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In this randomized-controlled trial, we study the effect of a mother-infant walk in a wooded area compared to staying indoors, combined with two types of proximity, namely pram walking and infant carrying, on physiological and behavioral outcomes in infants and their mothers. After exposing their infant to an ecologically-valid laboratory stressor, mother-infant dyads (N=100) were randomly allocated to one of the four conditions: a) outdoor pram (OP), b) outdoor carrier (OC), c) indoor pram (IP) or d) indoor carrier (IC). In the two outdoor conditions, mothers were instructed to go for a 30-minute walk in a green wooded area. In the two indoor conditions, mothers were asked to stay indoors with their infant for 30 minutes while sitting down or walking around in the research center. In the two pram conditions, the infant was lying in a pram. The infant was carried in a front carrier (facing the mother) in the carrier conditions. Infant and maternal cortisol were measured through five salivary samples taken during the lab visit. Infants’ total amount of sleep during the condition was measured through maternal report after the condition (between-subjects design). Maternal affect was measured through self-report on visual analogue scales before and after the assigned conditions (within-subjects design). We will assess the effect of environment and proximity on the following infant outcomes: 1a) cortisol recovery and 1b) amount of sleep; and the following maternal outcome: 2a) maternal affect. We will also explore the effect of the conditions on: 2b) maternal cortisol concentrations. Cortisol outcomes will be analyzed using multilevel modeling. Outcomes of infant sleep and maternal affect will be assessed using analyses of variance (see section ‘Design Plan ’).

Nutrition is important for health. The intake of unhealthy foods is associated with worse health outcomes such as cardiovascular diseases and cancer (Casas et al., 2018; Wiseman, 2019). In early life, parents have great influence on children’s dietary intake (Gubbels et al., 2011; Romanos-Nanclares et al., 2018). If parenting, whether it is early life or later life, can also affect healthy diet in adolescence is still unclear. However, reviews by Sleddens et al. (2011) and Hughes & Papaioannou (2018) showed that children in authoritative households, represented by higher parental sensitivity, had a healthier dietary intake. Parenting styles that were less sensitive were also associated with more child and adolescent emotional eating (Snoek et al., 2007), which is associated with higher intake of unhealthy foods and contributes to worse diet quality (Nguyen-Michel et al., 2007). Furthermore, some studies show that authoritarian parenting, low maternal support and high psychological control are associated with emotional eating in children and adolescents (Schuetzmann et al., 2008; Snoek et al., 2007; Topham et al., 2011). Although the focus was not on sensitivity, these authoritarian traits are a sign of low parenting sensitivity. One way how maternal sensitivity can predict adolescent diet and emotional eating is through inhibitory control. Indeed, after childhood, food choices become more dependent on the adolescents themselves and their inhibitory control. Having good inhibitory control may be reflected in the food choices that contribute to the overall adolescent diet quality, although to date research has found no clear links between inhibitory control and adolescent diet quality (i.e. sugar sweetened beverages, snacks intake and whole grain consumption) (Ames et al., 2014, 2016; Chung et al., 2012). Furthermore, better inhibitory control can help regulate stress and emotions. Indeed, inhibitory control deficits (assessed with multiple inhibitory control measures) are related to more emotional eating (Jasinska et al., 2012). Although, this relation was not seen in another study where the Stop signal task was used as inhibitory measure (Van Strien et al., 2014). Maternal sensitivity is related to child inhibitory control in the sense that the mother provides the child a safe environment where self-regulation can be practiced (Bernier et al., 2010; von Suchodoletz et al., 2011). In toddlers, early life maternal sensitivity was found to predict inhibitory control (Frick et al., 2019a, 2019b; Geeraerts et al., 2021; Kok et al., 2014; Vrijhof et al., 2020; Wu et al., 2022). Whether this prediction holds for adolescence is still under investigation as to our knowledge, only one previous study has been carried out (van der Voort et al., 2014). These authors found that maternal sensitivity during infancy and at age 7 years was associated with less over-inhibition (withdrawn and anxious-depressed behavior) at age 14 years. In this study, we aim to investigate if maternal sensitivity in early life, toddlerhood, childhood and/or adolescence is associated with diet quality and emotional eating in adolescents, and whether this association is mediated by adolescent inhibitory control. We also aim to see at what age maternal sensitivity has the largest impact on adolescent diet quality and emotional eating.

