Few studies have examined the associations between parents' own eating behaviors and their feeding practices. We aimed to study the associations between maternal eating behaviors and feeding practices in toddlerhood. In this cross-sectional analysis, maternal eating behaviors and feeding practices were assessed at 2-year follow-up by using the Three-Factor Eating Questionnaire (TFEQ-R21) and the Comprehensive Feeding Practices Questionnaire (CFPQ), respectively, among mothers of 1322 children from the EDEN mother-child cohort. Depending on their distributions, scores from the two questionnaires were considered continuous or binary variables, according to the median. Linear or logistic regression models were used as appropriate to assess the associations between maternal eating behaviors, considered simultaneously in a combined model, and their feeding practices. Maternal cognitive restraint was positively associated with maternal restriction for health and restriction for weight. Maternal uncontrolled eating was positively associated with pressure to eat and use of food to regulate the child's emotions. Maternal uncontrolled eating was also negatively associated with restriction for weight, but only among boys. This study supports that mothers' own eating behaviors are associated with their feeding practices in toddlerhood. Further studies are needed to understand the role of parental feeding practices in the familial transmission of eating behavior.

In utero exposure to environmental chemicals, such as synthetic phenols, may alter DNA methylation in different tissues, including placenta - a critical organ for fetal development. We studied associations between prenatal urinary biomarker concentrations of synthetic phenols and placental DNA methylation. Our study involved 202 mother-son pairs from the French EDEN cohort. Nine phenols were measured in spot urine samples collected between 22 and 29 gestational weeks. We performed DNA methylation analysis of the fetal side of placental tissues using the IlluminaHM450 BeadChips. We evaluated methylation changes of individual CpGs in an adjusted epigenome-wide association study (EWAS) and identified differentially methylated regions (DMRs). We performed mediation analysis to test whether placental tissue heterogeneity mediated the association between urinary phenol concentrations and DNA methylation. We identified 46 significant DMRs (≥5 CpGs) associated with triclosan (37 DMRs), 2,4-dichlorophenol (3), benzophenone-3 (3), methyl- (2) and propylparaben (1). All but 2 DMRs were positively associated with phenol concentrations. Out of the 46 identified DMRs, 7 (6 for triclosan) encompassed imprinted genes (APC, FOXG1, GNAS, GNASAS, MIR886, PEG10, SGCE), which represented a significant enrichment. Other identified DMRs encompassed genes encoding proteins responsible for cell signaling, transmembrane transport, cell adhesion, inflammatory, apoptotic and immunological response, genes encoding transcription factors, histones, tumor suppressors, genes involved in tumorigenesis and several cancer risk biomarkers. Mediation analysis suggested that placental cell heterogeneity may partly explain these associations. This is the first study describing the genome-wide modifications of placental DNA methylation associated with pregnancy exposure to synthetic phenols or their precursors. Our results suggest that cell heterogeneity might mediate the effects of triclosan exposure on placental DNA methylation. Additionally, the enrichment of imprinted genes within the DMRs suggests mechanisms by which certain exposures, mainly to triclosan, could affect fetal development.

Although an early adiposity rebound (AR) is an established risk factor for later obesity, little is known regarding its determinants, especially modifiable ones. Using data from the French EDEN mother-child cohort (1903 children born in 2003-2006), we aimed to examine the association between diet and activity-related behaviors at 2 years of age and the timing of the AR. Two-year-old children (n = 1138) with parent-reported data on their foods/drinks intake, TV/DVD watching time, outdoor playtime, and with an estimated (via growth modelling) age at AR were included in the present study. Two dietary patterns, labelled 'Nutrient-dense foods' and 'Processed and fast foods', were identified in a previous study. Multivariable linear and logistic regression models were used to assess the association between dietary patterns and activity-related behaviors and, respectively, the age at AR (continuous) and the likelihood of having a very early AR (before 3.6 years for girls and 3.8 years for boys, i.e., below the 10th percentile of sex-specific distribution). A higher score on the 'Processed and fast foods' dietary pattern was associated with a higher likelihood of having a very early AR (OR = 1.23; 95% CI: 1.00 to 1.50). No significant association was observed between the 'Nutrient-dense foods' dietary pattern, TV/DVD watching and outdoor playing times and the timing of the AR. This finding emphasizes the importance of reducing nutrient-dense and processed foods from the early years of life, and provides further support for early interventions aimed at helping parents establish healthy eating habits for their growing child from the complementary period.

