Risky Shifts: How the Timing and Course of Mothers' Depressive Symptoms Across the Perinatal Period Shape Their Own and Infant's Stress Response Profiles  

Oleh:

Laurent, Heidemarie K. ; Ablow, Jennifer C. ; Measelle, Jeffrey

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Development and Psychopathology vol. 23 no. 2 (May 2011), page 521-538.
Topik: Maternal Perinatal Depressive Symptoms; Mother–infant Hypothalamic–pituitary–drenal (HPA); Cortisol; Stress; Dysregulation

Ketersediaan

Perpustakaan Pusat (Semanggi) Nomor Panggil: DD21.20 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

We investigated the effects of timing and the course of maternal perinatal depressive symptoms on mother–infant hypothalamic–pituitary–adrenal (HPA) response profiles during an attachment stressor, as well as on within-dyad synchrony of stress profiles: coordination of HPA and sympathetic nervous system and infant–mother HPA attunement. Mothers (n = 86) completed the Center for Epidemiological Studies Depression Scale during pregnancy (Time 1 [T1]) and at 5 months (T2) and 18 months (T3) postnatal. At T3 mother–infant dyads completed the Strange Situation, and four saliva samples collected from both mothers and infants were assayed for cortisol and a-amylase. Hierarchical linear modeling was used to predict mother–infant cortisol response trajectories and within-dyad synchronies by main and interactive effects of T1–T3 Center for Epidemiological Studies Depression Scale scores. Main effects of earlier (T1, T2) depressive symptoms predicted mothers' cortisol trajectories and coordination, and interactions of T1 with postnatal (T2 and T3) symptoms predicted infants' cortisol trajectories, coordination, and attunement. Decomposition of interactions revealed more marked effects on infant cortisol trajectories when the mother shifted from higher to lower depressive symptoms (or vice versa) across the perinatal period. Shifts from lower to higher symptoms also predicted inverse coordination of cortisol with salivary a-amylase and greater attunement of infant with mother cortisol. Implications for the development and transmission of stress dysregulation are discussed.

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