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Evidence is limited regarding the effect of prenatal benzodiazepine and z-hypnotic exposure and long-term neurodevelopment in childhood. The objective of this study was to investigate the effects of initiating benzodiazepine or z-hypnotic treatment in early, mid, and late pregnancy on fifth-grade numeracy and literacy scholastic skills in children by emulating 3 target trials. The trials are identical except for the timing of enrollment and the number of eligible individuals. Eligibility to the trials required a history of anxiety and/or depression prior to pregnancy. We used data from the Norwegian Mother, Father and Child Cohort Study, linked to the Medical Birth Registry of Norway, to emulate the trials. We adjusted for baseline covariates that were available at time 0 for each trial by inverse probability of treatment weighting using the propensity score. The findings of this study did not show any effect of mothers' initiation of treatment with benzodiazepines or z-hypnotics in early, mid, or late pregnancy on the children's fifth-grade test scores in numeracy and literacy. The study results provide reassurance for patients in need of benzodiazepines and z-hypnotics during pregnancy; however, these findings need to be interpreted with caution due to low study power in some of the analyses. This article is part of a Special Collection on Pharmacoepidemiology. [ABSTRACT FROM AUTHOR]

Prenatal lead (Pb) and manganese (Mn) exposure can impair neurodevelopment, targeting the central nervous system. This study investigated the effects of prenatal exposure to Pb and Mn on neurodevelopment in children at 18 months of age, using data from 607 Italian mother–child pairs enrolled in the Northern Adriatic Cohort II (NAC-II). All children born at term (≥37 weeks) were assessed with the Bayley Scales of Infant and Toddler Development, third edition. Cord blood concentrations of Mn and Pb were categorized as low or high exposures based on the 75th percentile of their distribution. Sociodemographic and lifestyle information was collected via questionnaires. Using simple and multiple linear regressions, the study examined the relationship between the cognitive composite score (COGN) and Mn and Pb co-exposure, including their interaction. Stratified regressions explored how Mn exposure influenced the effect of Pb, in the whole cohort and by the child's sex. Beta coefficients (β) and the 90% confidence interval (90% CI) were estimated. Boys showed an interaction effect between Mn and Pb, with a reduction in COGN (β = −5.78, 90% CI: −11.17; −0.40), further described as a negative effect of high Pb on cognition when Mn exposure was also high (β = −6.98, 90% CI: −10.93; −3.04). No clear effects were observed in girls or the entire cohort at these levels of exposure. The findings highlight the harmful impact of combined prenatal Pb and Mn exposure on cognitive development in boys. [ABSTRACT FROM AUTHOR]

The intrauterine period is a time of high sensitivity in the development of the embryo and the fetus. Therefore, low levels of maternal stress are closely associated with healthy brain development in the neonatal and early childhood periods. There is increasing evidence linking natural disasters as prenatal maternal stress (PNMS) to neurodevelopmental disorders (including subclinical manifestations). Natural disasters involve many factors in addition to the trauma they cause, including loss and the physical and psychosocial difficulties that result from that trauma. This review article aims to bring together research findings on the neurodevelopmental effects of natural disasters on children as PNMS. It also looks at how factors such as gestational age and gender contribute to these effects. We conducted a systematic review on PubMed, Web of Science, and Scopus, with 30 studies meting the inclusion criteria. This systematic review was conducted in accordance with the PRISMA guidelines. A total of 1,327,886 mother–child dyads participated in the included studies. The results of the studies indicate that natural disasters have a negative impact on children's outcomes in terms of cognitive development, language development, autism/autism-like features, motor skills, performance in mathematics, mental development, sleep, attention, behavioral and emotional problems, and various psychiatric comorbidities. [ABSTRACT FROM AUTHOR]

Abstract Background The patterns of blood pressure (BP) change throughout the pregnancy were related to adverse birth outcomes. However, little is known about the long-term effect of BP change patterns on child neurodevelopment. This study aimed to explore the relationship between the BP trajectory and BP variability during pregnancy and early childhood neurodevelopment. Method A total of 2797 mother-newborn pairs were derived from the Wuhan Healthy Baby Cohort Study. BP was measured during each antenatal visit, and Mental and Psychomotor Development Indexes (MDI and PDI) were assessed using the Bayley Scales of Infant Development (BSID) when the children were 2 years old. Delayed neurodevelopment was defined as scores of PDI or MDI less than − 1SD relative to the mean score of the study population. A group-based multi-trajectory model was adopted to identify multi-trajectories of systolic blood pressure (SBP) and diastolic blood pressure (DBP). Visit-to-visit BP variability was assessed by the coefficient of variation (CV), standard deviation (SD), and average real variability (ARV). Generalized linear models and multivariate logistic regressions were used to assess the associations of BP trajectories and variability with BSID scores and delayed neurodevelopment, respectively. Results Five distinct trajectories for SBP and DBP were identified, namely, “Low-increasing,” “Low-stable,” “Moderate-decreasing,” “Moderate-increasing,” and “High-stable” groups. Compared with the “Low-stable” group, the children whose mothers’ BP fell into the other four groups had lower PDI scores, and mothers in the “Low-increasing,” “Moderate-increasing,” and “Moderate-decreasing” groups had 43% (OR: 1.43, 95% CI: 1.01, 2.03), 48% (OR: 1.48, 95% CI: 1.05, 2.08) and 45% (OR:1.45, 95% CI: 1.03, 2.04) higher risk of having offspring with delayed psychomotor neurodevelopment, respectively. High DBP variability was associated with lower BSID scores, and delayed psychomotor neurodevelopment (OR = 1.46, 95% CI: 1.10, 1.92 for DBP-SD; OR = 1.53, 95% CI: 1.16, 2.02 for DBP-CV). Conclusion Our findings suggest that BP change patterns assessed by multi-trajectory and visit-to-visit variability were associated with lower BSID scores and delayed neurodevelopment. Health professionals should be aware of the influence of BP level and its oscillations during pregnancy on the risk of delayed neurodevelopment.

Abstract Background Early pregnancy is a critical window for neural system programming; however, the association of first-trimester fetal size with children’s neurodevelopment remains to be assessed. This study aimed to explore the association between first-trimester fetal size and children’s neurodevelopment and to examine whether intrauterine accelerated growth could compensate for the detrimental effects of first-trimester restricted growth on childhood neurodevelopment. Methods The participants were from a birth cohort enrolled from March 2014 to March 2019 in Wuhan, China. A total of 2058 fetuses with crown to rump length (CRL) (a proxy of first-trimester fetal size) measurements in the first trimester and neurodevelopmental assessment at age 2 years were included. We measured the first-trimester CRL and defined three fetal growth patterns based on the growth rate of estimated fetal weight from mid to late pregnancy. The neurodevelopment was assessed using the Bayley Scales of Infant Development of China Revision at 2 years. Results Each unit (a Z score) increase of first-trimester CRL was associated with increased scores in mental developmental index (MDI) (adjusted beta estimate = 1.19, (95% CI: 0.42, 1.95), P = 0.03) and psychomotor developmental index (PDI) (adjusted beta estimate = 1.36, (95% CI: 0.46, 2.26), P

Prenatal lead (Pb) and manganese (Mn) exposure can impair neurodevelopment, targeting the central nervous system. This study investigated the effects of prenatal exposure to Pb and Mn on neurodevelopment in children at 18 months of age, using data from 607 Italian mother–child pairs enrolled in the Northern Adriatic Cohort II (NAC-II). All children born at term (≥37 weeks) were assessed with the Bayley Scales of Infant and Toddler Development, third edition. Cord blood concentrations of Mn and Pb were categorized as low or high exposures based on the 75th percentile of their distribution. Sociodemographic and lifestyle information was collected via questionnaires. Using simple and multiple linear regressions, the study examined the relationship between the cognitive composite score (COGN) and Mn and Pb co-exposure, including their interaction. Stratified regressions explored how Mn exposure influenced the effect of Pb, in the whole cohort and by the child’s sex. Beta coefficients (β) and the 90% confidence interval (90% CI) were estimated. Boys showed an interaction effect between Mn and Pb, with a reduction in COGN (β = −5.78, 90% CI: −11.17; −0.40), further described as a negative effect of high Pb on cognition when Mn exposure was also high (β = −6.98, 90% CI: −10.93; −3.04). No clear effects were observed in girls or the entire cohort at these levels of exposure. The findings highlight the harmful impact of combined prenatal Pb and Mn exposure on cognitive development in boys.