Sleep is essential for optimal child development and health during the life course. However, sleep disturbances are common in early childhood and increase the risk of cognitive, metabolic and inflammatory disorders throughout life. Sleep and immunity are mutually linked, and cytokines secreted by immune cells could mediate this interaction. The sleep modulation of cytokines has been studied mostly in adults and adolescents; few studies have focused on school-aged children and none on preschoolers. We hypothesized that night sleep duration affects cytokine levels in preschoolers. In a sample of 687 children from the EDEN French birth cohort, we studied the associations between night sleep duration trajectories from age to 2-5 years old and serum concentrations of four cytokines (Tumor necrosis factor alpha [TNF-alpha], Interleukin 6 [IL-6], IL-10, Interferon gamma [IFN)-gamma] at age 5, adjusting for relevant covariates. As compared with the reference trajectory (R-.111h30/night sleep, 37.4% of children), a shorter sleep duration trajectory (<10 h/night, 4.5% of children), and changing sleep duration trajectory (>= 11h30/night then 10h30/night, 5.6% of children) were associated with higher serum levels of IL-6 and TNF-alpha, respectively at age 5. We found no associations between sleep duration trajectories and IL-10 or IFN-gamma levels. This first longitudinal study among children aged 2-5 years old suggests an impact of sleep duration on immune activity in early childhood. Our study warrants replication studies in larger cohorts to further explore whether and how immune activity interacts with sleep trajectories to enhance susceptibility to adverse health conditions.

Detecting SGA (small for gestational age) during pregnancy improves the fetal and neonatal prognosis. To date, there is no valid antenatal biomarker of SGA used in clinical practice. Maternal circulating DLK1 (delta-like non-canonical notch ligand 1) levels have been shown to be significantly lower in pregnant women at 36 weeks of gestation (WG) who delivered a SGA newborn than in controls. Data in the literature are contradictory on the association between maternal circulating DLK1 levels and placental vascular dysfunction. The objective was to determine if maternal DLK1 levels in the second trimester of pregnancy are predictive of SGA, and to assess whether the measurement of DLK1 levels in maternal blood could be a means to distinguish SGA with placental vascular dysfunction from that due to other causes. We conducted a nested cased-control study within the EDEN mother-child cohort. 193 SGA (birth weight < 10th percentile) and 370 mother-child control (birth weight between the 25th and 75th percentile) matched pairs were identified in the EDEN cohort. Maternal circulating DLK1 levels at 26 WG were significantly lower for children born SGA than for controls (27.7 ± 8.7 ng/mL vs 30.4 ± 10.6 ng/mL, p = 0.001). Maternal blood DLK1 levels in the first quartile (DLK1 < 22.85 ng/mL) were associated with an odds ratio for SGA of 1.98 [1.15 - 3.37]. DLK1 was less predictive of SGA than ultrasound, with an area under the curve of 0.578. Maternal circulating DLK1 levels were not significantly different in cases of SGA with signs of placental vascular dysfunction (n = 63, 27.1 ± 9.2 ng/mL) than in those without placental dysfunction (n = 129, 28.0 ± 8.5 ng/mL, p = 0.53). The level of circulating DLK1 is reduced in the second trimester of pregnancy in cases of SGA at birth, independently of signs of placental vascular dysfunction. However, DLK1 alone cannot predict the risk of SGA.

