RESUMEN
Parental mental disorders increase the risk for insecure attachment in children. However, the quality of caregiver-infant interaction plays a key role in the development of infant attachment. Dyadic interaction is frequently investigated via global scales which are too rough to uncover micro-temporal mechanisms. Prior research found that the latency to reparation of uncoordinated dyadic states is associated with infant behavioral and neuroendocrine regulation. We investigated the hypothesis that this interactive mechanism is critical in predicting secure vs. insecure attachment quality in infancy. We also assessed the predictive quality of infant attachment regarding neuroendocrine reactivity later in childhood. A subsample of N = 58 dyads (n = 22 mothers with anxiety disorders, n = 36 controls) from a larger study were analyzed. At 3-8 months postpartum, maternal anxiety disorders were diagnosed via a structured clinical interview as well as dyadic interaction during the Face-to-Face-Still-Face (FFSF) was observed and coded on a micro-temporal scale. Infant attachment quality was assessed with the strange situation paradigm at 12-24 months of age. In an overlapping subsample of N = 39 (n = 13 mothers with anxiety disorder; n = 26 controls), we assessed child cortisol reactivity at 5 to 6 years of age. Generalized linear modeling revealed that longer latencies to interactive reparation during the reunion episode of the FFSF as well as maternal diagnosis at 3-8 months of age predict insecure attachment in children aged 12-24 months. Cox regressions demonstrated that dyads with infants who developed insecure attachment at 12-24 months of age were 48% less likely to achieve an interactive reparation at 3-8 months of age. Mixed models revealed that compared to securely attached children, children who had developed an insecure attachment at 12-24 months of age had an increased cortisol reactivity at 5 to 6 years of age during free play. The results confirm the hypothesis that the development of attachment is affected by experienced micro-temporal interactive patterns besides diagnostic categories. They also showed that infants of mothers with postpartum anxiety disorders have a more than fivefold increased risk of developing an insecure attachment than the infants of the control group. Moreover, results imply that these patterns may influence neurohormonal regulation even in preschool aged children.
RESUMEN
BACKGROUND: Each year, almost 35% of children are exposed to maternal depression and more grow up in persistent poverty, increasing the risk for stress-related disease and other socio-developmental deficits later in life. These impacts are likely related to chronic stress via the hypothalamic-pituitary-adrenal (HPA) axis. However, there is little evidence relating early windows of child HPA axis activity to multiple exposures. METHODS: We investigated chronic measures of hair-derived HPA axis hormones (cortisol and dehydroepiandrosterone (DHEA)) in 104 one-year old infants from rural Pakistan and longitudinal measures of maternal depression, intimate partner violence (IPV), socio-economic status (SES), and the home environment. RESULTS: Estimates from adjusted linear mixed effects models did not reveal consistent significant associations between infant cortisol and maternal depression or home adversities. By contrast, infants exposed to maternal depression during pregnancy had lower DHEA levels (ß= -0.18 95% confidence interval [CI]: -0.34, -0.02) as did those whose mothers experienced multiple types of IPV (ß=-4.14 95% CI: -7.42, -0.79) within one year postpartum. Higher SES had a significant positive association with infant DHEA levels (ß= 0.77 95% CI: 0.08, 1.47). Depression severity and chronicity at one year postpartum had near significant associations with infant DHEA. Measures of home environment had no observable impacts on infant HPA axis activity. LIMITATIONS: Limitations include the modest sample size and aggregation of hair samples for analysis. CONCLUSION: Results point to possible early HPA axis dysregulation driven by changes in DHEA activity, but not cortisol at one year of age. Findings contribute to growing research examining intergenerational transmissions of maternal depression, IPV, and household environment on infant stress-response systems.