Weerth, 2014; Coussons-Read, 2013), thus “programming” fetal development. This confers lasting susceptibility to health complications in the child (Accortt, Cheadle, Dunkel & Schetter, 2015) and potentially transgenerational risks through epigenetic programming (Cao-Lei, de Rooij, King, Matthews, Metz, Rosebloom, et al., 2017). Whereasile previous work has established connections between prenatal maternal stress and maladaptive child outcomes, more recent work is beginning to examine moderators such as timing of exposure and differences in outcomes based on fetal sex. It has been suggested that there may be evidence that not only do offspring outcomes differ by child sex, but the process of fetal programming is likely so sexually dimorphic that female and male development should be considered uniquely when investigatingexamining risk (Aiken & Ozanne, 2012). The current review examined the recent literature evaluating sex differences in the relation of PNMS to features of children’s psychological and neuropsychological development. Clarifying the nature of sex-dependent PNMS programming may lead to a stronger understanding of lifelong disease processes and facilitate tailored intervention approaches.
Studies published between 01/01/2015 and 12/31/18 listed on the engine PubMED were evaluated for inclusion based on four criteria: measurement of prenatal stress exposure, measurement of offspring psychological or neuropsychological functioning, empirical data published in a refereed journal, and a report of evaluation of sex in analyses. Nineteen studies were identified that met all study criteria. Five studies evaluated associations between PNMS and child neuroendocrine functioning as indicated by cortisol concentrations, with four showing sex-dependent associations. Four papers described epigenetic studies evaluating associations between PNMS and the expression of genes involved in stress and emotion regulation, with three reporting sex-dependent associations. Four papers examined child temperament, all finding evidence of sex-dependent effects. Six studies evaluated broad measures of psychopathology—including symptoms from multiple psychiatric disorders, with five showing evidence of sex-dependent associations. Characteristics of the articles included in the review are presented in Table 1.
Across the studies analyzed, a variety of measurement techniques were used in both the measurement of stress exposure (e.g. biological assay, trauma interview, documented natural disaster) and developmental outcomes (e.g. clinical interview, questionnaires); heterogeneity of measurement and analytic technique were apparent. Additionally, various types of statistical techniques were used to examine potential sex associations (e.g. additive interaction, stratification).
Of the nineteen studies analyzed, sixteen found evidence for sex-dependent associations. Although these associations varied in magnitude and direction across domains, there is sufficient evidence of sex-dependent associations to recommend that researchers consider the potential role of child sex in PNMS programming studies and report descriptive statistics for study outcomes stratified by child biological sex.