Higher maternal pre-pregnancy body mass index (ppBMI) is associated with increased neonatal morbidity, as well as with pregnancy complications and metabolic outcomes in offspring later in life. The placenta is a key organ in fetal development and has been proposed to act as a mediator between the mother and different health outcomes in children. The overall aim of the present work is to investigate the association of ppBMI with epigenome-wide placental DNA methylation (DNAm) in 10 studies from the PACE consortium, amounting to 2631 mother-child pairs. We identify 27 CpG sites at which we observe placental DNAm variations of up to 2.0% per 10 ppBMI-unit. The CpGs that are differentially methylated in placenta do not overlap with CpGs identified in previous studies in cord blood DNAm related to ppBMI. Many of the identified CpGs are located in open sea regions, are often close to obesity-related genes such as GPX1 and LGR4 and altogether, are enriched in cancer and oxidative stress pathways. Our findings suggest that placental DNAm could be one of the mechanisms by which maternal obesity is associated with metabolic health outcomes in newborns and children, although further studies will be needed in order to corroborate these findings.

The preconception period represents an important window for foetal and epigenetic programming. Some micronutrients (B vitamins, choline, betaine, methionine) implicated in one-carbon metabolism (OCM) are essential for major epigenetic processes that take place in early pregnancy. However, few studies have evaluated the implication of the micronutrients in placental DNA methylation. We investigated whether intake of OCM nutrients in the year before pregnancy was associated with placental DNA methylation in the EDEN mother–child cohort. Maternal dietary intake was assessed with a food-frequency questionnaire. Three dietary patterns, 'varied and balanced diet,' 'vegetarian tendency,' and 'bread and starchy food,' were used to characterize maternal OCM dietary intake. The Illumina Infinium HumanMethylation450 BeadChip was used to measure placental DNA methylation of 573 women included in the analyses. We evaluated the association of dietary patterns with global DNA methylation. Then, we conducted an agnostic epigenome-wide association study (EWAS) and investigated differentially methylated regions (DMRs) associated with each dietary pattern. We found no significant association between the three dietary patterns and global DNA methylation or individual CpG sites. DMR analyses highlighted associations between the 'varied and balanced' or 'vegetarian tendency' pattern and DMRs located at genes previously implicated in functions essential for embryonic development, such as neurodevelopment. The 'bread and starchy food' pattern was associated with regions related to genes whose functions involve various metabolic and cell synthesis-related processes. In mainly well-nourished French women without major deficiencies, OCM intake before pregnancy was not associated with major variation in DNA methylation.

BACKGROUND & AIMS:Maternal diet during pregnancy is a modifiable behaviour which plays an important role in maternal, neonatal and child health outcomes. Thus, knowledge of predictors of dietary quality and dietary inflammatory potential in European countries may contribute to developing maternal diet-related public health policies that target specific at-risk populations in Europe. METHODS:We used harmonised data from >26,000 pregnant women enrolled in the ALSPAC, EDEN, Generation R, Lifeways, REPRO_PL, ROLO and SWS cohorts, as part of the ALPHABET consortium. Maternal dietary quality and inflammatory potential were assessed using the Dietary Approaches to Stop Hypertension (DASH) and the energy-adjusted Dietary Inflammatory Index (E-DII). We conducted an individual participant data meta-analysis to investigate the maternal sociodemographic, health and behavioural predictors of maternal diet before and during pregnancy. RESULTS:DASH and E-DII scores were moderately correlated: from -0.63 (95% CI: -0.66, -0.59) to -0.48 (95% CI: -0.49, -0.47) across cohorts. Higher maternal age, education, household income, and physical activity during pregnancy were associated with a better dietary quality and a more anti-inflammatory diet. Conversely, multiparity and smoking during pregnancy were associated with a poorer dietary quality and a more proinflammatory diet. Women with obesity had a poorer pregnancy dietary quality than women with a normal body mass index range. CONCLUSIONS:The results will help identify population subgroups who may benefit from targeted public health strategies and interventions aimed at improving women's dietary quality during pregnancy.

