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Funding Information: This work was financially supported by Academy of Finland (grant no. 328674) (JL), the Dutch Scientific Council (NWO; VI.Veni.191G.025; MH), and the Sara van Dam z.l. Foundation, Royal Netherlands Academy of Arts and Sciences (MH and JL). Publisher Copyright: Copyright © 2022 Turk, Endevelt-Shapira, Feldman, van den Heuvel and Levy. Parent–infant EEG is a novel hyperscanning paradigm to measure social interaction simultaneously in the brains of parents and infants. The number of studies using parent–infant dual-EEG as a theoretical framework to measure brain-to-brain synchrony during interaction is rapidly growing, while the methodology for measuring synchrony is not yet uniform. While adult dual-EEG methodology is quickly improving, open databases, tutorials, and methodological validations for dual-EEG with infants are largely missing. In this practical guide, we provide a step-by-step manual on how to implement and run parent–infant EEG paradigms in a neurodevelopmental laboratory in naturalistic settings (e.g., free interactions). Next, we highlight insights on the variety of choices that can be made during (pre)processing dual-EEG data, including recommendations on interpersonal neural coupling metrics and interpretations of the results. Moreover, we provide an exemplar dataset of two mother–infant dyads during free interactions (“free play”) that may serve as practice material. Instead of providing a critical note, we would like to move the field of parent–infant EEG forward and be transparent about the challenges that come along with the exciting opportunity to study the development of our social brain within the naturalistic context of dual-EEG.

BACKGROUND: Maternal psychological distress during pregnancy is related to adverse child behavioral and emotional outcomes later in life, such as ADHD and anxiety/depression. The underlying mechanisms for this, however, are still largely unknown. The hypothalamic-pituitary-adrenal (HPA)-axis, with its most important effector hormone cortisol, has been proposed as a mechanism, but results have been inconsistent. The current study investigated the association between maternal psychological distress (i.e. anxiety and depressive symptoms) and maternal cortisol levels during pregnancy using a mixed models approach. METHOD: During three pregnancy trimesters, mothers (N = 170) collected four salivary samples for two consecutive days. Mothers reported symptoms of anxiety and depression three times during pregnancy (at 13.3 ± 1.1, 20.2 ± 1.5, and 33.8 ± 1.5 weeks of pregnancy, respectively) using the anxiety subscale of the Symptom Checklist (SCL-90), the Spielberger State and Trait Anxiety Inventory (STAI), and the Edinburgh Postnatal Depression Scale (EPDS). Specific fears and worries during pregnancy were measured with the short version of the Pregnancy Related Anxiety Questionnaire (PRAQ-R). RESULTS: We found a significant effect of SCL-90 anxiety subscale on cortisol levels at awakening (p = .008), indicating that mothers with higher anxiety showed lower cortisol at awakening. Maternal psychological variables explained 10.5% of the variance at the person level in awakening cortisol level, but none in the overall diurnal cortisol model. CONCLUSION: More research is necessary to unravel the underlying mechanisms of the association between maternal psychological distress and cortisol and the search for mechanisms other than the HPA-axis should be continued and extended. ispartof: Psychoneuroendocrinology vol:96 pages:52-60 ispartof: location:England status: published

Accumulating research shows that prenatal exposure to maternal stress increases the risk for behavioral and mental health problems later in life. This review systematically analyzes the available human studies to identify harmful stressors, vulnerable periods during pregnancy, specificities in the outcome and biological correlates of the relation between maternal stress and offspring outcome. Effects of maternal stress on offspring neurodevelopment, cognitive development, negative affectivity, difficult temperament and psychiatric disorders are shown in numerous epidemiological and case-control studies. Offspring of both sexes are susceptible to prenatal stress but effects differ. There is not any specific vulnerable period of gestation; prenatal stress effects vary for different gestational ages possibly depending on the developmental stage of specific brain areas and circuits, stress system and immune system. Biological correlates in the prenatally stressed offspring are: aberrations in neurodevelopment, neurocognitive function, cerebral processing, functional and structural brain connectivity involving amygdalae and (pre)frontal cortex, changes in hypothalamo-pituitary-adrenal (HPA)-axis and autonomous nervous system. Tessa Roseboom, Matthias Schwab and Bea van den Bergh, received support from EU FP7/Health.2011.2.22-2, GA2798219. Marius Lahti and Katri Räikkönen received funding from Academy of Finland and University of Helsinki. Katri Räikkönen also received funding from Signe and Ane Gyllenberg Foundation. Suzanne King received funding from the Canadian Institutes of Health Research (CIHR) for Project Ice Storm (MOP-111177), the Iowa Flood Study (MOP-93660), and the QF2011 Queensland Flood Study (MOP-1150067).

Epigenetic changes are associated with altered behavior and neuropsychiatric disorders and they modify the trajectory of aging. Maternal anxiety during pregnancy is a common environmental challenge for the fetus, causing changes in DNA methylation. Here, we determined the mediating role of DNA methylation and the moderating role of offspring sex on the association between maternal anxiety and children's behavioral measures. In 83 mother-child dyads, maternal anxiety was assessed in each trimester of pregnancy when the child was four years of age. Children's behavioral measures and children's buccal DNA methylation levels (NR3C1, IGF2/H19 ICR, and LINE1) were examined. Higher maternal anxiety during the third trimester was associated with more methylation levels of the NR3C1. Moderating effects of sex on the association between maternal anxiety and methylation were found for IGF2/H19 and LINE1 CpGs. Mediation analysis showed that methylation of NR3C1 could buffer the effects of maternal anxiety on children's behavioral measures, but this effect did not remain significant after controlling for covariates. In conclusion, our data support an association between maternal anxiety during pregnancy and DNA methylation. The results also underscore the importance of sex differences and timing effects. However, DNA methylation as underlying mechanism of the effect of maternal anxiety during pregnancy on offspring's behavioral measures was not supported. European Science Foundation (ESF) European Commission EuroSTRESS-PELS-99930AB6-0CAC-423B-9527-7487B33085F3 European Commission European Commission Joint Research Centre 279281 Erasmus+ travel grant