Suchergebnisse

AbstractThe origins of top‐down self‐regulation are attributed to genetic and socialization factors as evidenced by high heritability estimates from twin studies and the influential role of parenting. However, recent evidence suggests that parenting behavior itself is affected by parents' own top‐down self‐regulation. Because children's top‐down self‐regulation is influenced by genetic factors and parenting is influenced by top‐down self‐regulation, the effects of parenting on children's top‐down self‐regulation identified in prior studies may partially reflect passive gene–environment correlation. The goal of this study was to examine parenting influences on children's top‐down self‐regulation using a longitudinal, adoption‐at‐birth design, a method of identifying parenting influences that are independent of the role of shared genetic influences on children's characteristics because adoptive parents are genetically unrelated to their adopted child. Participants (N = 361) included adoptive families and biological mothers of adopted children. Adoptive mothers' and fathers' harsh/negative parenting were assessed when children were 27 months of age and biological mothers' top‐down self‐regulation was assessed when children were 54 months of age. Adopted children's top‐down self‐regulation was assessed when they were 54 and 72 months of age. Results, accounting for child gender, biological mother top‐down self‐regulation, and the potential evocative effects of adopted child anger, provide evidence that inherited influences and socialization processes uniquely contribute to children's top‐down self‐regulation. Furthermore, findings demonstrate the importance of both mother's and father's parenting behavior as an influence on young children's top‐down self‐regulation. The implications of these findings for understanding the complex mechanisms that influence children's top‐down self‐regulation are discussed.

AbstractLittle consideration has been given to the possibility of human infant development being shaped via lactocrine programming, and by breast milk cortisol levels specifically. Despite animal models indicating that glucocorticoid (GC) exposure via lactation might modify brain development and behavior, only one study has reported that milk cortisol levels were positively associated with infant negative affectivity, especially fearfulness and sadness—early emerging risk factors for internalizing difficulties such as anxiety. The aim of the current study was to investigate whether human milk cortisol is associated with mother‐reported fearfulness and experimentally induced infant fear reactivity. Mother‐infant dyads (n = 65) enrolled in the FinnBrain Cohort Study participated. Breast milk samples were obtained 2.5 months postpartum, and milk cortisol concentrations were ascertained using validated luminescence immunoassay methodology. Infant fear reactivity was assessed using maternal reports 6 months postpartum and in a laboratory 8 months postpartum. There was a significant interaction between infant sex and milk cortisol such that higher milk cortisol was related to higher infant fear reactivity in a laboratory setting in girls (β = 0.36, p = .04) but not in boys (β = −0.15, p = .40). Milk cortisol was not associated with mother‐reported infant fearfulness. Results suggest that higher human milk cortisol concentrations are associated with elevated experimentally induced fear in infancy. Findings support lactocrine programming, and suggest that mothers may "communicate" vital information about stressful environments via cortisol contained in breast milk, shaping girls' early emotional reactivity.