Background Early adiposity rebound (AR) has been associated with increased risk of overweight or obesity in adulthood. However, little is known about early predictors of age at AR. We aimed to study the role of perinatal factors and genetic susceptibility to obesity in the kinetics of AR. Methods Body mass index (BMI) curves were modelled by using mixed-effects cubic models, and age at AR was estimated for 1415 children of the EDEN mother–child cohort study. A combined obesity risk-allele score was calculated from genotypes for 27 variants identified by genome-wide association studies of adult BMI. Perinatal factors of interest were maternal age at delivery, parental education, parental BMI, gestational weight gain, maternal smoking during pregnancy, and newborn characteristics (sex, prematurity, and birth weight). We used a hierarchical level approach with multivariable linear regression model to investigate the association between these factors, obesity risk-allele score, and age at AR. Results A higher genetic susceptibility to obesity score was associated with an earlier age at AR. At the most distal level of the hierarchical model, maternal and paternal educational levels were positively associated with age at AR. Children born to parents with higher BMI were more likely to exhibit earlier age at AR. In addition, higher gestational weight gain was related to earlier age at AR. For children born small for gestational age, the average age at AR was 88 [±39] days lower than for children born appropriate for gestational age and 91 [±56] days lower than for children born large for gestational age. Conclusion The timing of AR seems to be an early childhood manifestation of the genetic susceptibility to adult obesity. We further identified low birth weight and gestational weight gain as novel predictors of early AR, highlighting the role of the intrauterine environment in the kinetics of adiposity.

Abstract Women with thyroid diseases at the beginning of pregnancy may have suboptimal thyroid hormone levels because of potential difficulties in compensating for the physiological thyroid hormone changes occurring in pregnancy. Our objective was to study the association between preexisting thyroid diseases, pregnancy complications, and neonatal anthropometry. In total, 16,395 women from the ELFE French longitudinal birth cohort were included, and 273 declared pre-pregnancy thyroid diseases. Associations were investigated with multivariable regression models, with adjustment for relevant potential confounders. Body mass index (BMI) was additionally adjusted for in a second stage. As compared with other women, women with pre-pregnancy thyroid diseases were more frequently obese (19.6% vs. 9.8%) and had greater odds of gestational diabetes development (odds ratio [OR] = 1.58 [95% confidence interval [CI] 1.08, 2.30]) or had undergone treatment for infertility (OR = 1.57 [95% CI 1.07, 2.31]). After adjustment for BMI, the association with gestational diabetes was no longer significant (OR = 1.27 [95% CI 0.86, 1.88]). After excluding women with another medical history, those with pre-pregnancy thyroid diseases had increased odds of premature rupture of membranes (OR = 1.51 [95% CI 1.01, 2.25]). Children born from mothers with hypothyroidism before conception due to a disease or as a potential side effect of treatment had a smaller head circumference at birth than other children (β = −0.23 [95% CI −0.44, −0.01] cm). In conclusion, pre-pregnancy thyroid diseases were associated with risk of infertility treatment, gestational diabetes, and premature rupture of membranes. The association between history of hypothyroidism and moderate adverse effects on fetal head circumference growth needs replication.

