The developmental origins of health and disease hypothesis applied to neurodevelopmental outcomes asserts that the fetal origins of future development are relevant to mental health. There is a third pathway for the familial inheritance of risk for psychiatric illness beyond shared genes and the quality of parental care: the impact of pregnant women's distress—defined broadly to include perceived stress, life events, depression, and anxiety—on fetal and infant brain–behavior development. We discuss epidemiological and observational clinical data demonstrating that maternal distress is associated with children's increased risk for psychopathology: For example, high maternal anxiety is associated with a twofold increase in the risk of probable mental disorder in children. We review several biological systems hypothesized to be mechanisms by which maternal distress affects fetal and child brain and behavior development, as well as the clinical implications of studies of the developmental origins of health and disease that focus on maternal distress. Development and parenting begin before birth.

IMPORTANCE Selective serotonin reuptake inhibitor (SSRI) use among pregnant women is increasing, yet the association between prenatal SSRI exposure and fetal neurodevelopment is poorly understood. Animal studies show that perinatal SSRI exposure alters limbic circuitry and produces anxiety and depressive-like behaviors after adolescence, but literature on prenatal SSRI exposure in humans is limited and mixed.OBJECTIVE To examine associations between prenatal SSRI exposure and brain development using structural and diffusion magnetic resonance imaging (MRI).

IMPORTANCE Despite evidence of an association between prenatal acetaminophen exposure and attention-deficit/hyperactivity disorder (ADHD) in offspring, the drug is not contraindicated during pregnancy, possibly because prior studies have relied on maternal self-report, failed to quantify acetaminophen dose, and lacked mechanistic insight.OBJECTIVE To examine the association between prenatal acetaminophen exposure measured in meconium (hereinafter referred to as meconium acetaminophen) and ADHD in children aged 6 to 7 years, along with the potential for mediation by functional brain connectivity. DESIGN, SETTING, AND PARTICIPANTSThis prospective birth cohort study from the Centre Hospitalier Université de Sherbrooke in Sherbrooke, Québec, Canada, included 394 eligible children, of whom 345 had meconium samples collected at delivery and information on ADHD diagnosis. Mothers were enrolled from September 25, 2007, to September 10, 2009, at their first prenatal care visit or delivery and were followed up when children were aged 6 to 7 years. When children were aged 9 to 11 years, resting-state brain connectivity was assessed with magnetic resonance imaging. Data for the present study were collected from September

Attention deficit hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) are among the most common childhood disorders and frequently co-occur. The present study sought to advance our understanding of how comorbidity between ADHD and ODD develops during the preschool years by testing a cross-lagged model that integrates two prominent models: the developmental precursor model and the correlated risk factors model. Participants were 199 children (107 boys) who took part in a longitudinal study of preschoolers with behavior problems. Parent reports of ADHD and ODD symptoms were collected annually from ages 3 to 6 and a family history interview was administered at age 3. In support of the developmental precursors model, ADHD symptoms predicted later argumentative/defiant symptoms. In support of the correlated risk factors model, family histories of ADHD and ODD/CD symptoms were correlated risk factors that uniquely predicted ADHD and anger/irritable symptoms in children. Results suggest that the correlated risk factors model may best explain the development of comorbidity between symptoms of ADHD and anger/irritability, whereas the developmental precursors model may better explain the development of comorbidity between symptoms of ADHD and argumentative/defiance.