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Poster #21 - Infant and Mother Cortisol Responses to the Still-Face Procedure

Sat, March 23, 12:45 to 2:00pm, Baltimore Convention Center, Floor: Level 1, Exhibit Hall B

Integrative Statement

Functioning of the hypothalamic-pituitary-adrenal (HPA) axis, a biological stress response system, is associated with a range of health outcomes (McEwen, 2013). The HPA axis develops rapidly in the first year of life (Jansen et al., 2010). Through interactions with their caregivers, infants learn to regulate their stress responses—a process that may be associated with infant–caregiver bio-behavioral synchrony (Atzil & Gendron, 2017). Infant bio-behavioral responses to socioemotional stress are commonly assessed using the Still Face Procedure (SFP), a laboratory-based parent–child interaction that challenges dyadic communication (Tronick et al., 1978). However, research examining whether exposure to the SFP evokes HPA-axis reactivity in infants has yielded inconsistent findings (Provenzi et al., 2016); moreover, few studies have considered concordance in caregiver–infant physiological responses to this stressor. In the present study, we investigated infant and mother cortisol reactivity to the SFP and analyzed the degree of synchrony between their cortisol responses.

A socio-economically diverse sample (annual income = $15,001-$30,000 to more than $150,000; 25% low-income) consisting of ninety-six 6-month-old infants (mean age = 6.13 [0.45] months) and their mothers (mean age=33.81 [4.77] years) completed the repeated SFP (Haley & Stansbury, 2003). Up to five saliva samples were collected from infants to assess cortisol responses to the SFP. A subset of 50 mothers provided saliva samples contemporaneous with those of their infants. We used latent class mixture modeling to identify trajectories of infant cortisol reactivity to the SFP.

A model with two latent class trajectories of infant cortisol reactivity to the SFP provided the best fit for the data (mean posterior probabilities: trajectory 1=.95, trajectory 2=.85). The first trajectory, comprising 75% of the sample, was characterized by significant decreases in cortisol (B=-0.02, SE=.01, Wald=-3.20, p=.001). The second trajectory, comprising 25% of the sample, was characterized by significant increases in cortisol (B=-0.02, SE=.05 Wald=5.29, p<.001; see Figure 1). Infants in the two classes did not differ in cortisol levels at arrival to laboratory or immediately prior to the SFP; however, infants in the increasing trajectory evidenced significantly higher total cortisol production, quantified by area under the curve relative to ground (AUCg), compared to infants in the decreasing trajectory (t(74)=5.07, p<.001). On average, mothers had significantly decreasing cortisol secretion in response to the SFP (B=-.05, SE=.03, t(47.65)=-4.37, p<.001). Although infant cortisol trajectories were not associated with maternal cortisol reactivity to the SFP, infant AUCg was significantly positively associated with maternal AUCg (r(41)=.312, p=.041); in fact, maternal and infant cortisol levels tended to be positively associated at each sampling occasion (rs=.109-.308; Figure 2). There was no linear effect of time across the session on cortisol concordance.

Our findings suggest that only a minority of infants exhibit a heightened cortisol response to the SFP, and that, on average, mothers do not show such a response. However, irrespective of their reactivity patterns, mothers’ and infants’ levels of cortisol production were correlated across sampling occasions, indicating synchronous HPA-axis functioning. In future analyses, we will examine predictors and outcomes associated with trajectories of infant cortisol reactivity to the SFP.

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