Certaines études suggèrent une transmission familiale des comportements alimentaires. Néanmoins, peu d’études se sont intéressées à la place éventuelle des pratiques parentales vis-à-vis de l’alimentation dans ce processus. Dans ce contexte, notre objectif était d’examiner dans quelle mesure le statut pondéral et le propre comportement alimentaire des mères étaient associés à leurs pratiques vis-à-vis de l’alimentation de l’enfant. Au total, 1340 enfants de la cohorte mère–enfant Étude des Déterminants pré et post natals de la santé de l’ENfant (EDEN) ont été inclus dans cette étude. L’IMC de la mère avant la grossesse a été calculé à partir du poids et de la taille recueillis à la maternité. Le comportement alimentaire de la mère et ses pratiques parentales vis-à-vis de l’alimentation de l’enfant ont été évalués à 2 ans à l’aide de questionnaires standardisés : le TFEQ-R21 (restriction cognitive, alimentation incontrôlée et alimentation émotionnelle) et le CFPQ (restriction pour la santé, restriction pour le poids, pression à manger, liberté laissée à l’enfant vis-à-vis de son alimentation, utilisation des aliments à des fins non nutritionnelles : comme récompense ou pour gérer les émotions de l’enfant), respectivement. Pour chacune des échelles, les scores ont été dichotomisés à la médiane. Les associations entre l’IMC ou le comportement alimentaire de la mère et ses pratiques parentales ont été évaluées à l’aide de modèles de régressions logistiques, ajustées sur les principaux facteurs de confusion. Un modèle a été effectué par exposition (IMC ou score de comportement) et par pratique parentale. L’IMC maternel était positivement associé à la restriction parentale pour le poids (OR [IC95 %] = 1,04 [1,01 ; 1,06]) et négativement à la pression à manger (0,97 [0,95 ; 1,00]). En comparaison à un faible niveau de restriction cognitive chez la mère, un niveau élevé était associé à une plus forte utilisation des pratiques parentales coercitives (restriction pour la santé : 1,90 [1,50 ; 2,40], restriction pour le poids : 2,14 [1,69 ; 2,70] mais aussi pression à manger : 1,33 [1,06 ; 1,68]). Un niveau élevé d’alimentation incontrôlée chez la mère était associé à une plus forte pression parentale à manger (1,43 [1,14 ; 1,80]). De plus, pour chacun des scores de comportement maternel considérés (restriction cognitive, alimentation incontrôlée ou alimentation émotionnelle), un niveau élevé était associé à une plus forte utilisation de la nourriture à des fins non nutritionnelles (comme récompense et pour gérer les émotions de l’enfant). Le propre comportement alimentaire des mères, et dans une moindre mesure leur IMC, sont donc fortement associés à leurs pratiques parentales vis-à-vis de l’alimentation de leur enfant.

Abstract Introduction There is a reciprocal interaction between sleep and the immune system. Activation of the immune system changes the quality of sleep, and sleep regulates innate and adaptive immune responses. While these interactions have been studied in adults and adolescents, only a few studies have focused on school age children and none on preschoolers. Here, we have studied the association between night sleep trajectories between the age of 2 and 5 and serum levels of four cytokines in 5-year-old children. Methods A total of 687 children (44% girls) from the EDEN French birth cohort were included. Information on night sleep trajectories between 2 and 5 was available in all included individuals, as well as the levels of Tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, interferon gamma (IFN-gamma), and IL-10 in 5-year-old children. The associations between sleep trajectories and cytokines were assessed by multivariate linear regressions adjusted for socioeconomic, familial, maternal, perinatal and child factors. Results A shorter sleep duration trajectory (<10h/night, 4.5% of children) was associated with higher levels of IL-6 when compared to the reference trajectory (≈11h30/night, 37.4% of children). A longer sleep duration trajectory (≥11h3/night, 40.9% of children) was associated with higher levels of IL-10. A changing sleep duration trajectory (≥11h30/night followed by 10h30/night, 5.6% of children) was associated with increased levels of TNF-alpha. No statically significant association was observed between sleep duration trajectories and IFN-gamma. Conclusion This first longitudinal study in preschoolers demonstrates an association between sleep duration trajectories and blood levels of IL-6, IL-10 and TNF-alpha. While association does not imply causation, our results are compatible with an impact of sleep duration on low-grade inflammation in preschool children. Should our results be replicated in an independent study sample, it would pave the way for a better understanding of the interactions between sleep and the immune system. Support (if any):

Studies in children have reported associations of screen time and background TV on language skills as measured by their parents. However, few large, longitudinal studies have examined language skills assessed by trained psychologists, which is less prone to social desirability. We assessed screen time and exposure to TV during family meals at ages 2, 3 and 5–6 years in 1562 children from the French EDEN cohort. Language skills were evaluated by parents at 2 years (Communicative Development Inventory, CDI) and by trained psychologists at 3 (NEPSY and ELOLA batteries) and 5–6 years (verbal IQ). Cross-sectional and longitudinal associations were assessed by linear regression adjusted for important confounders. Overall, daily screen time was not associated with language scores, except in cross-sectional at age 2 years, where higher CDI scores were observed for intermediate screen time. Exposure to TV during family meals was consistently associated with lower language scores: TV always on (vs never) at age 2 years was associated with lower verbal IQ (− 3.2 [95% IC: − 6.0, − 0.3] points), independent of daily screen time and baseline language score. In conclusion, public health policies should better account for the context of screen watching, not only its amount.

