Background Early life experiences have persisting influence on brain function throughout life. Maternal signals constitute a primary source of early life experiences, and their quantity and quality during sensitive developmental periods exert enduring effects on cognitive function and emotional and social behaviors. Here we examined if, in addition to established qualitative dimensions of maternal behavior during her interactions with her infant and child, patterns of maternal signals may contribute to the maturation of children's executive functions. We focused primarily on effortful control, a potent predictor of mental health outcomes later in life. Methods In two independent prospective cohorts in Turku, Finland ( N = 135), and Irvine, CA, USA ( N = 192) that differed significantly in race/ethnicity and sociodemographic parameters, we assessed whether infant exposure to unpredictable patterns of maternal-derived sensory signals portended poor effortful control. Outcomes In both the Irvine and Turku cohorts, unpredictable sequences of maternal behavior during infancy were associated with worse effortful control at one year of age. Longitudinal analyses demonstrated that this association persisted for as long as each cohort was assessed-until two years of age in the Turku cohort and to 9.5 years in the Irvine cohort. The relation of unpredictable maternal signals during infancy and the measures of executive function persisted after adjusting for covariates. Interpretations The consistency of our findings across two cohorts from different demographic backgrounds substantiated the finding that patterns, and specifically unpredictable sequences, of maternal behaviors may influence the development of executive functions which may be associated with vulnerability to subsequent psychopathology. Fund This research was supported by the National Institutes of Health (NIH) awards P50MH096889, HD051852, NS041298, HD02413, HD050662, HD065823, and by the FinnBrain funders: Academy of Finland (129839, 134950, 253270, 286829, 287908, 308176, 308252), Jane and Aatos Erkko Foundation, Signe and Ane Gyllenberg Foundation, Yrjö Jahnsson Foundation, and State Research Grants (P3498, P3654).

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Little 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.

Maternal prenatal symptoms of depression and anxiety have been suggested to impose differential effects on later offspring development, depending on their characteristics, such as timing, intensity and persistence. Paternal symptoms have been less investigated. While knowledge on these trajectory characteristics is essential for improved comprehension of prenatal stress, prospective studies including both expecting parents have been scarce. We aim at identifying and comparing the trajectories of prenatal depressive and anxiety symptoms in both parents in a pregnancy cohort design. The sample included 3202 mothers and 2076 fathers who were recruited to the FinnBrain Birth Cohort study (www.finnbrain.fi). Depressive symptoms were assessed using the Edinburgh Postnatal Depression Scale (EPDS) and general anxiety by the anxiety scale of the Symptom Checklist -90 (SCL-90) repeatedly at 14, 24, and 34 gestational weeks. Five differential depressive and four anxiety symptom trajectories were identified across pregnancy both in mothers and in fathers. The trajectories of consistently low depressive or anxiety symptoms were associated with higher educational level in both parents, and with nulliparity and non-smoking during pregnancy in mothers. Parents with consistently high or increasing levels of symptoms had more often prenatal SSRI medication. The congruences between elevated depressive and anxiety symptoms at any point in pregnancy, as well as parental trajectories within families were low. However, in this population-based sample, the self-reported symptom levels of both parents were generally very low. Variance in timing and persistence of parent-reported prenatal depressive and anxiety symptoms is potentially important, while symptom trajectories are very similar in mothers and fathers. These differential symptom trajectories and the significance of their correlates should be acknowledged when studying prenatal stress exposures and the related outcomes in children.