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Childhood obesity is a predictor of adult obesity and has its roots in the pre-pregnancy or pregnancy period. This review presents an overview of the prenatal risk factors for childhood obesity, which were categorized into 2 groups: biological risk factors (maternal pre-pregnancy body mass index, gestational weight gain, diabetes in pregnancy, and caesarean section), and environmental and behavioural risk factors (maternal smoking and exposure to obesogens, maternal dietary patterns, maternal intestinal microbiome and antibiotics exposure, and maternal psychosocial stress). Identifying modifiable predisposing prenatal factors for obesity will inform further development of inventions to prevent obesity over the life course, and future directions for research and intervention are discussed. Key words: risk factors, obesity, pregnancy, body mass index, childhood. L'obesite chez l'enfant est un facteur predictif de l'obesite chez l'adulte ayant ses racines dans les periodes de grossesse ou precedant la grossesse. Cet article de synthese presente un apercu des facteurs de risque prenataux pour l'obesite chez l'enfant, que nous avons categorises en 2 groupes : facteurs de risque biologiques (indice de masse corporelle maternel avant la grossesse, prise de poids pendant la grossesse, diabete de grossesse, ainsi que cesarienne) et facteurs de risque environnementaux et comportementaux (tabagisme chez la mere et exposition aux << obesogenes >>, habitudes alimentaires de la mere, microbiome intestinal maternel et prise d'antibiotiques, ainsi que stress psychosocial chez la mere). L'identification de facteurs predisposants modifiables prenataux d'obesite chez Ia mere apportera des donnees pour le developpement a venir d'inventions destinees a la prevention de l'obesite tout au long de la vie, et nous discutons d'avenues pour des recherches et des interventions futures. [Traduit par la Redaction] Mots-cles : facteurs de risque, obesite, grossesse, indice de masse corporelle, enfance., Introduction Obesity is generally defined as a condition in which the degree of excess body fat has the potential to negatively impact health outcomes (WHO 2017). Body mass index (BMI) [...]

Introduction: Approximately 5.5% of pregnant women take antidepressants. Studies on prenatal exposure to antidepressants reported no association with child cognition, and inconsistent results with motor function and language development. A limitation has been the failure to adjust for prenatal maternal distress. Objectives: Assess the associations between prenatal exposure to antidepressants and child development at age two, while adjusting for maternal depressive symptoms and stress during pregnancy. Explore indirect effects through birth complications and consider sex-specific associations. Methods: This is an ancillary study of the 3D (Design Develop, Discover) Study initiated during pregnancy. Data on antidepressants were collected through medication logs spanning the entire pregnancy. Depressive symptoms and stress were assessed during pregnancy by self-reported questionnaires, motor and cognitive development with the Bayley Scales of Infant and Toddler Development (BSID-III), and language development with the MacArthur Communicative Development Inventories at age 2. Multiple linear regressions were used to assess the associations between exposure and developmental outcomes. Mediation models were used to assess indirect effects. Interaction terms were introduced to assess sex-specific associations. Results: 1,489 mother-child dyads were included, of whom 61 (4.1%) reported prenatal antidepressant use. Prenatal exposure was negatively associated with motor development (B = -0.91, 95% CI -1.73, -0.09 for fine motor, B = -0.89, 95% CI -1.81, 0.02 for gross motor), but not with cognitive (B = -0.53, 95% CI -1.82, 0.72) and language (B = 4.13, 95% CI -3.72, 11.89) development. Adjusting for maternal prenatal distress only slightly modified these associations. No indirect effect or differential effect according to child sex were found. Conclusion: This study supports evidence of a negative association between prenatal exposure to antidepressants and motor development at age two, after adjusting for maternal distress, but the effect size remains very small, with about only one BSID-III point lower in average. [ABSTRACT FROM AUTHOR]

Acetaminophen is the only over-the-counter pain reliever that is not contraindicated during pregnancy, but recent studies have questioned whether acetaminophen is safe for the fetus, particularly the developing brain. This prospective birth cohort study probed the previously observed association between in utero exposure to acetaminophen and neurodevelopment by using concentrations of acetaminophen measured in meconium, which more objectively captures exposure of the fetus than maternal report. Exposure, measured by liquid chromatography coupled with tandem mass spectrometry, was categorized into nondetection, low detection, and high detection levels. At age 6–8 years, children completed a set of subtests from the Wechsler Intelligence Scale for Children, 4th edition. Additionally, this study examined potential effect modification by child sex on the association between acetaminophen exposure and neurodevelopment. In fully adjusted models, in utero exposure to acetaminophen was not statistically significantly associated with decreased scores on any of the examined subtests in all children combined (n  = 118). The effect of in utero acetaminophen exposure on the Coding subtest was marginally significantly different among boys and girls, with girls performing significantly better on the task with higher levels of acetaminophen compared with girls with undetectable levels of exposure (βgirls, low = 2.83 [0.97, 4.70], βgirls, high = 1.95 [−0.03, 3.93], βboys, low = .02 [−1.78, 1.81], βboys, high = −.39 [−2.09, 1.31], p interaction = .06). Effect modification by child sex was not observed on other subtests. These results do not support prior reports of adverse neurodevelopmental effects of in utero exposure to acetaminophen. [ABSTRACT FROM AUTHOR]