Previous findings suggest that parental feeding practices may adapt to children's eating behavior and sex, but few studies assessed these associations in toddlerhood. We aimed to study the associations between infant's appetite or children's genetic susceptibility to obesity and parental feeding practices. We assessed infant's appetite (three-category indicator: low, normal or high appetite, labelled 4-to-24-month appetite) and calculated a combined obesity risk-allele score (genetic risk score of body mass index (BMI-GRS)) in a longitudinal study of respectively 1358 and 932 children from the EDEN cohort. Parental feeding practices were assessed at 2-year-follow-up by the CFPQ. Three of the five tested scores were used as continuous variables; others were considered as binary variables, according to the median. Associations between infant's appetite or child's BMI-GRS and parental feeding practices were assessed by linear and logistic regression models, stratified on child's sex if interactions were significant. 4-to-24-month appetite was positively associated with restrictive feeding practices among boys and girls. Among boys, high compared to normal 4-to-24-month appetite was associated with higher use of food to regulate child's emotions (OR [95% CI] = 2.24 [1.36; 3.68]). Child's BMI-GRS was not related to parental feeding practices. Parental feeding practices may adapt to parental perception of infant's appetite and child's sex.

Abstract Better adherence to dietary guidelines during pregnancy is supposed to result in healthier perinatal outcomes. We aim to characterize the diets of pregnant women by hypothesis‐driven and exploratory approaches and describe potential social determinants. Analyses included 12 048 mothers from the French nationwide ELFE birth cohort. Dietary intake over the last three months of the pregnancy was assessed by a food frequency questionnaire. Two hypothesis‐driven scores (the Diet Quality score, based on benchmarks derived from the National Health and Nutrition Program Guidelines, and the PANDiet score, based on nutrient intake) were calculated. Exploratory dietary patterns were also identified by principal component analysis. Multiple linear regressions were used to assess associations of maternal social characteristics with dietary patterns, accounting for the possible effect modification by their migration status. Five dietary patterns were identified: the Western, Balanced, Bread and toppings, Processed products, and Milk and breakfast cereals. Younger maternal age, single motherhood, unemployment and the presence of older children in the household were related to a suboptimal diet during pregnancy. The less acculturated the women were, the healthier and less processed their diets were, independent of their socio‐economic position. Several social determinants of the quality of women's diets were however moderated by their migration status. These findings shed light on the relations between indicators of social vulnerability, such as single motherhood and unemployment, and poorer diet quality. Given the reduced diet quality that accompanies the acculturation process, it is of paramount importance to identify the specific factors or obstacles that affect migrant women in maintaining their diet quality advantage over the majority population.

