Iron is essential for the functioning of all cells and organs, most critically for the developing brain in the fundamental neuronal processes of myelination, energy and neurotransmitter metabolism. Iron deficiency, especially in the first 1000 days of life, can result in long-lasting, irreversible deficits in cognition, motor function and behaviour. Pregnant women, infants and young children are most vulnerable to iron deficiency, due to their high requirements to support growth and development, coupled with a frequently inadequate dietary supply. An unrecognised problem is that even if iron intake is adequate, common pregnancy-related and lifestyle factors can affect maternal–fetal iron supply in utero, resulting in an increased risk of deficiency for the mother and her fetus. Although preterm birth, gestational diabetes mellitus and intrauterine growth restriction are known risk factors, more recent evidence suggests that maternal obesity and delivery by caesarean section further increase the risk of iron deficiency in the newborn infant, which can persist into early childhood. Despite the considerable threat that early-life iron deficiency poses to long-term neurological development, life chances and a country's overall social and economic progress, strategies to tackle the issue are non-existent, too limited or totally inappropriate. Prevention strategies, focused on improving the health and nutritional status of women of reproductive age are required. Delayed cord clamping should be considered a priority. Better screening strategies to enable the early detection of iron deficiency during pregnancy and early-life should be prioritised, with intervention strategies to protect maternal health and the developing brain.

The putative role of vitamin D in muscle function and strength throughout the life course is of interest because muscle strength is required for engagement in physical activity at all ages. As vitamin D deficiency is widely reported in the population, especially in countries at high latitude, the potential importance of vitamin D in muscle function throughout life, and the potential impacts on growth and development, participation in physical activity, and effects on skeletal and cardio‐metabolic health, comprise an important topic for discussion. This review provides an overview of muscle function and summarises the role of the vitamin D receptor and the proposed molecular mechanisms of action of vitamin D in muscle cells. In addition, the review provides a comprehensive assessment of the clinical evidence surrounding the association between vitamin D and muscle strength. Among adults, particularly older adults, cross‐sectional and cohort studies reported a positive association between vitamin D status and muscle strength. These associations have been largely confirmed by intervention studies. Limited research has been carried out in adolescents and children; two cross‐sectional studies in adolescents have suggested an association between serum 25‐hydroxyvitamin D concentrations and muscle strength. However, the two intervention studies in adolescents have yielded conflicting results. Other than a single observational study, data in young children are very limited and further investigation in under 12‐year‐olds is warranted.

Iron is critical to the developing brain, but fetal iron accretion is compromised by several maternal and pregnancy-related factors. Little consideration has been given to the long-term neurologic consequences of neonatal iron deficiency, especially in generally healthy, low-risk populations. We aimed to investigate the association between neonatal iron deficiency and neurologic development at 2 and 5 y of age. We measured umbilical cord serum ferritin concentrations in the prospective maternal-infant Cork BASELINE (Babies after SCOPE: Evaluating the Longitudinal Impact Using Neurological and Nutritional Endpoints) Birth Cohort. Lifestyle and clinical data were collected from 15 weeks of gestation to 5 y of age. Standardized neurologic assessments were performed at 2 y [Bayley Scales of Infant Development/Child Behavior Checklist (CBCL)] and 5 y (Kaufman Brief Intelligence Test/CBCL). Among 697 maternal-infant pairs, median (IQR) cord ferritin concentrations were 200.9 (139.0, 265.8) µg/L; 8% had neonatal iron deficiency (ferritin <76 µg/L). Using fully adjusted models, there was no association between neonatal iron deficiency and cognitive or behavioral outcomes at 2 or 5 y. We conducted an a priori sensitivity analysis in 306 high-risk children, selected using known risk factors for neonatal iron deficiency (smoking/obesity/cesarean section delivery/small-for-gestational age birth). In this high-risk subgroup, children with iron deficiency at birth (12%) had similar cognitive outcomes, but the behavioral assessments showed higher internalizing [9.0 (5.3, 12.0) compared with 5.0 (3.0, 10.0), P = 0.006; adjusted estimate (95% CI): 2.8 (0.5, 5.1), P = 0.015] and total [24.5 (15.3, 40.8) compared with 16.0 (10.0, 30.0), P = 0.009; adjusted estimate (95% CI): 6.6 (0.1, 13.1), P = 0.047] problem behavior scores at 5 y compared with those born iron sufficient. We have demonstrated lasting behavioral consequences of neonatal iron deficiency in high-risk children from our generally healthy, low-risk maternal-infant cohort. Although larger investigations are warranted, this study provides strong association data to suggest that interventions and strategies targeting the fetal and neonatal period should be prioritized for the prevention of iron deficiency and associated neurologic consequences.