Background Maternal obesity is associated with increased risk of adverse neurodevelopmental outcomes and obesity in offspring, yet their comorbidity among preschoolers and underlying mechanisms remain unclear.Objective To examine associations between maternal obesity in pregnancy and offspring preschool psychopathology, focusing on clinical and biological pathways.Methods In a cohort of 462 women with obesity in pregnancy (body mass index (BMI) ≥30 kg/m²) from the UK Pregnancies Better Eating and Activity Trial, followed up with their children at 3–4 years postpartum (49% boys), structural equation models assessed effects of antenatal exposures (measured at three visits) on child risk of psychopathology: maternal inflammation (by interleukin-6), glycaemia (by random glucose or gestational diabetes diagnosis), placental function (by placental growth factor) and depressive symptoms. Child outcomes were derived from the Strengths and Difficulties Questionnaire scores and psychological phenotypes from latent class analysis (LCA). Child adiposity and eating behaviours were compared across phenotypes.Findings High-risk of psychopathology was identified in 11.3% of children (boys 14.7%, girls 8%). Higher antenatal maternal depression and lower placental function predicted increased risk of psychopathology, while inflammation and glycaemia were not associated (R 2=44.5%). LCA identified externalising (8%) and internalising (4.1%) phenotypes. An externalising phenotype was associated with higher BMI, weight-for-age z-scores and waist circumference; both phenotypes showed greater food fussiness than well-adjusted children.Conclusions One in 10 children of women with obesity showed early risk of psychopathology, which was linked to adiposity. Antenatal maternal depression emerged as the primary risk factor, with a novel role for placental dysfunction.Clinical implication Screening for maternal depression and placental function in pregnancies affected by obesity may help reduce adverse neurodevelopmental and metabolic outcomes in offspring.
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Sigurðardottir et al. (2026) studied this question.
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