ADHD symptoms and body composition changes in childhood: a longitudinal study evaluating directionality of associations.

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is linked to increased risk of overweight/obesity among children and adults. Studies have also implicated obesity as a risk factor for ADHD. However, no studies have evaluated bidirectional, longitudinal associations between childhood fat mass and ADHD symptom severity. OBJECTIVES: We investigate bidirectional associations between ADHD symptoms and measures of body composition between ages 1.5 and 9. We further examine effects of specific eating patterns linked to ADHD on associations between symptom severity and body composition. METHODS: The study utilized data from children (N = 3903) participating in the Generation R cohort (Netherlands). Children were enrolled at birth and retained regardless of ADHD symptoms over time. Cross-lagged and change models examined bidirectional associations between body composition (body mass index/dual-energy X-ray absorptiometry) and ADHD symptoms at four time points in childhood. RESULTS: A child with a clinically concerning ADHD symptom z-score two standard deviations above the mean at age 6 would be expected to experience about 0.22 kg greater fat mass gain measured via dual-energy x-ray absorptiometry between ages 6 and 9, even if they displayed healthy eating patterns (95% CI: 0.11 - 0.28, p < 0.001). Conversely, fat mass at any age did not predict worse ADHD symptoms later. CONCLUSIONS: Beginning in early childhood, more ADHD symptoms predict higher fat mass at later ages. We did not find evidence of a reverse association. Based on these and prior findings, lifestyle counselling during treatment for children with a diagnosis of ADHD should be considered, even if they are diagnosed in early childhood and do not yet have a body mass index of clinical concern.

Fetal sex specific differences in human placentation: a prospective cohort study.

INTRODUCTION: Our objective was to assess fetal sex specific differences in first trimester placental biomarkers of both physiological and pathological pregnancies and their interaction with environmental influences. This study is embedded in the Generation R Study, a prospective cohort study. METHODS: Only live singleton births were included. Linear regression was performed to assess the effect of sex on first trimester placental biomarkers. Interaction analyses were performed to assess interaction of fetal sex with environmental influences. First trimester soluble fms-like tyrosine kinase (s-Flt1), placental growth factor (PLGF), plasminogen activator inhibitor (PAI-2) and homocysteine levels were assessed. RESULTS: Significant fetal sex specific differences in placental biomarkers were observed. S-Flt1, PAI-2 and PLGF log transformated concentrations were 0.08 ng/mL (95% CI 0.05; 0.11), 0.07 ng/mL (95% CI 0.06; 0.09) and 0.04 pg/mL (95% CI 0.01; 0.06) higher in case of female as compared to male placentas. In pregnancies complicated by pre-eclampsia (PE), preterm birth (PTB) or a newborn being small for gestational age (SGA) no fetal sex specific differences were observed. Interaction analyses suggest that concentrations of s-Flt1, PLGF and PAI-2 decrease in male placentas in the case of hyperhomocysteinemia but remain equal in female placentas. DISCUSSION: Fetal sex affects early placentation processes with discrepancies regarding pregnancies complicated by PE, PTB or a newborn being SGA. This suggests that other mechanisms causing these complications may dominate the fetal sex effect. The differences concerning homocysteine suggest that fetal sex dependent placental gene-environment interactions exist. CONCLUSION: Fetal sex specific differences in placental biomarkers exist.