Background: The patterns of blood pressure (BP) change throughout the pregnancy were related to adverse birth outcomes. However, little is known about the long-term effect of BP change patterns on child neurodevelopment. This study aimed to explore the relationship between the BP trajectory and BP variability during pregnancy and early childhood neurodevelopment. Method: A total of 2797 mother-newborn pairs were derived from the Wuhan Healthy Baby Cohort Study. BP was measured during each antenatal visit, and Mental and Psychomotor Development Indexes (MDI and PDI) were assessed using the Bayley Scales of Infant Development (BSID) when the children were 2 years old. Delayed neurodevelopment was defined as scores of PDI or MDI less than − 1SD relative to the mean score of the study population. A group-based multi-trajectory model was adopted to identify multi-trajectories of systolic blood pressure (SBP) and diastolic blood pressure (DBP). Visit-to-visit BP variability was assessed by the coefficient of variation (CV), standard deviation (SD), and average real variability (ARV). Generalized linear models and multivariate logistic regressions were used to assess the associations of BP trajectories and variability with BSID scores and delayed neurodevelopment, respectively. Results: Five distinct trajectories for SBP and DBP were identified, namely, "Low-increasing," "Low-stable," "Moderate-decreasing," "Moderate-increasing," and "High-stable" groups. Compared with the "Low-stable" group, the children whose mothers' BP fell into the other four groups had lower PDI scores, and mothers in the "Low-increasing," "Moderate-increasing," and "Moderate-decreasing" groups had 43% (OR: 1.43, 95% CI: 1.01, 2.03), 48% (OR: 1.48, 95% CI: 1.05, 2.08) and 45% (OR:1.45, 95% CI: 1.03, 2.04) higher risk of having offspring with delayed psychomotor neurodevelopment, respectively. High DBP variability was associated with lower BSID scores, and delayed psychomotor neurodevelopment (OR = 1.46, 95% CI: 1.10, 1.92 for DBP-SD; OR = 1.53, 95% CI: 1.16, 2.02 for DBP-CV). Conclusion: Our findings suggest that BP change patterns assessed by multi-trajectory and visit-to-visit variability were associated with lower BSID scores and delayed neurodevelopment. Health professionals should be aware of the influence of BP level and its oscillations during pregnancy on the risk of delayed neurodevelopment. [ABSTRACT FROM AUTHOR]

Background: Early pregnancy is a critical window for neural system programming; however, the association of first-trimester fetal size with children's neurodevelopment remains to be assessed. This study aimed to explore the association between first-trimester fetal size and children's neurodevelopment and to examine whether intrauterine accelerated growth could compensate for the detrimental effects of first-trimester restricted growth on childhood neurodevelopment. Methods: The participants were from a birth cohort enrolled from March 2014 to March 2019 in Wuhan, China. A total of 2058 fetuses with crown to rump length (CRL) (a proxy of first-trimester fetal size) measurements in the first trimester and neurodevelopmental assessment at age 2 years were included. We measured the first-trimester CRL and defined three fetal growth patterns based on the growth rate of estimated fetal weight from mid to late pregnancy. The neurodevelopment was assessed using the Bayley Scales of Infant Development of China Revision at 2 years. Results: Each unit (a Z score) increase of first-trimester CRL was associated with increased scores in mental developmental index (MDI) (adjusted beta estimate = 1.19, (95% CI: 0.42, 1.95), P = 0.03) and psychomotor developmental index (PDI) (adjusted beta estimate = 1.36, (95% CI: 0.46, 2.26), P < 0.01) at age 2 years, respectively. No significant association was observed between fetal growth rate and PDI. For children with restricted first-trimester fetal size (the lowest tertile of first-trimester CRL), those with "intrauterine accelerated growth" pattern (higher growth rates) had significantly higher MDI (adjusted beta estimate = 6.14, (95% CI: 3.80, 8.49), P < 0.001) but indistinguishable PDI compared to those with "intrauterine faltering growth" pattern (lower growth rates). Main limitations of this study included potential misclassification of gestational age due to recall bias of the last menstrual period and residual confounding. Conclusions: The current study suggests that restricted first-trimester fetal size is associated with mental and psychomotor developmental delay in childhood. However, in children with restricted first-trimester fetal size, intrauterine accelerated growth was associated with improved mental development but had little effect on psychomotor development. Additional studies are needed to validate the results in diverse populations. [ABSTRACT FROM AUTHOR]

Objective: To review the evidence on the association between maternal exposure to ultraprocessed food (UPF) categories, UPF diet items, and overall diet quality, as assessed by recognized dietary indices, and neurodevelopmental outcomes in offspring. Methods: PubMed, MEDLINE, EMBASE, Scopus, Ovid, and Scholar databases were searched for original articles on female gestational exposure to UPF categories, individual elements of the UPF diet, or indices of diet quality, in relation to outcomes regarding their offspring's neurocognitive development, according to neuropsychometric and behavioral scales, anthropometric/psychomotor indices, and symptoms/diagnosis of neurodevelopmental disorders (NDDs). Results: Fourteen articles were selected and underwent the quantitative analysis. Six of these examined diet quality, and eight exposure to UPF categories or specific UPF foods. The maternal population was adult (18+). Child cognitive development was negatively impacted by a diet featuring many processed foods, saturated fats, and sugars. Conversely, a Med-diet led to better neurodevelopment, particularly verbal intelligence and executive functions, in middle childhood. Discussion: A maternal diet with many UPFs, saturated fats, and total sugars (especially those added or hidden in packaged carbonated beverages) can adversely affect a child's cognitive development. Knowledge needs to be further extended and managed from a prevention perspective in light of the well-known negative effects of UPFs on human health in all age groups. [ABSTRACT FROM AUTHOR]

Objective: Treatment indication of maternal subclinical hypothyroidism (SCH) is undetermined, despite the wide administration of levothyroxine for maternal overt hypothyroidism (OH). This study aimed to evaluate the therapeutic effect of levothyroxine for maternal SCH and OH in real‐world practice, with a focus on early child neurodevelopment. Design: Prospective cohort study. Patients and Measurements: Pregnant women diagnosed with SCH at the first antenatal visit were enroled and compared to those diagnosed with OH. Thyroid follow‐ups were conducted during pregnancy. Early child neurodevelopment was assessed using the Gesell Development Diagnosis Scale (GDDS) at 1, 3, 6, 12 and 24 months of age. Results: From January 2012 to December 2013, a total of 442 pregnant women were included in final analysis, among whom 194 and 248 were assigned to the SCH and OH groups, respectively. The percentage of levothyroxine therapy at the first antenatal visit was significantly lower in the SCH group than that in the OH group (91.24% vs. 97.58%, p <.01), with a similar treatment rate at delivery (99.4% vs. 100%, p >.05). Notably, GDDS scores were lower in the SCH group than those in the OH group at 6 months to 2 years of age, which was confirmed by subgroup analyses and sensitivity analyses. Conclusions: Children born with maternal SCH demonstrated slightly lower neuropsychological scores at 6 months to 2 years of age compared to those with maternal OH in the clinical practice. The therapeutic effect of maternal SCH on the child neurodevelopment requires further exploration. [ABSTRACT FROM AUTHOR]

