The role of early life nutrition's impact on relevant health outcomes across the lifespan laid the foundation for the field titled the developmental origins of health and disease. Studies in this area initially concentrated on nutrition and the risk of adverse cardio-metabolic and cancer outcomes. More recently the role of nutrition in early brain development and the subsequent influence of later mental health has become more evident. Scientific breakthroughs have elucidated two mechanisms behind long-term nutrient effects on the brain, including the existence of critical periods for certain nutrients during brain development and nutrient-driven epigenetic modifications of chromatin. While multiple nutrients and nutritional conditions have the potential to modify brain development, iron can serve as a paradigm to understand both mechanisms. New horizons in nutritional medicine include leveraging the mechanistic knowledge of nutrient–brain interactions to propose novel nutritional approaches that protect the developing brain through better timing of nutrient delivery and potential reversal of negative epigenetic marks. The main challenge in the field is detecting whether a change in nutritional status truly affects the brain's development and performance in human subjects. To that end, a strong case can be made to develop and utilise bioindicators of a nutrient's effect on the developing brain instead of relying exclusively on biomarkers of the nutrient's status.

Accumulating evidence indicates that the fetal environment plays an important role in brain development and sets the brain on a trajectory across the life span. An abnormal fetal environment results when factors that should be present during a critical period of development are absent or when factors that should not be in the developing brain are present. While these factors may acutely disrupt brain function, the real cost to society resides in the long-term effects, which include important mental health issues. We review the effects of three factors, fetal alcohol exposure, teratogen exposure, and nutrient deficiencies, on the developing brain and the consequent risk for developmental psychopathology. Each is reviewed with respect to the evidence found in epidemiological and clinical studies in humans as well as preclinical molecular and cellular studies that explicate mechanisms of action.

The human brain undergoes a remarkable transformation during fetal life and the first postnatal years from a relatively undifferentiated but pluripotent organ to a highly specified and organized one. The outcome of this developmental maturation is highly dependent on a sequence of environmental exposures that can have either positive or negative influences on the ultimate plasticity of the adult brain. Many environmental exposures are beyond the control of the individual, but nutrition is not. An ever-increasing amount of research demonstrates not only that nutrition shapes the brain and affects its function during development but also that several nutrients early in life have profound and long-lasting effects on the brain. Nutrients have been shown to alter opening and closing of critical and sensitive periods of particular brain regions. This paper discusses the roles that various nutrients play in shaping the developing brain, concentrating specifically on recently explicated biological mechanisms by which particularly salient nutrients influence childhood and adult neural plasticity.

Researchers, institutional review boards (IRBs), participants in human subjects research, and their families face an important but largely neglected problem — how should incidental findings (IFs) be managed in human subjects research. If researchers unexpectedly stumble upon information of potential health or reproductive significance, should they seek expert evaluation, contact the participant’s physician, tell the research participant, or respond with some combination? What should consent forms and the entire consent process say about how IFs will be handled in research? What should IRBs require?

The aim of the present research was to investigate the impact of abnormal fetal environment on explicit memory performance. Based on animal models, it was hypothesized that infants of diabetic mothers (IDMs) experience perturbations in memory performance due to exposure to multiple neurologic risk factors including: chronic hypoxia, hyperglycemia/reactive hypoglycemia, and iron deficiency. Memory performance, as measured by the elicited/deferred imitation paradigm, was compared between 13 IDMs (seven females, six males; mean age 365 days, SD 11) and 16 typically developing children (seven females, nine males; mean age 379 days, SD 9). The IDM group was characterized by shorter gestational age (mean 38w, SD 2), greater standardized birthweight scores (mean 3797g, SD 947), and lower iron stores (mean ferritin concentration 87μg/L, SD 68) in comparison with the control group (mean gestational age: 40w, SD 1; mean birthweight: 3639g, SD 348; mean newborn ferritin concentration 140μg/L, SD 46). After statistically controlling for both gestational age and global cognitive abilities, IDMs demonstrated a deficit in the ability to recall multi-step event sequences after a delay was imposed. These findings highlight the importance of the prenatal environment on subsequent mnemonic behavior and suggest a connection between metabolic abnormalities during the prenatal period, development of memory, circuitry, and behavioral mnemonic performance.

The prenatal and early postnatal periods constitute a time of rapid development when the brain is in a state of both heightened plasticity and vulnerability. Premature infants and infants of diabetic mothers represent two experiments of nature that allow researchers to observe how the developing brain responds to early biological challenge of either a global or regionally specific nature. We outline a set of organizing principles for conceptualizing the mechanisms by which early adverse experience may be encoded in the brain and subsequently expressed in behavior. We then review the available literature on developmental outcomes for infants born premature and infants of diabetic mothers. Research examining the relative influence of experience and maturation in the development of preterm infants indicates that advance experience does not accelerate the advent of specific cognitive capacities, but may enhance performance once the particular ability has emerged. Long-term follow-up of preterm infants also reveals evidence for plasticity and cognitive improvement into early adolescence for later maturing executive functions. Finally we offer an integrated model for investigating cognitive outcomes in infants of diabetic mothers that incorporates data from animal, electrophysiological, and behavioral measures.

The aim of this study was to determine whether there are primary effects of prematurity on the development of explicit memory. Elicited imitation of action sequences was used to compare immediate and 15-minute delayed memory in term and preterm infants (19 months corrected age; n=48) who were at low risk: none had experienced the medical or social risk factors often associated with preterm birth. Relative to infants born at term (38 to 40 weeks' gestation), children who had been born at 27 to 34 weeks' gestation showed lower levels of ordered recall; performance of healthy infants born at 35 to 37 weeks' gestation was intermediate and did not differ significantly from that of the other groups. These results suggest that specific cognitive deficits can occur as a function of preterm birth even in low-risk infants.