BACKGROUND AND AIM: Foetal growth and development strongly depend upon the health of the placenta. Prenatal exposure to phthalates has been hypothesized to be associated with differential DNA methylation, however epigenome-wide studies on placental tissue are lacking. The aim of this study was to characterize associations between pregnancy urinary concentrations of phthalate metabolites and placental DNA methylation. METHODS: We measured concentrations of 11 phthalate metabolites in maternal spot urine samples collected between 22-29 gestational weeks in 202 mother-son pairs. We analysed DNA methylation levels in term placental tissue using IlluminaHM450 BeadChips. We performed an adjusted epigenome-wide association study (EWAS) and identified differentially methylated regions (DMRs, ≥ 5 CpGs). We also evaluated DNA methylation of repetitive elements Alu and LINE-1. RESULTS:We identified 6 DMRs associated with urinary concentrations of phthalate metabolites. Monoethyl phthalate (MEP) was positively associated with 2 DMRs encompassing imprinted genes (SGCE/PEG10) and a gene involved in the immunological response (GCA). Other positive associations were detected for: monocarboxy-iso-nonyl-phthalate (MCNP) and HSPA1A/HSPA1L genes encoding heat shock proteins; mono(3-carboxypropyl)-phthalate (MCPP) and ART5 encoding protein responsible for protein function regulation; mono-iso-buthyl-phthalate (MiBP) and transcription factor coding REPIN1 gene. The only negative association was identified between mono(2-ethylhexyl)-phthalate (MEHP) exposure and DMR encompassing transcription factor coding ZSCAN16 gene. Finally, we found that pregnancy monobenzyl phthalate concentrations were negatively associated with placental methylation of Alu repeats. CONCLUSIONS:Our study is the first one to describe the genome-wide epigenetic modifications of placental DNA in association with pregnancy exposure to phthalates. Some phthalates may be associated with differential methylation of placental DNA, including changes in repetitive element methylation. Interestingly, 1 of the 5 highlighted phthalate metabolites has been associated with the placental-to-foetal weight ratio in a previous study relying on EDEN cohort. KEYWORDS: Phthalates, Endocrine disrupting chemicals, Chemical exposures, Birth outcomes, Epigenomics

Refractive errors are common, especially in children and adolescents, leading to global health issues, academic implications and economic costs. Circadian rhythm and sleep habits may play a role. The study included 1130 children from the EDEN birth-cohort. Data were collected through parental questionnaires at age 2 and 5 for sleep duration and timing, and at age 5 for refractive error. At 5 years, 20.4% were prescribed glasses (2% for myopia, 11.9% for hyperopia and 6.8% for unknown reason). Children slept on average (SD) 11h05/night (± 30 min) and 10h49/night (± 48 min) at age 2 and 5, respectively. Average bedtime and midsleep was 8.36 pm (± 30 min), 2.06 am (± 36 min), and 8.54 pm (± 30 min), 2.06 am (± 24 min) at age 2 and 5, respectively. A U-shaped association was observed between sleep duration at age 2 and eyeglass prescription at age 5. Later midsleep and bedtime at age 2 were associated with an increased risk of eyeglass prescription at age 5. Associations became borderline significant after adjustment for confounding factors. Sleep duration and timing at age 2 were associated with subsequent refractive errors in preschoolers from general population. Sleep hygiene might be a target for refractive errors prevention.

BACKGROUND:Maternal diet quality during pregnancy has been linked to offspring's physical and mental health outcomes across the lifespan. However, few studies have examined its association with subsequent offspring's anxiety and depression issues.OBJECTIVES:The objective of the study was to examine the relationship between maternal prenatal dietary patterns and offspring's anxiety and depression symptoms from 3 to 8 years.METHODS:We used data from 1242 children enrolled in the French EDEN (Etude des déterminants pré- et postnatals précoces du développement et de la santé de l'enfant) birth cohort. Maternal third trimester dietary patterns-namely, "Healthy" (i.e., high intake in fruit, vegetables, fish, and whole-grain cereals) and "Western" (i.e., high intake in processed and snacking foods) patterns-were evaluated using a validated qualitative FFQ. Children's anxiety and depression symptoms (i.e., fears, worries, misery, nervousness, and somatic symptoms) were assessed by mothers using the Strengths and Difficulties Questionnaire at ages 3, 5, and 8 years, from which trajectories were derived using group-based trajectory modeling. We used logistic regressions to analyze the associations between maternal dietary patterns and children's anxiety and depression symptom trajectories.RESULTS:We identified 2 trajectories of anxiety and depression symptoms from 3 to 8 years of age: low to moderate (n = 1058; reference group) and moderately high (n = 184). Maternal low adherence to the Healthy dietary pattern in the third trimester was significantly associated with moderately high children's anxiety and depression symptom trajectories from 3 to 8 years (OR, 1.87; 95% CI, 1.40-2.51), in crude and adjusted analyses. The maternal Western dietary pattern was not significantly associated with anxiety and depression symptom trajectories.CONCLUSIONS:High maternal prenatal adherence to a Healthy dietary pattern was negatively related to anxiety and depression symptoms in children. As maternal diet is a key lifestyle factor, further research should investigate its association with subsequent offspring anxiety and depression symptoms in aiming to later inform prevention strategies focusing on pregnancy.

