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Postnatal infant autonomic regulation may be programmed by prenatal exposure to maternal stress, at least in animal models (Hartman et al., 2018). However, in humans, there are few studies which document direct effects of prenatal maternal stress on infant physiological functioning. This empirical gap suggests that there may be unexamined moderators that could explain why prenatal stress is related to stress response system functioning in some infants but not others. A mother’s history of her own parental bonding may be one such moderator. Gaining a better understanding of how prenatal stress and maternal past parental bonding may affect infant autonomic regulation will help identify specific parenting elements that are amenable to intervention.
It was hypothesized that infants whose mothers have been exposed to higher levels of prenatal stress will be less able to regulate their parasympathetic nervous system, as will be evidenced by higher RSA reactivity. It was also hypothesized that mothers who have a history of secure parental bonding will be less affected by high levels of prenatal stress such that their infants will exhibit lower levels of RSA reactivity when compared to mothers who have a history of low-quality parental bonding and also experience a high level of prenatal stress.
Participants (N = 69) are mothers and their 7-month-old infants recruited from a longitudinal study of prenatal exposure to maternal emotion dysregulation. Pregnant women are recruited from OB/GYN clinics and are 10.3% Hispanic or Latino, 7.7% American Indian or Alaskan native, 15.4% Asian or Pacific Islander, 64% White, and 2.6% Black/African American. Infants are 55% Male, 45% Female. Average maternal age was 28.78 years. A history of the mothers’ own bonding experience with their parents was evaluated by the Parental Bonding Instrument (PBI; Parker, Tupling, & Brown, 1979). Dyads performed the still-face paradigm (SFP) at 7 months (Tronick, Als, Adamson, Wise, & Brazelton, 1978).
The main effects of prenatal acute stress exposure and parental bonding history were not significant (all p’s > .57). There was a significant prenatal acute stress x parental bonding history interaction, b = -.33, p = .03 (Figure 1). The effect of prenatal maternal stress on infant autonomic reactivity at 7 months depended on the mother’s past parental bonding with her own mother. Under conditions of low prenatal stress, mothers with a history of high-quality parental bonding had infants who exhibited more RSA withdrawal to the still-face episode. Mothers with poor-quality parental bonding had infants who showed increases in RSA in response to the still-face, which suggests active attempts at coping. Under conditions of high prenatal stress exposure, infants showed modest increases or decreases in RSA, regardless of their mother’s past parental bonding history. Our future work will consider the effects of maternal sensitivity as it relates to a past history of parental bonding, prenatal stress exposure, and infant stress reactivity during the still-face.