Biological aging is an umbrella term that refers to a complex biological process which entails the aging of cells, their organelles and DNA (Hägg & Jylhävä, 2021). Biological aging processes have been associated with a variety of diseases, including cancer and atherosclerosis (Adams & White, 2004; Dugué et al., 2018), and are a good predictor for higher morbidity and mortality rates (Perna et al., 2016). Therefore, a growing body of research is focused on potential factors affecting biological aging. Biological aging can be operationalized by different biomarkers, including telomere length and epigenetic clocks (Belsky et al., 2018; Pearce et al., 2022). Telomeres are repetitive TTAGGG sequences at the end of chromosomes that protect the chromosomes from shortening during cell division. Telomeres shorten throughout the lifespan, and accelerated telomere shortening is an index of accelerated biological aging (Tempaku et al., 2015; Vaiserman & Krasnienkov, 2021). Furthermore, the epigenetic clock concerns DNA methylation levels, namely the accumulation of methyl groups to DNA molecules, and is an estimator of chronical age (Chen et al., 2016; Jylhävä et al., 2017). These clocks capture methylation of certain sets of CpG sites in the DNA, and methylation levels correlate with age. Accordingly, the biological age of the cells can be calculated in years (Chen et al., 2016; Horvath et al., 2012; McEwen et al., 2020). It has been found that, besides genetic factors (Gibson et al., 2019), also environmental factors, such as smoking and diet, are associated with both of the previous biomarkers of accelerated biological aging (Gao et al., 2016; Horvath et al., 2014; Huang et al., 2019; Vaiserman & Krasnienkov, 2021). Accelerated biological aging in terms of accelerated telomere attrition and advanced epigenetic age has also been associated with sleeping problems in adults (Carskadon et al., 2019; Carroll & Prather, 2021; Cribbet et al., 2014; Gao et al., 2022; James et al., 2017; Jin et al., 2022). Sleep is a complex behavioral and homeostatically regulated state of all mammals (Zielinski et al., 2016). Sleep has many vital functions, including development, modulation of immune responses, memory consolidation and endocrine functions (Krueger et al., 2016; Zielinski et al., 2016). Previous research has demonstrated associations between poor quality of sleep, shorter sleep duration, and delayed sleep onset with shortened telomere lengths (Cribbet et al., 2014; Wynchank et al., 2019). Additionally, reduced sleep duration and poor sleep quality have also been linked to the acceleration of the epigenetic clock (Carskadon et al., 2019; Gao et al., 2022) This association between sleep and accelerated biological aging was not only observed in adults. James and colleagues (2017) found an association of shorter telomeres with shorter sleep durations in nine-year-old children, indicating that the relationship between biological aging and sleep already emerges early in development (James et al., 2017). However, to our knowledge, this is the only study that has looked at children’s sleep in relation to markers for biological aging. Therefore, to date, there is a lack of research on the association of sleep quality with biological aging in children. Additionally, the previously mentioned study on this association in children was cross-sectional, hence the directionality of the relationship between biological aging and sleep quality in children remains unclear. On the one hand, previous studies in adults have largely assumed that more sleeping problems cause alterations in neuro-chemical processes, which, in turn, cause accelerated aging. But on the other hand, studies on the elderly population suggest that accelerated aging can cause significant alterations in the sleep stages and in the quantity and quality of sleep (Tempaku et al., 2015), indicating that aging could also bring about sleep changes. Accordingly, Carrol and Prather (2021) suggest that there is also a possibility that accelerated biological aging causes alterations in brain areas that regulate sleep states, hereby causing sleep difficulties (Carroll & Prather, 2021). Since previous research on the association of sleep and biological aging in children was solely cross-sectional, the directionality of the association remains to be assessed. In the current study we assess the association of sleep with accelerated biological aging in children bi-directionally between chronological ages 6 years (T1) and 10 years (T2). As telomere length and epigenetic clocks have been shown to capture different biological aging processes (Belsky et al., 2018; Pearce et al., 2022), both will be used in this study to measure biological aging. In previous studies, the Pediatric-Buccal-Epigenetic (PedBE) clock has been reported to be the most reliable epigenetic clock for pediatrics (McEwen et al., 2020), and will hence be used in the current study. In this study, we will assess the following goals: 1) Our first goal is to assess cross-sectional associations at T1 and T2 between our biomarkers of biological aging (telomere length and PedBE clock) with child sleeping problems. 2) Our second goal is to determine whether sleeping problems at T1 forecasts biological aging, defined as a) telomere length at T2; b) telomere erosion between T1 – and T2; c) PedBE clock at T2. 3) Our third goal is to determine whether our biomarkers of biological aging (a, b & c) predict sleeping problems at T2. a) telomere length; b) telomere erosion from T1 to T2; c) PedBE clock at T1. 4) Lastly, we will assess the directionality between sleeping problems and biological aging by comparing the explained variance between question 2 and 3. Note that we do not include the change in PedBE from T1 to T2, as the PedBE clock already incorporates the difference between biological aging and chronological aging as an age acceleration. Given that telomere length and/or erosion varies by sex (Barrett & Richardson, 2011), z-score body mass index index (zBMI; Clemente et al., 2019; Gielen et al., 2018), and maternal education (Broer et al., 2013), we will statistically control for these aspects in our analyses. This will be done by using child sex determined at birth, child zBMI at T2 and maternal education defined as the highest level of education completed when assessed at T2 (Beijers, Hartman, et al., 2020; Shalev et al., 2013).