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Background: There are limited population studies on the neurodevelopmental effects of bisphenol F (BPF), a substitute for bisphenol A. Furthermore, the role of placental estradiol as a potential mediator linking these two factors remains unclear. Objective: To examine the association between maternal prenatal BPF exposure and infant neurodevelopment in a prospective cohort study and to explore the mediating effects of placental estradiol between BPF exposure and neurodevelopment in a nested case-control study. Methods: The prospective cohort study included 1077 mother-neonate pairs from the Wuhu city cohort study in China. Maternal BPF was determined using the liquid/liquid extraction and Ultra-performance liquid chromatography tandem mass spectrometry method. Children's neurodevelopment was assessed at ages 3, 6, and 12 months using Ages and Stages Questionnaires. The nested case-control study included 150 neurodevelopmental delay cases and 150 healthy controls. Placental estradiol levels were measured using enzyme-linked immunosorbent assay kits. Generalized estimating equation models and robust Poisson regression models were used to examine the associations between BPF exposure and children's neurodevelopment. In the nested case-control study, causal mediation analysis was conducted to assess the role of placental estradiol as a mediator in multivariate models. Results: In the prospective cohort study, the pregnancy-average BPF concentration was positively associated with developmental delays in gross-motor, fine-motor, and problem-solving ( ORtotal ASQ: 1.14(1.05, 1.25), ORgross-motor: 1.22(1.10, 1.36), ORfine-motor: 1.19(1.07, 1.31), ORproblem-solving: 1.11(1.01, 1.23)). After sex-stratified analyses, pregnancy-average BPF concentration was associated with an increased risk of neurodevelopmental delays in the gross-motor (ORgross-motor:1.30(1.12, 1.51)) and fine-motor (ORfine-motor: 1.22(1.06, 1.40)) domains in boys. In the nested case-control study, placental estradiol mediated 16.6% (95%CI: 4.4%, 35.0%) of the effects of prenatal BPF exposure on developmental delay. Conclusions: Our study supports an inverse relationship between prenatal BPF exposure and child neurodevelopment in infancy, particularly in boys. Decreased placental estradiol may be an underlying biological pathway linking prenatal BPF exposure to neurodevelopmental delay in offspring.

Background: ‘Epigenetic clocks’ have been developed to accurately predict chronologic gestational age and have been associated with child health outcomes in prior work. Methods: We meta-analysed results from four prospective U.S cohorts investigating the association between epigenetic age acceleration estimated using blood DNA methylation collected at birth and preschool age Childhood Behavior Checklist (CBCL) scores. Results: Epigenetic ageing was not significantly associated with CBCL total problem scores (β = 0.33, 95% CI: −0.95, 0.28) and DSM-oriented pervasive development problem scores (β = −0.23, 95% CI: −0.61, 0.15). No associations were observed for other DSM-oriented subscales. Conclusions: The meta-analysis results suggest that epigenetic gestational age acceleration is not associated with child emotional and behavioural functioning for preschool age group. These findings may relate to our study population, which includes two cohorts enriched for ASD and one preterm birth cohort.; future work should address the role of epigenetic age in child health in other study populations. Abbreviations: DNAm: DNA methylation; CBCL: Child Behavioral Checklist; ECHO: Environmental Influences on Child Health Outcomes; EARLI: Early Autism Risk Longitudinal Investigation; MARBLES: Markers of Autism Risk in Babies – Learning Early Signs; ELGAN: Extremely Low Gestational Age Newborns; ASD: autism spectrum disorder; BMI: body mass index; DSM: Diagnostic and Statistical Manual of Mental Disorders.

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Introduction: Subclinical hypothyroidism (SCH) during pregnancy is reported to have detrimental impact on pregnancy and child development. However, its treatment indications require further investigation in different thyroid peroxidase antibody (TPOAb) status. Material and methods: This was a secondary analysis of a Chinese prospective cohort in a real‐world setting. Pregnant women with gestational SCH were enrolled at the first antenatal visit and grouped by TPOAb positivity. Child neurodevelopment was assessed by the Gesell development diagnosis scale (GDDS) at one, three, six, 12, and 24 months of age. Subgroup analyses and sensitivity analyses were also conducted. Clinical trial registration: ClinicalTrials.gov NCT01744743. Results: From January 2012 to December 2013, a total of 171 participants were enrolled, including 116 of SCH with TPOAb negative (SCH‐TPOAb [−]) and 55 of SCH with TPOAb positive (SCH‐TPOAb [+]). Compared to women in the SCH‐TPOAb (+) group, those in the SCH‐TPOAb (−) group had lower thyroid‐stimulating hormone (TSH) levels at enrollment and 12–16+6 gestational weeks, and unexpectedly higher TSH levels at 30–34+6 gestational weeks and delivery, with a correspondingly lower levothyroxine dosage throughout pregnancy (all p < 0.05). Offspring in the SCH‐TPOAb (−) group displayed lower GDDS scores at one year old than did their counterparts (adjusted p < 0.05), which was possibly related to the worse thyroid function control of maternal SCH‐TPOAb (−). No statistically significant difference was found in the GDDS assessments of children at one, three, six, and 24 months of age. These results were also confirmed in subgroup analyses stratified by maternal thyroid characteristics at enrollment, namely TSH levels, free levothyroxine (T4) levels, and anti‐thyroglobulin antibody (TgAb) status, as well as in sensitivity analyses excluding participants with no levothyroxine treatment at enrollment. Conclusions: In the current clinical practice, infants born to mothers with SCH‐TPOAb (−) displayed slightly lower neurodevelopmental scores at one year old than did those born to mothers with SCH‐TPOAb (+) but this difference was not seen at two years. [ABSTRACT FROM AUTHOR]

The impact of maternal exposure to Bisphenol A on child cognitive development as well as its sex dimorphism remains uncertain. This study used data of 215 mothers and their children from a birth cohort in Shanghai. Urinary BPA were measured in spot urine samples of mothers at late pregnancy and children at age 2 years. Cognitive development was evaluated by Ages & Stages Questionnaires, Third Edition (ASQ-3) at age 2 years. Urinary BPA was detectable in 98.9% of mothers (geometric mean, GM: 2.6 μg/g. creatinine) and 99.8% children (GM: 3.4 μg/g. creatinine). Relative to the low and medium BPA tertiles, high tertile of maternal urinary BPA concentrations were associated with 4.8 points lower (95% CI: −8.3, −1.2) in gross motor and 3.7 points lower (95% CI: −7.4, −0.1) in problem-solving domain in girls only, with adjustment for maternal age, maternal education, pre-pregnancy BMI, passive smoking during pregnancy, parity, delivery mode, birth-weight for gestational age, child age at ASQ-3 test. This negative association remained with additional adjustment for child urinary BPA concentrations at age 2 years. No association was observed in boys. These results suggested the sex-dimorphism on the associations of maternal BPA exposure with gross motor and problem-solving domains in children at age 2 years. This study also indicated that optimal early child development should start with a healthy BPA-free “in utero” environment.

Background: Perfluoroalkyl acids (PFAAs) within the broader class of per- and polyfluoroalkyl substances (PFAS) are present in human serum as isomer mixtures, but epidemiological studies have yet to address isomer-specific associations with child development and behavior. Objectives: To examine associations between prenatal exposure to 25 PFAAs, including perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) isomers, and child neurodevelopment among 490 mother–child pairs in a prospective Canadian birth cohort, the Alberta Pregnancy Outcomes and Nutrition (APrON) study. To consider the influence of a classic neurotoxicant, total mercury (THg), based on its likelihood of co-exposure with PFAAs from common dietary sources. Methods: Maternal blood samples were collected in the second trimester and child neurodevelopment was assessed at 2 years of age using the Bayley Scales of Infant and Toddler Development, 3rd Edition (Bayley-III). Linear or curvilinear multiple regression models were used to examine associations between exposures and neurodevelopment outcomes. Results: Select PFAAs were associated with lower Cognitive composite scores, including perfluoroheptanoate (PFHpA) (β = −0.88, 95% confidence interval (CI): −1.7, −0.06) and perfluorododecanoate (PFDoA) (β = −2.0, 95% CI: −3.9, −0.01). Non-linear relationships revealed associations of total PFOS (β = −4.4, 95% CI: −8.3, −0.43), and linear-PFOS (β = −4.0, 95% CI: −7.5, −0.57) and 1m-PFOS (β = −1.8, 95% CI: −3.3, −0.24) isomers with lower Language composite scores. Although there was no effect modification, including THg interaction terms in PFAA models revealed negative associations between perfluorononanoate (PFNA) and Motor (β = −3.3, 95% CI: −6.2, −0.33) and Social-Emotional (β = −3.0, 95% CI: −5.6, −0.40) composite scores. Discussion: These findings reinforce previous reports of adverse effects of maternal PFAA exposure during pregnancy on child neurodevelopment. The unique hazards posed from isomers of PFOS justify isomer-specific analysis in future studies. To control for possible confounding, mercury co-exposure may be considered in studies of PFAAs.

