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Introduction: The fetal programming hypothesis suggests that high exposure to prenatal maternal stress and anxiety affects an infant’s developmental trajectory, potentially increasing vulnerability to later psychopathology (Glover, 2011). One way to measure whether children are affected by maternal anxiety is through indicators such as sympathetic nervous system functioning at rest and in response to stress measured by electrodermal activity (EDA; Borelli et al., 2015). Little is known about the pathways through which a mother’s anxiety affects her infant’s physiological response systems. The purpose of this study was to examine prenatal patterns of self-reported maternal trait anxiety on infant EDA measured 7 months postpartum.
Hypothesis: High levels of prenatal maternal anxiety will be associated with higher infant EDA baseline at 7 months as well as higher electrodermal reactivity to stress, above and beyond maternal anxiety at 7 months.
Study population: Pregnant mothers participated in a NIMH-funded study whose purpose was to understand the effects of maternal prenatal stress and emotion dysregulation on their infants postpartum. Sixty-six mother-infant dyads (38 male infants) participated in lab visits prenatally and 7 months after birth. Mean household income fell in the range of $40,000-$49,999 annually, and 82.5% of mothers identified as non-Hispanic Caucasian.
Method: Mothers reported their trait anxiety via the State/Trait Anxiety Inventory-Trait (STAI-T) questionnaire (Spielberger et al., 1983) at prenatal and 7 months postpartum visits. Also at 7 months, participants watched a two-minute Baby Einstein clip to capture baseline autonomic functioning and participated in the Haley and Stansbury still-face paradigm (Haley & Stansbury, 2003), comprised of 2-minute segments beginning with regular play, then alternating between still-face and recovery segments twice. During still-face episodes, mothers were asked to maintain a flat affect and refrain from infant interaction, and during recovery periods the dyads played normally. EDA data was gathered in the form of non-specific skin conductance responses in 30-second epochs throughout the visit. EDA reactivity scores were calculated as EDAstill-face episode (1 or 2) – EDAbaseline. Therefore, positive reactivity scores indicate an increase in sympathetic nervous system activity from baseline to task.
Results: Covariates examined include infant sex, maternal race and ethnicity, household income, maternal education, and maternal age. Significant partial correlations were found when controlling for household income and maternal race in relation to EDA reactivity and STAI-T score (see Table 1). We examined the bivariate correlations between both prenatal and 7-month STAI-T scores, and baseline EDA responses as well as EDA reactivity to the first and second still-face episodes. Significant correlations were found between prenatal maternal anxiety and infant baseline EDA response (r = .286, p < .05); EDA reactivity to the first still-face (r =-.419, p < .01); and EDA reactivity to the second still-face (r =-.365, p < .05). There were no significant relations between 7-month maternal anxiety and infant EDA. In other words, infants exposed to prenatal maternal anxiety show heightened baseline sympathetic nervous system functioning, and attenuated reactivity under stress above and beyond the effects of exposure to concurrent levels of maternal anxiety (t(30) = -2.24, p < .05).
Dylan Neff, University of Utah Department of Psychology
Presenting Author
Mindy Brown, University of Utah
Non-Presenting Author
Sarah Terrell, University of Utah
Non-Presenting Author
Brendan Ostlund, University of Utah
Non-Presenting Author
Parisa Kaliush, University of Utah
Non-Presenting Author
Robert Dennis Vlisides-Henry, University of Utah
Non-Presenting Author
Sheila Crowell, University of Utah
Non-Presenting Author
Elisabeth Conradt, University of Utah
Non-Presenting Author