This study is part of the longitudinal Dutch COPE study (COVID-19 and Perinatal Experiences) on experiences of (future) parents during the COVID-19 crisis.

This is a meta-analytic review of the extant literature regarding synchrony (both biological and behavioral) and its relation to cognitive outcomes in children.

The World Health Organization (WHO, 2003) and UNICEF (2019) recommend exclusive breastfeeding (BF) and parent-infant room-sharing (RS) for the first 6 postnatal months, because of the significant benefits for infant health outcomes and safety (WHO, 2013; AAP Task Force on Sudden Infant Death Syndrome, 2016). However, not all parents meet these recommendations. In The Netherlands, for example, only 19% of infants receive exclusive BF (NCJ, 2020) and only 25% share a room with their parents (Beijers et al., 2013), for the first 6 postnatal months. One explanation for prematurely stopping (exclusive) BF and RS may be parents’ return to work (Lanting et al., 2005, Goldberg & Keller, 2007). During the COVID-19 pandemic, however, being at home became a regularity for many parents, especially during times of lockdown. Parents for example lost jobs or moved to working from home. The COVID-19 lockdown may thus have led to more time spent with the infant, and/or more time to rest and pump milk when back at work, possibly resulting in longer (exclusive) BF and RS duration. As such, the COVID-19 lockdown represents a natural experiment that mimics to some extent prolonged parental work leave. Nevertheless, it is likely that the COVID-19 lockdown affected parents in different ways, leading to individual differences, which may in turn may influence (exclusive) BF and RS duration. Our study seeks to investigate (exclusive) BF and RS practices in a Dutch cohort during the COVID-19 pandemic and its contributing factors. The goal of our study is threefold: 1) characterize (exclusive) BF and RS rates in 0-to-6-month-old infants in the first Dutch COVID-19 lockdown (April-May 2020), and report the (exclusive) BF and RS prevalence rates in 6-month-old infants (April 2020-ongoing); 2) investigate whether mothers and their partners being at home for a longer period throughout the pandemic results in longer (exclusive) BF and RS duration; 3) examine whether the association between longer duration of being at home for mothers and their partners and (exclusive) BF and RS duration is moderated by education, household income, parity, employment, and working from home.

Mothers are faced with a change in their routines and for many, motherhood also entails breastfeeding, which not only represents an essential nutritional source for the baby but it also carries numerous health benefits for both the mother and her offspring (Labbok, 2001). The benefits of breastfeeding have long been acknowledged for infants’ neurodevelopmental outcomes (e.g. for a meta-analysis see: Anderson et al., 1999; Belfort et al., 2013; Colen & Ramey, 2014; Kramer et al., 2008). Yet, less is known about the determinants of breast milk composition during early weeks of motherhood. Pioneering work showed an increase in postpartum breast milk cortisol concentrations from week 2 to week 12 (Hechler et al., 2018). Moreover, maternal psychosocial distress (i.e. stress, anxiety, and depressive symptoms) has been linked to breastmilk composition (i.e. cortisol, microbial diversity) in the same time period (Aparicio et al., 2020; Browne et al., 2019). Cortisol is a crucial hormone, responsible for a wide range of psychobiological functions and behaviour (Bergman et al., 2010; Hinde et al., 2015). Particularly, previous studies provided evidence on associations between maternal prenatal and postnatal cortisol, and offspring behaviour in humans (e.g. temperament; Glynn et al., 2021; Grey et al., 2013) and in primates (Hinde et al., 2015). Yet little is known about what determines cortisol concentrations in the breastmilk in the first postnatal months. To investigate the determinants of maternal breastmilk cortisol, a data-driven exploratory approach will examine the role of: 1) maternal trait-like prenatal and 2) situational postnatal factors that may account for changes in breastmilk cortisol concentrations. Precisely, we plan to examine the maternal factors of mother's own early caregiving experiences (attachment security, childhood trauma, adversity) and her resiliency. To examine situational factors, we will explore: a) partner aspects (sensitivity towards the infant, help with childcare activities); b) infant aspects (crying); c) maternal parenting self-efficacy and separation from infant for childcare.