Amsalu Taye Wondemagegn,1 Abay Mulu2 1Department of Biomedical Sciences, School of Medicine, Debre Markos University, Debre Markos, Ethiopia; 2Department of Anatomy, College of Health Sciences, Addis Ababa University, Addis Ababa, EthiopiaCorrespondence: Amsalu Taye Wondemagegn, Department of Biomedical Sciences, School of Medicine, Debre Markos University, P.O. Box: 269, Debre Markos, Amhara Regional State, Ethiopia, Tel +251 921815441, Email 50amsalu@gmail.comIntroduction: Scientific evidence regarding relationships between developmental status and nutritional status of children aged under five years old is scarce, particularly in Africa. Thus, the objective of the present study is to evaluate the relationships between nutritional status and developmental status among children aged under five in Gojjam, Ethiopia.Methods: A cross-sectional study was conducted on 390 child–mother pairs from December 1– 30 2021. Developmental status, nutritional status and related data were collected using age and stage questionnaire 3rd edition (ASQ-3) and measurements of body dimensions and other physical characteristics. Body dimensions data was obtained by measurement of height and weight of children aged under five years. Logistic regression analysis was executed to identify factors related with poor child developmental status. Adjusted odds ratio (AOR) and 95% CI was estimated to reveal the strength of association and statistical significance were declared at p-value less than 5%.Results: The overall prevalence of developmental delay in the current study among under five years children was 22.6%. Moreover, in this study the prevalence of stunting, wasting and being underweight was 36.3%, 14.2% and 20.3%, respectively. Developmental delay among under-five children was significantly associated with experiencing repeated diseases during pregnancy (AOR: 2.43; 95% CI:1.38, 4.28), short birth interval (AOR: 2.78; 95% CI :1.52, 5.09), stunting (AOR: 2.61;95% CI: 1.41, 4.84), wasting (AOR: 3.68;95% CI: 1.61, 8.37) and being underweight (COR: 3.28;95% CI: 1.91, 5.63).Conclusion: The overall developmental delay prevalence among under-five children in the present study was 22.6%. The prevalence of stunting, wasting and being underweight was 36.3%, 14.2% and 20.3%, respectively. Maternal diseases, birth interval and nutritional status of children aged under five years were among the factors which revealed statistically significant associations with developmental delay of under-five children. We recommend the concerned body to work on improving maternal health status during pregnancy, to enable mothers to adequately space subsequent births, and to work on improving the nutritional status of women and children in the current study area in order to improve the developmental status of children aged under five.Keywords: child neurodevelopment, child developmental status, nutritional status, under-five children, Ethiopia

Many young children in low- and middle-income countries (LMICs) are at risk of developmental delays. Early child development (ECD) interventions have been shown to improve outcomes, but few interventions have targeted culturally normative violence such as corporal punishment (CP). We partnered with an existing community-based ECD organization in the LMIC of Grenada to implement a parallel controlled-trial single-blind responsive caregiving intervention that educates parents about the developing brain and teaches alternatives to corporal punishment while building parental self-regulation skills and strengthening social-emotional connections between parent and child. Parents and primary caregivers with children under age two were eligible. Allocation to the intervention and waitlist control arms was unblinded and determined by recruitment into the program. Neurodevelopment was assessed by blinded testers when each child turned age two. Primary comparison consisted of neurodevelopmental scores between the intervention and waitlist control groups (Clinicaltrials.gov registration # NCT04697134). Secondary comparison consisted of changes in maternal mental health, home environment, and attitudes towards CP. Children in the intervention group (n = 153) had significantly higher scores than children in the control group (n = 151) on measures of cognition (p = .022), fine motor (p < .0001), gross motor (p = .015), and language development (p = .013). No difference in secondary outcomes, including CP, was detected.

Background: 'Epigenetic clocks' have been developed to accurately predict chronologic gestational age and have been associated with child health outcomes in prior work. Methods: We meta-analysed results from four prospective U.S cohorts investigating the association between epigenetic age acceleration estimated using blood DNA methylation collected at birth and preschool age Childhood Behavior Checklist (CBCL) scores. Results: Epigenetic ageing was not significantly associated with CBCL total problem scores (ß = 0.33, 95% CI: -0.95, 0.28) and DSM-oriented pervasive development problem scores (ß = -0.23, 95% CI: -0.61, 0.15). No associations were observed for other DSM-oriented subscales. Conclusions: The meta-analysis results suggest that epigenetic gestational age acceleration is not associated with child emotional and behavioural functioning for preschool age group. These findings may relate to our study population, which includes two cohorts enriched for ASD and one preterm birth cohort.; future work should address the role of epigenetic age in child health in other study populations. Abbreviations: DNAm: DNA methylation; CBCL: Child Behavioral Checklist; ECHO: Environmental Influences on Child Health Outcomes; EARLI: Early Autism Risk Longitudinal Investigation; MARBLES: Markers of Autism Risk in Babies - Learning Early Signs; ELGAN: Extremely Low Gestational Age Newborns; ASD: autism spectrum disorder; BMI: body mass index; DSM: Diagnostic and Statistical Manual of Mental Disorders. [ABSTRACT FROM AUTHOR]

Background: An increase in the prevalence of neurodevelopmental conditions worldwide, alongside resource constraints within clinical services, has led to increased interest in health information technologies, such as apps and digital resources. Digital tools are often viewed as a solution to bridge this divide and to increase supports for families. There is, however, a paucity of research that has evaluated digital health tools, their potential benefits for child neurodevelopment and associated concerns (eg, mental health, well-being), and their benefit for families., Objective: This study conducted the first review of existing mobile apps and digital resources targeted at supporting the needs of children with developmental concerns or neurodevelopmental conditions., Methods: We identified 3435 separate resources, of which 112 (43 apps and 69 digital resources) met the criteria. These resources were categorized according to their purpose or target and were then reviewed based on their engagement, information quality, and evidence base using the Adapted Mobile App Rating Scale., Results: The most common condition of concern targeted by apps and digital resources was autism (19/112, 17% resources), with retrieved resources focusing on supporting challenging behaviors, promoting speech, language, and social development, and providing options for alternative and assistive communication. Other common areas of concern targeted by apps and digital resources included language and communication (16/112, 14.3%) and attention-deficit/hyperactivity disorder (11/112, 9.8%). Results showed that reviewed resources were engaging, with high levels of accessibility and functionality. Resources had various functions, including developmental or behavioral tasks targeted at children, assistive communication support, scheduling support, journaling, and advice, activities, and strategies for parents. The information quality of resources, such as credibility of source and evidence base was, however, mostly low. Apps and digital resources with good credibility and an existing evidence base were largely developed in partnership with research, health, or government institutions, and were rated significantly higher on overall quality compared with apps and digital resources not developed in partnership with such institutions (apps; t 41 =-4.35, P<.001; digital resources; t 67 =-4.95, P<.001)., Conclusions: The lack of evidence base across resources means that it is extremely difficult to provide recommendations to families with respect to apps or digital resources that may support their needs. Frameworks for the development of new tools are discussed, highlighting the novel approaches required to demonstrate the efficacy of tools for improving outcomes for children and families. Such a framework requires collaboration with multiple stakeholders (software developers, researchers, regulatory bodies, clinicians, children, and families) and engagement across multiple levels of expertise (app development, implementation, and dissemination within services, policy, and clinical regulations), to harness the potential of digital health for improving outcomes and promoting support in child neurodevelopment, which at this juncture remains largely underdeveloped., (©Kelsie Ann Boulton, Makana Hilton, Emilia Sutton, Adam John Guastella. Originally published in the Journal of Medical Internet Research (https://www.jmir.org), 01.01.2025.)

