Exposure to a High-Fat Diet during Early Development Programs Behavior and Impairs the Central Serotonergic System in Juvenile Non-Human Primates.

Perinatal exposure to maternal obesity and high-fat diet (HFD) consumption not only poses metabolic risks to offspring but also impacts brain development and mental health. Using a non-human primate model, we observed a persistent increase in anxiety in juvenile offspring exposed to a maternal HFD. Postweaning HFD consumption also increased anxiety and independently increased stereotypic behaviors. These behavioral changes were associated with modified cortisol stress response and impairments in the development of the central serotonin synthesis, with altered tryptophan hydroxylase-2 mRNA expression in the dorsal and median raphe. Postweaning HFD consumption decreased serotonergic immunoreactivity in area 10 of the prefrontal cortex. These results suggest that perinatal exposure to HFD consumption programs development of the brain and endocrine system, leading to behavioral impairments associated with mental health and neurodevelopmental disorders. Also, an early nutritional intervention (consumption of the control diet at weaning) was not sufficient to ameliorate many of the behavioral changes, such as increased anxiety, that were induced by maternal HFD consumption. Given the level of dietary fat consumption and maternal obesity in developed nations these findings have important implications for the mental health of future generations.

Early identification of ADHD risk via infant temperament and emotion regulation: a pilot study.

BACKGROUND: Attention deficit hyperactivity disorder (ADHD) is theorized to have temperamental precursors early in life. These are difficult to identify because many core features of ADHD, such as breakdowns in executive function and self-control, involve psychological and neural systems that are too immature to reliably show dysfunction in early life. ADHD also involves emotional dysregulation, and these temperamental features appear earlier as well. Here, we report a first attempt to utilize indices of emotional regulation to identify ADHD-related liability in infancy. METHODS: Fifty women were recruited in the 2nd trimester of pregnancy, with overselection for high parental ADHD symptoms. Measures of maternal body mass index, nutrition, substance use, stress, and mood were examined during pregnancy as potential confounds. Offspring were evaluated at 6 months of age using LABTAB procedures designed to elicit fear, anger, and regulatory behavior. Mothers completed the Infant Behavior Questionnaire about their child's temperament. RESULTS: After control for associated covariates, including maternal depression and prenatal stress, family history of ADHD was associated with measures of anger/irritability, including infant negative vocalizations during the arm restraint task (p = .004), and maternal ratings of infant distress to limitations (p = .036). In the regulation domain, familial ADHD was associated with less parent-oriented attention seeking during the still face procedure (p < .001), but this was not echoed in the maternal ratings of recovery from distress. CONCLUSIONS: Affective response at 6 months of age may identify infants with familial history of ADHD, providing an early indicator of ADHD liability. These preliminary results provide a foundation for further studies and will be amplified by enlarging this cohort and following participants longitudinally to evaluate ADHD outcomes.