Abstract Introduction Refractive errors are very common, in particular in children and adolescents, leading to global health issues, academic implications and economic costs. The process of emmetropization in child development is a multifactorial and active mechanism, and is yet to be fully understood. Light exposure and endogenous circadian rhythmicity are thought to have an important role in this process. They are also known to be both cause and consequence of various sleep habits. The study aims at investigating the role of sleep duration and timing in refractive error development of preschoolers. Methods Sleep duration and timing were assessed at age 2 and 5 years, and vision problems at age 5 through parental auto-questionnaires in 1,130 children from the EDEN birth-cohort. We performed both cross-sectional and longitudinal analyses using logistic regression models, before and after adjusting for age, sex, socio-economic status, nap duration, time spent outdoors and daily screen-time. We conducted multiple imputations to deal with missing data on covariates. The shape of the association was considered by splitting sleep duration into tertiles. Results At age 5 years, 20.4% of the children were prescribed glasses (2% for myopia, 11.9% for hyperopia and 6.8% for unknow reason). Children slept on average (SD) 11h05 (30 min) per night at age 2 and 10h49 (48 min) at age 5. Average bedtime and midsleep were 8.36 pm (30 min), 2.06 am (36 min), and 8.54 pm (30 min), 2.06 am (24 min) at age 2 and 5, respectively. In the raw longitudinal analysis, a U-shaped association was observed between nocturnal sleep duration at age 2 and eyeglass prescription at age 5: 2-years-old children sleeping 11h30 had a higher risk to have an eyeglass prescription by the age of 5. Later midsleep and bedtime at age 2 were associated with an increased risk of eyeglass prescription at age 5. All associations, except the one concerning bedtime, were barely changed after adjustment while becoming borderline significant. Conclusion Duration and timing of sleep at age 2 were associated with subsequent onset of refractive errors in preschoolers from a general population. Sleep and light hygiene might be targets for prevention. Support (if any):

Objectif Les troubles de la refraction sont tres courants. Le sommeil et les rythmes circadiens pourraient etre impliques dans leur developpement. Methodes L’etude inclus 1133 enfants d’une cohorte de naissance ayant des donnees sur le sommeil a 2 ans et les troubles de la refraction a 5 ans (myopie, hypermetropie et prescription de lunettes). La duree de sommeil a ete categorisee en tertiles ( 11h30) pour etudier une possible relation non lineaire suggeree par la litterature. Les associations longitudinales ont ete estimees par regression logistique ajustee sur des facteurs de confusion (dont âge, sexe, statut socio-economique, duree de sieste, activite exterieure, temps d’ecrans). Resultats A 5 ans, 2 % des enfants presentaient une myopie, 12 % une hypermetropie et 20 % ont eu une prescription de lunettes. En moyenne, les enfants dormaient 11h05 (± 30 min)/nuit a 2 ans, se couchaient a 20h54 (± 30 min) et avaient un milieu de nuit a 2h06 (± 36 min). Une relation en U a ete observee entre duree de sommeil a 2 ans et prescription de lunettes a 5 ans, le risque etant accru de 45 % pour les plus courts et plus longs dormeurs. Les enfants avec un milieu de nuit plus tardif a 2 ans avaient un risque accru de prescription de lunettes a 5 ans de 30 %/heure. Les associations persistaient apres ajustement bien qu’a la limite de la significativite. Conclusion La duree du sommeil et son timing a 2 ans sont associees a l’apparition ulterieure de troubles de refraction chez les enfants d’âge prescolaire en population generale. Ces resultats doivent etre confirmes dans des cohortes de plus grande taille.