Background: The amount of people affected by traffic-related air pollution and noise is continuously increasing, but limited research has been conducted on the association between these environmental exposures and functional brain connectivity in children. Objective: This exploratory study aimed to analyze the associations between the exposure to traffic-related air pollution and noise during pregnancy and childhood, and functional brain connectivity amongst a wide-swath of brain areas in preadolescents from 9 to 12 years of age. Methods: We used data of 2,197 children from the Generation R Study. Land use regression models were applied to estimate nitrogen oxides and particulate matter levels at participant’s homes for several time periods: pregnancy, birth to 3 years, 3 to 6 years, and 6 years of age to the age at magnetic resonance imaging (MRI) assessment. Existing noise maps were used to estimate road traffic noise exposure at participant’s homes for the same time periods. Resting-state functional MRI was obtained at 9–12 years of age. Pair-wise correlation coefficients of the blood-oxygen-level-dependent signals between 380 brain areas were calculated. Linear regressions were run and corrected for multiple testing. Results: Preadolescents exposed to higher levels of NO2, NOx, and PM2.5 absorbance, from birth to 3 years, and from 3 to 6 years of age showed higher correlation coefficients among several brain regions (e.g. from 0.16 to 0.19 higher correlation coefficient related to PM2.5 absorbance exposure, depending on the brain connection). Overall, most identified associations were between brain regions of the task positive and task negative networks, and were mainly inter-network (20 of 26). Slightly more than half of the connections were intra-hemispheric (14 of 26), predominantly in the right hemisphere. Road traffic noise was not associated with functional brain connectivity. Conclusions: This exploratory study found that exposure to traffic-related air pollution during the first years of life was related to higher functional brain connectivity predominantly in brain areas located in the task positive and task negative networks, in preadolescents from 9 to 12 years of age. These results could be an indicator of differential functional connectivity in children exposed to higher levels of air pollution.

Copyright of Psychosocial Intervention is the property of Colegio Oficial de Psicologos de Madrid and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: The PPARα gene may be crucial to the neurotoxic effect of phthalates. However, epidemiological studies considering the neurodevelopmental influence of phthalates interacting with genetic susceptibility are limited. We hypothesized phthalates could interact with the PPARα gene, synergistically affecting neurocognitive development. Methods: A total of 961 mother-infant pairs were involved in this study. The concentrations of phthalate metabolites in maternal urine during pregnancy were detected. Children's neurocognitive development was estimated with the Bailey Infant Development Inventory (BSID). Genetic variations in PPARα were genotyped with the Illumina Asian Screening Array. We applied generalized linear regression models to estimate genotypes and phthalate metabolites' association with children's neurocognitive development. Results: After adjusting for potential confounders, the mono-n-butyl phthalate (MnBP) concentration was negatively associated with Psychomotor Development Index (PDI) (β = −0.86, 95% CI: −1.67, −0.04). The associations between MnBP and neurocognitive development might be modified by PPARα rs1800246. Compared with low-MnBP individuals carrying rs1800246 GG genotypes, high-MnBP individuals with the AG + AA genotype had a higher risk of neurocognitive developmental delay, with the odds ratio of 2.76 (95% CI:1.14, 6.24). Conclusions: Our current study revealed that prenatal exposure to MnBP was negatively correlated with children's neurocognitive development, and PPARα rs1800246 might modify the association. [ABSTRACT FROM AUTHOR]

Background: The PPARα gene may be crucial to the neurotoxic effect of phthalates. However, epidemiological studies considering the neurodevelopmental influence of phthalates interacting with genetic susceptibility are limited. We hypothesized phthalates could interact with the PPARα gene, synergistically affecting neurocognitive development.Methods: A total of 961 mother-infant pairs were involved in this study. The concentrations of phthalate metabolites in maternal urine during pregnancy were detected. Children’s neurocognitive development was estimated with the Bailey Infant Development Inventory (BSID). Genetic variations in PPARα were genotyped with the Illumina Asian Screening Array. We applied generalized linear regression models to estimate genotypes and phthalate metabolites’ association with children’s neurocognitive development.Results: After adjusting for potential confounders, the mono-n-butyl phthalate (MnBP) concentration was negatively associated with Psychomotor Development Index (PDI) (β = −0.86, 95% CI: −1.67, −0.04). The associations between MnBP and neurocognitive development might be modified by PPARα rs1800246. Compared with low-MnBP individuals carrying rs1800246 GG genotypes, high-MnBP individuals with the AG + AA genotype had a higher risk of neurocognitive developmental delay, with the odds ratio of 2.76 (95% CI:1.14, 6.24).Conclusions: Our current study revealed that prenatal exposure to MnBP was negatively correlated with children’s neurocognitive development, and PPARα rs1800246 might modify the association.

South Africa has the highest burden of human immunodeficiency virus (HIV) per capita and the largest antiretroviral treatment program globally. It is a country with a deeply entrenched history of differentiation based on race, which limited access to quality health care, education, and employment to most of its citizens. The purpose of this paper is to explore past and present disparities with a particular focus on HIV and neurocognitive development in children. We describe developments around the history of HIV and treatment in South Africa and how inequality affected HIV transmission and management. By highlighting the HIV-focused research at the Family Centre for Research with UBUNTU (FAMCRU) in Cape Town, South Africa, we aim to demonstrate that HIV related health disparities can be addressed through continued research focused approaches. At FAMCRU, special reference is made to improving the neurodevelopmental trajectories of children living with HIV. We conclude with some recommendations how to improve health outcomes in a research-driven environment. [ABSTRACT FROM AUTHOR]

Background: Despite a clear association seen in congenitally infected children, the effect of postnatal cytomegalovirus (CMV) infection during early childhood on cognitive development has not yet been determined.Methods: CMV-infection status was obtained based on serological measurements when children were 7 years old. Using population-based longitudinal data, we employed multivariate Poisson regression with a robust variance estimator to characterize the relationship between childhood CMV infection and adverse neurocognitive outcomes in children. Suboptimal neurocognitive outcomes were compared between CMV-positive and CMV-negative children using various cognitive assessments from 8 to 15 years of age. Children were evaluated on the cognitive domains of language, reading, memory and general intelligence, with a suboptimal score being >2 standard deviations lower than the mean score. Approximate Bayes factor (ABF) analysis was used to determine the level of evidence for the observed associations.Results: With adjustment for potential confounders, we observed that early-childhood CMV infection was associated with suboptimal total intelligence quotient (IQ) at 8 years of age [incidence-rate ratio (IRR) = 2.50, 95% confidence interval (CI) 1.35-4.62, ABF = 0.08], but not with suboptimal total IQ at 15 years of age (IRR = 0.97, 95% CI 0.43-2.19, ABF = 1.68). Suboptimal attentional control at 8 years (IRR = 1.74, 95% CI 1.13-2.68, ABF = 0.18) and reading comprehension at 9 years (IRR = 1.93, 95% CI 1.12-3.33, ABF = 0.24) were also associated with CMV infection. ABF analysis provided strong evidence for the association between CMV infection and total IQ at 8 years, and only anecdotal evidence for attentional control at 8 years and reading comprehension at 9 years. All other cognitive measures assessed were not associated with CMV infection.Conclusion: In this large-scale prospective cohort, we observed some evidence for adverse neurocognitive effects of postnatal CMV infection on general intelligence during early childhood, although not with lasting effect. If confirmed, these results could support the implementation of preventative measures to combat postnatal CMV infection. [ABSTRACT FROM AUTHOR]

