Faculty Bibliography

Introduction: Over the course of the 20th century, there has been a sharp increase in the consumption of saturated fat and refined sugars. This so-called "western diet" (WD) has been extensively linked to biological alterations and associated functional deficits in the hippocampus of animals. However, the effects of a WD on the human hippocampus are less well-characterized. This preliminary study aimed to extend prior animal work by investigating the effects of a WD on hippocampal volume in children. Methods: Twenty-one healthy children (ages 5-9) completed a structural T1-weighted magnetic resonance imaging scan. Bilateral hippocampal volumes (as regions-of-interest) and bilateral amygdala volumes (as medial temporal lobe control regions-of-interest) were calculated. WD variables were derived from the parent-completed Youth/Adolescent Food Frequency Questionnaire. Specifically, variables were calculated as percent of daily calories consumed from sugars, fats, or a combination of these (WD). Results: While the relationships between overall WD consumption and bilateral hippocampal volumes were not significant, increased fat consumption was significantly related to decreased left hippocampal volume. Sugar consumption was not related to hippocampal size. Control region volumes were not related to any diet variables. Discussion: This study is the first to directly link diet-specifically fat consumption-to decreased left hippocampal volume in children. This extends previous work showing smaller left hippocampal volume related to obesity in pediatric samples. Though preliminary, findings represent an important step toward understanding the impact of diet on child brain development.

This chapter provides an overview of current research discoveries beginning to uncover the neurobiology of maternal mental illness. Results are described according to standard diagnostic categories (specifically, perinatal depression, perinatal anxiety and OCD, postpartum psychosis and bipolar disorder, and trauma and posttraumatic stress disorder), yet we aim to put this approach in context with the introduction of a classification model for psychiatric research, the research domain criteria, gaining traction in basic and clinical translational fields. We first review a new area of study, the neuroplasticity of the pregnant and postpartum brain, as work here has relevance for understanding the pathophysiology of mental disorders and may provide clues to changes in brain functioning that are related to compromised parenting in the context of postpartum depression. We next provide background information on neuroendocrine and immune changes during pregnancy and, to a lesser extent, the postpartum period, as alterations in these systems are significantly implicated in underlying neurobiology of mental illness for peripartum women. Our discussion of the major mental illnesses for pregnant and postpartum women includes neuroendocrine changes, neuroinflammation, and neurotransmitter alterations, as well as circuit dysfunction. Overall, remarkable progress has been made in identifying variations in neurobiology (and related systems) involved in maternal mental illness; yet, it is clear that, as classified with standard diagnostic systems, these are heterogeneous disorders and there is individual variability in the alterations in neurobiology for the same illness.

The vast individual differences in the developmental origins of risk and resilience pathways combined with sophisticated capabilities of big data science increasingly point to the imperative of large, neurodevelopmental consortia to capture population heterogeneity and key variations in developmental trajectories. At the same time, such large-scale population-based designs involving multiple independent sites also must weigh competing demands. For example, the need for efficient, scalable assessment strategies must be balanced with the need for nuanced, developmentally sensitive phenotyping optimized for linkage to neural mechanisms and specification of common and distinct exposure pathways. Standardized epidemiologic batteries designed for this purpose such as PhenX (consensus measures for Phenotypes and eXposures) and the National Institutes of Health (NIH) Toolbox provide excellent "off the shelf" assessment tools that are well-validated and enable cross-study comparability. However, these standardized toolkits can also constrain ability to leverage advances in neurodevelopmental measurement over time, at times disproportionately advantaging established measures. In addition, individual consortia often expend exhaustive effort "reinventing the wheel," which is inefficient and fails to fully maximize potential synergies with other like initiatives. To address these issues, this paper lays forth an early childhood neurodevelopmental assessment strategy, guided by a set of principles synthesizing developmental and pragmatic considerations generated by the Neurodevelopmental Workgroup of the HEALthy Brain and Child Development (HBCD) Planning Consortium. These principles emphasize characterization of both risk- and resilience-promoting processes. Specific measurement recommendations to HBCD are provided to illustrate application. However, principles are intended as a guiding framework to transcend any particular initiative as a broad neurodevelopmentally informed, early childhood assessment strategy for large-scale consortia science.