Effect of parental obesity and gestational diabetes on child neuropsychological and behavioral development at 4 years of age: the Rhea mother-child cohort, Crete, Greece

Studies have suggested an association between maternal obesity pre-pregnancy and gestational diabetes (GDM) with impaired offspring neurodevelopment, but it is not clear if these associations are explained by shared familiar characteristics. We aimed to assess the associations of maternal and paternal obesity, maternal glucose intolerance in early pregnancy and GDM, with offspring neurodevelopment at 4 years of age. We included 772 mother-child pairs from the "Rhea" Mother-Child cohort in Crete, Greece. Data on maternal/paternal body mass index (BMI) and maternal fasting serum samples for glucose and insulin measurements were collected at 12 weeks of gestation. GDM screening was performed at 24-28 weeks. Neurodevelopment at 4 years was assessed using the McCarthy Scales of Children's Abilities. Behavioral difficulties were assessed by Strengths and Difficulties Questionnaire and Attention Deficit Hyperactivity Disorder Test. Multivariate linear regression analyses showed that maternal obesity was associated with a significant score reduction in general cognitive ability (beta-coeff -4.03, 95% CI: -7.08, -0.97), perceptual performance (beta-coeff -4.60, 95% CI: -7.74, -1.47), quantitative ability (beta-coeff -4.43, 95% CI: -7.68, -1.18), and executive functions (beta-coeff -4.92, 95% CI: -8.06, -1.78) at 4 years of age, after adjustment for several confounders and paternal BMI. Maternal obesity was also associated with increased behavioral difficulties (beta-coeff 1.22, 95% CI: 0.09, 2.34) and ADHD symptoms (beta-coeff 4.28, 95% CI: 1.20, 7.36) at preschool age. Paternal obesity maternal glucose intolerance in early pregnancy and GDM was not associated with child neurodevelopment. These findings suggest that maternal obesity may impair optimal child neurodevelopment at preschool age independently of family shared characteristics

Maternal mild thyroid dysfunction and offspring cognitive and motor development from infancy to childhood: the Rhea mother-child cohort study in Crete, Greece

BACKGROUND: Maternal thyroid hormones’ supply is crucial for fetal neurodevelopment; however, the role of maternal mild thyroid dysfunction is not clear. We aimed to assess the association of maternal mild thyroid dysfunction with child neuropsychological development from infancy to early childhood. METHODS: We included 757 mother-child pairs from the prospective “Rhea” cohort on Crete, Greece. Maternal thyroid functioning was assessed by quantitative analysis of serum thyroid stimulating hormone (TSH), free thyroxine (fT4), thyroid peroxidase antibodies (TPO-Abs), and thyroglobulin antibodies (Tg-Abs) at early gestation (mean=14 weeks). Neuropsychological assessment was based on Bayley Scales of Infant Development (18 months of age), McCarthy Scales of Children’s Abilities (4 years of age), Raven’s Coloured Progressive Matrices, Trail Making Test, and Finger Tapping Test (6 years of age). RESULTS: In multivariate adjusted linear regression analyses maternal hypothyroxinemia was associated with decreased verbal scores at 4 years and reduced motor speed at 6 years of age. Maternal thyroid autoimmunity was associated with decreased child perceptual and motor ability at 4 years of age. Four trajectories of longitudinal non-verbal cognitive development were identified and children exposed to maternal thyroid autoimmunity had increased risk for belonging to an adverse trajectory (“Low”: adjusted-RRR = 2.7 95%CI: [1.4, 5.2], “High-decreasing”: adjusted-RRR = 2.2 95%CI: [1.2, 4.0], “Low-increasing”: adjusted-RRR = 1.8 95%CI: [1.0, 3.2]). CONCLUSION: Maternal hypothyroxinemia is associated with reduced offspring verbal and motor ability. Maternal thyroid autoimmunity is associated with decreased offspring perceptual performance and motor ability and increased risk for adverse non-verbal cognitive development from infancy to childhood

Cord Leptin is Associated with Neuropsychomotor Development in Childhood

Objective: Leptin is critical for central nervous system development and maturation. This study aimed to evaluate the potential regulatory role of cord leptin in the neuropsychomotor development of children ages 18 months to 6 years. Methods: This study included 424 children from a prospective mother-child cohort (Rhea Study; Crete, Greece) with available cord leptin levels and data on neurodevelopmental outcomes at 18 months (Bayley Scales of Infant and Toddler Development, Third Edition), 4 years (McCarthy Scales of Children's Abilities), and 6 years (Raven's Coloured Progressive Matrices and Trail Making Test). Multivariable linear regression models were used to explore the associations. Results: Each 10-ng/mL increase in the cord leptin level was associated with increased scores on the gross motor scale at 18 months (β coefficient: 3.8; 95% CI: 0.0-7.5), with decreased scores in the general cognitive performance (β coefficient: −3.0; 95% CI: −5.5 to −0.4), perceptual performance (β coefficient: −3.4; 95% CI: −6.0 to −9.9), working memory (β coefficient: −3.1; 95% CI: −5.7 to −0.4), executive function (β coefficient −3.1; 95% CI: −5.7 to −0.5), and functions of the posterior cortex (β coefficient: −2.7; 95% CI: −5.2 to −0.1) scales at 4 years, and with a 3.7-unit decrease in the Raven's Coloured Progressive Matrices score at 6 years (β coefficient: −3.7; 95% CI: −6.9 to −0.5). Conclusions: Increased cord leptin levels are associated with enhanced gross motor development at 18 months but decreased cognitive performance in early and middle childhood. © 2019 The Obesity Societ