Purpose: Current knowledge of the effect of prenatal caffeine exposure on the child's neurodevelopment is contradictory. The current study aimed to study whether caffeine intake during pregnancy was associated with impaired child neurodevelopment up to 8 years of age. Method: A total of 64,189 full term pregnancies from the Norwegian Mother, Father and Child Cohort Study were included. A validated food-frequency questionnaire administered at gestational week 22 was used to obtain information on maternal caffeine intake from different sources. To assess child neurodevelopment (behaviour, temperament, motor development, language difficulties) validated scales were used to identify difficulties within each domain at 6, 18, 36 months as well as 5 and 8 years of age. Adjusted logistic regression models and mixed linear models were used to evaluate neurodevelopmental problems associated with maternal caffeine intake. Results: Prenatal caffeine exposure was not associated with a persistently increased risk for behaviour, temperament, motor or language problems in children born at full-term. Results were consistent throughout all follow-ups and for different sources of caffeine intake. There was a minor trend towards an association between consumption of caffeinated soft drinks and high activity level, but this association was not driven by caffeine. Conclusion: Low to moderate caffeine consumption during pregnancy was not associated with any persistent adverse effects concerning the child's neurodevelopment up to 8 years of age. However, a few previous studies indicate an association between high caffeine consumption and negative neurodevelopment outcomes. [ABSTRACT FROM AUTHOR]

Background: Emerging evidence suggests that phthalate exposure may be associated with behavior problems in children and that these associations may be sex specific. Methods: In a follow up study of 411 inner-city minority mothers and their children, mono-n-butyl phthalate (MnBP), monobenzyl phthalate (MBzP), monoisobutyl phthalate (MiBP), monethyl phthalate (MEP) and four di-2-ethylhexyl phthalate metabolites (DEHP) were quantified in maternal urine samples collected during the third trimester and in child urine samples at ages 3 and 5 years. The Conners’ Parent Rating Scale-Revised: Long Form (CPRS) and Child Behavior Checklist (CBCL) were administered to the mothers to assess children’s behavior problems at 7 years of age. The analysis included children with available measures of CBCL, CPRS and phthalates measured in maternal urine. We performed both Quasi-Poisson regression and a mixture analysis using Weighted Quantile Sum(WQS) regression to assess the risk for CPRS scores and for internalizing and externalizing behaviors (from the CBCL) following intra-uterine exposure to the phthalate metabolites for boys and girls separately. Results: Among boys, increases in in anxious-shy behaviors were associated with prenatal exposure to MBzP (Mean Ratio [MR] = 1.20, 95%CI 1.05–1.36) and MiBP (Mean Ratio (MR) = 1.22, 95%CI 1.02–1.47). Among girls, increases in perfectionism were associated with MBzP (MR = 1.15, 95%CI 1.01–1.30). In both boys and girls, increases in psychosomatic problems were associated with MiBP (MR = 1.28, 95%CI 1.02–1.60), and MnBP (MR = 1.28, 95%CI 1.02–1.59), respectively. Among girls, decreased hyperactivity was associated with two DEHP metabolites, mono(2-ethyl-5-oxohexyl) phthalate (MR = 0.83, 95%CI 0.71–0.98) and mono(2-ethyl-5-hydroxyhexyl) phthalate (MR = 0.85, 95%CI 0.72–0.99). Using weighted Quantile Sum logistic regression, no associations were found between the Weighted Quantile Sum (WQS) of phthalate metabolites and CPRS scores or externalizing and internalizing behaviors. Nonetheless, when the analysis was performed separately for DEHP and non-DEHP metabolites significant associations were found between the WQS of DEHP metabolites and social problems in boys (OR = 2.15, 95%CI 1.13–4.06, p-value = 0.02) anxious-shy problems in girls (OR = 2.19, 95%CI 1.15–4.16, p = 0.02), and emotional lability problems in all children (OR = 0.61, 95%CI 0.38–0.97, p = 0.04). MEHP and MEOHP were the most highly weighted DEHP metabolites in WQS mixture. The analysis performed with CBCL scale corroborated these associations. Conclusion: Concentration of non-DEHP metabolites was associated with anxious-shy behaviors among boys. DEHP phthalate metabolites were associated with decreased hyperactivity and impulsivity among girls on CPRS scores. These findings lend further support to the adverse associations between prenatal phthalate exposure and childhood outcomes, and clearly suggest that such associations are sex and mixture specific.

Objective: Prenatal exposure to heavy metals, pesticides and phenols has been suggested to interfere with neurodevelopment, but the neurotoxicity of their mixtures is still unclear. We aimed to elucidate the associations of maternal urinary concentrations of selected chemical mixtures with intelligence quotient (IQ) in children. Methods: Maternal urinary concentrations of selected heavy metals, pesticide metabolites, and phenols were quantified in pregnant women who participated in the Sheyang Mini Birth Cohort Study (SMBCS) from June 2009 to January 2010. At age 7 years, child’s IQ score was assessed using the Chinese version of Wechsler Intelligence Scale for Children (C-WISC) by trained pediatricians. Generalized linear regression models (GLM), Bayesian kernel machine regression (BKMR) models and elastic net regression (ENR) models were used to assess the associations of urinary concentrations individual chemicals and their mixtures with IQ scores of the 7-year-old children. Results: Of 326 mother-child pairs, single-chemical models indicated that prenatal urinary concentrations of lead (Pb) and bisphenol A (BPA) were significantly negatively associated with full intelligence quotient (FIQ) among children aged 7 years [β = −2.31, 95% confidence interval (CI): −4.13, −0.48; p = 0.013, sex interaction p-value = 0.076; β = −1.18, 95% CI: −2.21, −0.15; p = 0.025; sex interaction p-value = 0.296, for Pb and BPA, respectively]. Stratified analysis by sex indicated that the associations were only statistically significant in boys. In multi-chemical BKMR and ENR models, statistically significant inverse association was found between prenatal urinary Pb level and boy’s FIQ scores at 7 years. Furthermore, BKMR analysis indicated that the overall mixture was associated with decreases in boy’s IQ when all the chemicals’ concentrations were at their 75th percentiles or higher, compared to at their 50th percentiles. ENR models revealed that maternal urinary Pb levels were statistically significantly associated with lower FIQ scores (β = −2.20, 95% CI: −4.20, −0.20; p = 0.031). Conclusions: Prenatal exposure to selected chemical mixtures may affect intellectual performance at 7 years of age, particularly in boys. Pb and BPA were suspected as primary chemicals associated with child neurodevelopment.

Abstract Background Child neurodevelopment has been positively linked to maternal intake of polyunsaturated fatty acids (PUFAs) during pregnancy; however, it is unknown if that relationship persists among populations exposed to environmental neurotoxicants. Objective The aim of this work was to assess whether maternal dietary intake of PUFAs during pregnancy is positively associated with child neurodevelopment, whose mothers were environmentally exposed to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT). Methods A prospective cohort study with 276 mother–child pairs was performed in Mexico. Neurodevelopment was assessed by Bayley Scales II from children age 1 to 30 months. Dietary PUFAs intake was estimated by Food Frequency Questionnaire at 1st and 3rd trimester of pregnancy. DDE (1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene, the main metabolite of DDT) maternal serum levels were determined by electron capture gas chromatography. Longitudinal multivariate linear mixed-effects analysis, which combines mental (MDI) and motor (PDI) Bayley scales in a single model, were performed. Results Our results show that in a sample environmentally exposed to DDT, maternal ingestion of DPA during the first trimester of pregnancy was positively associated with MDI (β = 0.10, 95% CI 0.02, 0.18) in children from 1 to 30 months. Likewise, our results suggest that dietary ALA may be also related to MDI. Conclusion DPA may benefit neurodevelopment even in populations exposed to DDT. Our results strengthen the importance of PUFAs intake during the prenatal period.

