Nutrients and growth factors regulate brain development during fetal and early postnatal life. The rapidly developing brain is more vulnerable to nutrient insufficiency yet also demonstrates its greatest degree of plasticity. Certain nutrients have greater effects on brain development than do others. These include protein, energy, certain fats, iron, zinc, copper, iodine, selenium, vitamin A, choline, and folate. The effect of any nutrient deficiency or overabundance on brain development will be governed by the principle of timing, dose, and duration. The ability to detect the specific effects of nutrient deficiencies is dependent on knowing which area of the brain is preferentially affected and on having neurologic assessments that tap into the functions of those specific areas. As examples, protein-energy malnutrition causes both global deficits, which are testable by general developmental testing, and area-specific effects on the hippocampus and the cortex. Iron deficiency alters myelination, monoamine neurotransmitter synthesis, and hippocampal energy metabolism in the neonatal period. Assessments of these effects could include tests for speed of processing (myelination), changes in motor and affect (monoamines), and recognition memory (hippocampus). Zinc deficiency alters autonomic nervous system regulation and hippocampal and cerebellar development. Long-chain polyunsaturated fatty acids are important for synaptogenesis, membrane function, and, potentially, myelination. Overall, circuit-specific behavioral and neuroimaging tests are being developed for use in progressively younger infants to more accurately assess the effect of nutrient deficits both while the subject is deficient and after recovery from the deficiency.

Background: Serum ferritin measurements are used in clinical populations to estimate total body iron stores and the risk of subsequent iron deficiency or overload. The lack of normative newborn serum ferritin concentration data between 23 and 41 weeks has led to difficulty in establishing the incidence and degree of abnormal iron status in the neonatal period. Objectives: The primary objective of this review was to summarize the maternal and gestational factors that determine ferritin concentrations in full-term and pre-term newborn infants and to generate comprehensive reference values. The secondary objective was to assess serum ferritin concentrations in newborn infants at risk for abnormal fetal iron metabolism, including maternal diabetes mellitus, intrauterine growth restriction and maternal smoking during pregnancy. Methods: Serum ferritin and gestational age data at birth from 457 low-risk pre-term and term infants of 23–41 weeks gestation obtained from 35 published studies reviewed from a period of 25 years and from recently collected data from our centers were assessed by regression analysis. Slopes and intercepts of the high-risk groups were compared with the standard curve. Results: Umbilical cord serum ferritin concentrations increased with advancing gestational age, from a mean of 63 µg/l at 23 weeks to 171 µg/l at 41 weeks gestation (p < 0.001). The infants of diabetic mothers had a lower intercept than the control infants (p < 0.001). Conclusions: Iron deficiency and overload have been implicated in neurodevelopmental impairments. Normative cord serum ferritin data may permit a more precise assessment of infants who are at risk for abnormal iron status at birth.

Early iron deficiency not only affects brain and behavioral function during the period of iron deficiency, it persists long after treatment. The mech