The causal relationship between iron deficiency and physical work capacity is evaluated through a systematic review of the research literature, including animal and human studies. Iron deficiency was examined along a continuum from severe iron-deficiency anemia (SIDA) to moderate iron-deficiency anemia (MIDA) to iron deficiency without anemia (IDNA). Work capacity was assessed by aerobic capacity, endurance, energetic efficiency, voluntary activity and work productivity. The 29 research reports examined demonstrated a strong causal effect of SIDA and MIDA on aerobic capacity in animals and humans. The presumed mechanism for this effect is the reduced oxygen transport associated with anemia; tissue iron deficiency may also play a role through reduced cellular oxidative capacity. Endurance capacity was also compromised in SIDA and MIDA, but the strong mediating effects of poor cellular oxidative capacity observed in animals have not been demonstrated in humans. Energetic efficiency was affected at all levels of iron deficiency in humans, in the laboratory and the field. The reduced work productivity observed in field studies is likely due to anemia and reduced oxygen transport. The social and economic consequences of iron-deficiency anemia (IDA) and IDNA have yet to be elucidated. The biological mechanisms for the effect of IDA on work capacity are sufficiently strong to justify interventions to improve iron status as a means of enhancing human capital. This may also extend to the segment of the population experiencing IDNA in whom the effects on work capacity may be more subtle, but the number of individuals thus affected may be considerably more than those experiencing IDA.

Background: Food-based strategies to reduce nutritional iron deficiency have not been universally successful. Biofortification has the potential to be

Background: Iron deficiency without anemia has been shown to reduce both muscle-tissue oxidative capacity and endurance in animals. However, the consequences of iron deficiency in humans remain unclear. Objective: We investigated the effects of iron supplementation on adaptation to aerobic training among marginally iron-depleted women. We hypothesized that iron supplementation for 6 wk would significantly improve iron status and maximal oxygen uptake (V̇O₂max) after 4 wk of concurrent aerobic training. Design: Forty-one untrained, iron-depleted, nonanemic women were randomly assigned to receive either 50 mg FeSO₄ or a placebo twice daily for 6 wk in a double-blind trial. All subjects trained on cycle ergometers 5 d/wk for 4 wk, beginning on week 3 of the study. Results: Six weeks of iron supplementation significantly improved serum ferritin and serum transferrin receptor (sTfR) concentrations and transferrin saturation without affecting hemoglobin concentrations or hematocrit. Average V̇O₂max and maximal respiratory exchange ratio improved in both the placebo and iron groups after training; however, the iron group experienced significantly greater improvements in V̇O₂max. Both iron-status and fitness outcomes were analyzed after stratifying by baseline sTfR concentration (> and ≤8.0 mg/L), which showed that the previously observed treatment effects were due to iron-status and fitness improvements among subjects with poor baseline iron status. Conclusions: Our findings strongly suggest that iron deficiency without anemia but with elevated sTfR status impairs aerobic adaptation among previously untrained women and that this can be corrected with iron supplementation.

Background: Iron deficiency is the most widespread nutritional deficiency in the world.Objective: The objective of this randomized efficacy trial was

The objective of this review is to examine the degree of variation that exists in the achieved height of preadolescent and adolescent children across populations experiencing favorable conditions that support linear growth. Fifty-three population groups were identified that reported mean heights for economically privileged populations from all major continents. Graphic representation of the heights for these populations indicates that the mean height of preadolescent children differs by 3 to 5 cm, whereas population means begin to diverge from the National Center for Health Statistics/World Health Organization (NCHS/WHO) reference at puberty, with most non-European populations falling to approximately 5 cm below the reference and northern European populations exceeding the reference by a similar amount. We conclude that the evidence for limited interpopulation variation in the height of preadolescents supports consideration of a single growth reference for children up to puberty, but the uncertainty of the causes of the divergence in achieved height during puberty requires further research in order to establish an appropriate adolescent growth reference.

An emerging body of research suggests the trajectory of a family’s income affects children’s health and development more profoundly than the often-measured income at a single time point. The purpose of this study was to examine the associations between changes in family income status, early-life risk factors, and body mass index (BMI) z-score trajectory from age 2 to 15 years.