Background Fish is a primary source of protein and n-3 PUFA but also contains methylmercury (MeHg), a naturally occurring neurotoxicant to which, at sufficient exposure levels, the developing fetal brain is particularly sensitive. Objectives To examine the association between prenatal MeHg and maternal status of n-3 and n-6 PUFA with neurodevelopment, and to determine whether PUFA might modify prenatal MeHg associations with neurodevelopment. Methods We examined the Seychelles Child Development Study Nutrition Cohort 2 (NC2) at age 7 y. We used a sophisticated and extensive neurodevelopmental test battery that addressed 17 specific outcomes in multiple neurodevelopmental domains: cognition, executive and psychomotor function, language development, behavior, scholastic achievement, and social communication. Analyses were undertaken on 1237 mother-child pairs with complete covariate data (after exclusions) and a measure of at least 1 outcome. We examined the main and interactive associations of prenatal MeHg exposure (measured as maternal hair mercury) and prenatal PUFA status (measured in maternal serum at 28 weeks' gestation) on child neurodevelopmental outcomes using linear regression models. We applied the Bonferroni correction to account for multiple comparisons and considered P values <0.0029 to be statistically significant. Results Prenatal MeHg exposure and maternal DHA and arachidonic acid (20:4n-6) (AA) status were not significantly associated with any neurodevelopmental outcomes. Findings for 4 outcomes encompassing executive function, cognition, and linguistic skills suggested better performance with an increasing maternal n-6:n-3 PUFA ratio (P values ranging from 0.004 to 0.05), but none of these associations were significant after adjusting for multiple comparisons. No significant interaction between MeHg exposure and PUFA status was present. Conclusions Our findings do not support an association between prenatal MeHg exposure or maternal DHA and AA status with neurodevelopmental outcomes at age 7 y. The roles of n-6 and n-3 PUFA in child neurodevelopment need further research. [ABSTRACT FROM AUTHOR]

Copyright of Medicina (Buenos Aires) is the property of Medicina (Buenos Aires) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background Mild-to-moderate iodine deficiency, particularly in pregnancy, is prevalent; this is of concern because observational studies have shown negative associations with child neurodevelopment. Although neither the benefits nor the safety of iodine supplementation in pregnancy in areas of mild-to-moderate deficiency are well researched, such supplementation is increasingly being recommended by health authorities in a number of countries. Objectives By reviewing the most recent published data on the effects of iodine supplementation in mildly-to-moderately deficient pregnant women on maternal and infant thyroid function and child cognition, we aimed to determine whether the evidence was sufficient to support recommendations in these areas. Methods A systematic review of randomized controlled trials (RCTs), non-RCT interventions, and observational studies was conducted. To identify relevant articles, we searched the PubMed and Embase databases. We defined mild-to-moderate iodine deficiency as a baseline median urinary iodine concentration (UIC) of 50–149 µg/L. Eligible studies were included in meta-analyses. Results In total, 37 publications were included—10 RCTs, 4 non-RCT interventions, and 23 observational studies. Most studies showed no effect of iodine supplementation on maternal or infant thyroid-stimulating hormone and free thyroxine. Most RCTs found that supplementation reduced maternal thyroglobulin and in 3 RCTs, it prevented or diminished the increase in maternal thyroid volume during pregnancy. Three RCTs addressed child neurodevelopment; only 1 was adequately powered. Meta-analyses of 2 RCTs showed no effect on child cognitive [mean difference (MD): −0.18; 95% CI: −1.22, 0.87], language (MD: 1.28; 95% CI: −0.28, 2.83), or motor scores (MD: 0.28; 95% CI: −1.10, 1.66). Conclusions There is insufficient good-quality evidence to support current recommendations for iodine supplementation in pregnancy in areas of mild-to-moderate deficiency. Well-designed RCTs, with child cognitive outcomes, are needed in pregnant women who are moderately deficient (median UIC < 100 µg/L). Maternal intrathyroidal iodine stores should be considered in future trials by including appropriate measures of preconceptional iodine intake. This review was registered at www.crd.york.ac.uk/prospero as CRD42018100277. [ABSTRACT FROM AUTHOR]

Background: Recent studies have suggested an association between prenatal paracetamol exposure and adverse neurodevelopmental outcomes in children. However, these findings may be confounded by unmeasured factors related to maternal use of paracetamol and child outcomes.Objective: To examine the association between duration and timing of prenatal paracetamol exposure on parent-reported communication skills, behaviour, and temperament in preschool-aged children, with focus on the role of unmeasured confounding.Methods: We used data from the Norwegian Mother and Child Cohort Study. Linear and generalised linear models with inverse probability weights and robust standard errors were used to quantify the association between prenatal paracetamol exposure and continuous and categorical outcomes.Results: Of the 32 934 children included in our study, 8374 (25.4%), 4961 (15.1%), and 1791 (5.4%) were prenatally exposed to paracetamol in one, two, and three trimesters, respectively. Children exposed to paracetamol in two trimesters scored lower on shyness compared with unexposed children (β -0.62, 95% confidence interval [CI] -1.05, -0.19). Children exposed to paracetamol in three trimesters had a moderate increased risk of internalising behaviour problems (relative risk (RR) 1.36, 95% CI 1.02, 1.80) and borderline externalising behaviour problems (RR 1.22, 95% CI 0.93, 1.60) compared with unexposed children. Children exposed to paracetamol in 2nd/3rd trimester scored lower on shyness (β -0.32, 95% CI -0.66, 0.02) compared with unexposed children. Sensitivity analyses indicated that unmeasured confounders play an important role and may potentially bias the effect estimates away from the null.Conclusions: Timing of exposure and short-term use of paracetamol during pregnancy do not seem to pose any substantial risk of the outcomes examined. Although we found an association between paracetamol use in multiple trimesters and lower shyness and greater internalising behaviour in preschool-aged children, we cannot rule out chance or unmeasured confounding as possible explanations for these findings. [ABSTRACT FROM AUTHOR]

• Maternal perinatal psychiatric disorders determine important biological variations in breast milk composition. • Breast milk is a fundamental source of many different nutritional, immune and hormonal components. • Changes in milk composition can contribute to cognitive impairments and alterations in child development. • Milk fatty acids and immune molecules mediate the relationship between maternal psychopathology and child development. Perinatal psychopathologies affect more than 25% of women during and after their gestational period. These psychiatric disorders can potentially determine important biological variations in their organisms, affecting many different physiological and metabolic pathways. Of relevance, any of these changes occurring in the mother can alter the normal composition of breast milk, particularly the concentration of nutritional and inflammatory components, which play a role in child brain functioning and development. Indeed, there is evidence showing that changes in milk composition can contribute to cognitive impairments and alterations in mental abilities in children. This review aims to shed light on the unique intergenerational role played by breast milk composition, from maternal psychopathologies to child development. [ABSTRACT FROM AUTHOR]

Abstract Background Intra-amniotic inflammation is associated with adverse pregnancy and neonatal outcomes. However, the impact on child neurodevelopment remains unclear. We aim to assess the effect of intra-amniotic inflammation on neurodevelopmental outcomes in children. Methods The databases MEDLINE, Embase, CINAHL, and Cochrane will be searched from their inception until November 2017. Randomized trials and cohort studies in which inflammatory markers were measured in amniotic fluid collected by amniocentesis and in which infant’s neurodevelopment was assessed will be eligible. Two reviewers will independently select eligible studies, assess their risk of bias, and extract data. Results will be compared and a third party will be consulted in case of disagreement. Our primary outcome of interest is child neurodevelopment, assessed with either a validated tool or by revision of medical records for specific diagnosis. Secondary outcomes will include abnormal brain imaging. Relative risks will be pooled and sensitivity analyses will be performed for the indication of amniocentesis, gestational age at amniocentesis, gestational age at delivery, and fetal sex. Risk of bias will be assessed using the Cochrane Collaboration’s tool for assessing the risk of bias in randomized trials or an adapted version of the ROBINS-1 for the risk of bias in non-randomized studies. Discussion This systematic review will report the current evidence regarding the association between amniotic inflammation and child neurodevelopment, and the modifiers of this association. The review will generate new hypotheses on pathological pathways and will guide future research. Systematic review registration PROSPERO 2017 65065

Background: The Australian Early Development Census (AEDC) provides a measure of early child development upon school entry. Understanding which combination of factors influences Aboriginal child neurodevelopment is important to inform policy and practice.Objective: The primary objective was to use latent class analysis (LCA) to model AEDC profiles and identify the highest need profiles. The secondary objective was to determine the associations of these high need profiles on the likelihood of a child becoming developmentally vulnerable.Methods: We designed a prospective population-based birth cohort study (n = 2715) using linked data sets with information on Aboriginal cohort children, and their mothers and siblings in Western Australia. Specific developmental indicators in the 2009 and 2012 AEDC were used to assess developmental vulnerability. LCA methods were used to determine need profiles and their association with developmental vulnerability.Results: 49.3% of Aboriginal children were vulnerable on at least one developmental domain, and 37.5% were vulnerable on two or more domains. LCA found six unique profiles. High needs family, High needs young mother, and Preterm infant comprised 42% of the cohort and were considered to have high need configurations. These groups were at least 1.7 times as likely to have children who had at least one or two developmental vulnerabilities compared with the Healthy family group.Conclusion: Many Aboriginal children in Western Australia enter school with at least one developmental vulnerability. This study highlights a range of unique profiles that can be used to empower Aboriginal families for change and develop targeted programmes for improving the early development of young Aboriginal children. [ABSTRACT FROM AUTHOR]

Our aim in this study was to estimate the strength of associations between prenatal diet quality and child behavioral, language, and motor functions in the Norwegian Mother and Child Cohort Study (1999–2008). We created a prenatal diet quality index (PDQI) based on adherence to Norwegian dietary guidelines. Child outcomes were defined as sum scores on the Child Behavior Checklist, the Ages and Stages Questionnaire, and the Child Development Index at ages 18, 36, and 60 months. Using a longitudinal cohort study design and Bayesian hierarchical modeling, we estimated association strengths using inverse probability weighting to account for selection bias. In total, 27,529 mother-child pairs were eligible for inclusion. A 1–standard-deviation increase in PDQI score was associated with an absolute reduction in outcome sum scores of 0.02–0.21 and a 3%–7% relative decrease, with larger decreases seen for language and motor functions than for behavioral functions. PDQI scores were inversely associated with all child functions, but the estimated strength of each association was low. The results indicate that the observed variations in PDQI scores in an industrialized Western society may not profoundly influence the child functions studied. [ABSTRACT FROM AUTHOR]

Effective treatment of maternal antenatal depression may ameliorate adverse neurodevelopmental outcomes in offspring. We performed two follow-up rounds of children at age 2 and age 5 whose mothers had received either specialized cognitive-behavioural therapy or routine care for depression while pregnant. Of the original cohort of 54 women, renewed consent was given by 28 women for 2-year follow-up and by 24 women for 5-year follow-up. Child assessments at the 2-year follow-up included the Parenting Stress Index (PSI), Bayley Scales of Infant Development (BSID-III) and the Child Behaviour Checklist (CBCL). The 5-year follow-up included the Wechsler Preschool and Primary Scales of Intelligence (WPPSI-III) and again the CBCL. Treatment during pregnancy showed significant benefits for children's development at age 2, but not at age 5. At 2 years, intervention effects were found with lower scores on the PSI Total score, Parent Domain and Child domain (d =1.44, 1.47, 0.96 respectively). A non-significant trend favoured the intervention group on most subscales of the CBCL and the BSID-III (most notably motor development: d =0.52). In contrast, at 5-year follow-up, no intervention effects were found. Also, irrespective of treatment allocation, higher depression or anxiety during pregnancy was associated with higher CBCL and lower WPPSI-III scores at 5 years. This is one of the first controlled studies to evaluate the long-term effect of antenatal depression treatment on infant neurodevelopmental outcomes, showing some benefit. Nevertheless, caution should be taken interpreting the results because of a small sample size, and larger studies are warranted. [ABSTRACT FROM AUTHOR]

There are limited population studies on the neurodevelopmental effects of bisphenol F (BPF), a substitute for bisphenol A. Furthermore, the role of placental estradiol as a potential mediator linking these two factors remains unclear. To examine the association between maternal prenatal BPF exposure and infant neurodevelopment in a prospective cohort study and to explore the mediating effects of placental estradiol between BPF exposure and neurodevelopment in a nested case-control study. The prospective cohort study included 1077 mother-neonate pairs from the Wuhu city cohort study in China. Maternal BPF was determined using the liquid/liquid extraction and Ultra-performance liquid chromatography tandem mass spectrometry method. Children's neurodevelopment was assessed at ages 3, 6, and 12 months using Ages and Stages Questionnaires. The nested case-control study included 150 neurodevelopmental delay cases and 150 healthy controls. Placental estradiol levels were measured using enzyme-linked immunosorbent assay kits. Generalized estimating equation models and robust Poisson regression models were used to examine the associations between BPF exposure and children's neurodevelopment. In the nested case-control study, causal mediation analysis was conducted to assess the role of placental estradiol as a mediator in multivariate models. In the prospective cohort study, the pregnancy-average BPF concentration was positively associated with developmental delays in gross-motor, fine-motor, and problem-solving (OR total ASQ : 1.14(1.05, 1.25), OR gross-motor : 1.22(1.10, 1.36), OR fine-motor : 1.19(1.07, 1.31), OR problem-solving : 1.11(1.01, 1.23)). After sex-stratified analyses, pregnancy-average BPF concentration was associated with an increased risk of neurodevelopmental delays in the gross-motor (OR gross-motor :1.30(1.12, 1.51)) and fine-motor (OR fine-motor : 1.22(1.06, 1.40)) domains in boys. In the nested case-control study, placental estradiol mediated 16.6% (95%CI: 4.4%, 35.0%) of the effects of prenatal BPF exposure on developmental delay. Our study supports an inverse relationship between prenatal BPF exposure and child neurodevelopment in infancy, particularly in boys. Decreased placental estradiol may be an underlying biological pathway linking prenatal BPF exposure to neurodevelopmental delay in offspring. [Display omitted] ● Prenatal BPF exposure was associated with infant neurodevelopmental delays. ● Prenatal BPF exposure was associated with neurodevelopmental delays in boys. ● Placental estradiol mediated the effects of BPF exposure on neurodevelopment. [ABSTRACT FROM AUTHOR]

Background: In 2009, the Australian government mandated the fortification of bread salt with iodine. In 2010, pregnant and lactating women were also advised to take an iodine-containing supplement. Our assessment of this policy in an iodine-sufficient population showed that children whose mothers were in the highest and lowest quartiles of iodine intake performed more poorly on early childhood tests of cognition and language than those in the second quartile. However, we did not quantify the iodine intake associated with optimal neurodevelopment., Objectives: The aim was to establish the iodine intake range in pregnancy associated with optimal child neurodevelopment., Methods: A prospective cohort study of pregnant women and their young children (n = 699). Iodine intake was assessed by a validated food frequency questionnaire at 16 and 28 wk of gestation. Child neurodevelopment at 18 mo of age was measured using the Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III). The relationship between average iodine intake during pregnancy and child neurodevelopment was assessed using linear regression with fractional polynomials and adjustment for confounders., Results: Mean (SD) iodine intake was similar at study entry and 28 wk, 308 (120) μg/d, with 82% of women taking iodine supplements at study entry. The relationship between iodine intake during pregnancy and Bayley-III cognitive and language scores was curvilinear (P = 0.001 and P = 0.004, respectively), with the lowest Bayley-III scores observed at lower and higher iodine intakes. The inflection point that drove the association between lower iodine intake in pregnancy and poorer child neurodevelopment scores was around 185 μg/d; for the higher pregnancy iodine intakes, language and cognitive scores were negatively affected from ∼350 μg/d to 370 μg/d, respectively. Higher iodine intakes were being driven by supplement use., Conclusions: Targeted, not blanket, iodine supplementation may be needed for pregnant women with low-iodine intake from food., (Copyright © 2023 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)