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Nutrients
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Iron Deficiency and Iron-Related Disorders
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Iron Deficiency and Iron-Related Disorders

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Micronutrients and Human Health".

Deadline for manuscript submissions: closed (25 April 2024) | Viewed by 8710

Special Issue Editors

Dr. Phu V. Tran

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Guest Editor
Department of Pediatrics, University of Minnesota at Twin Cities, Minneapolis, MN 55455, USA
Interests: developmental neuroscience; epigenetics; fetal-neonatal nutrition; neurobehavioral development; DOHaD
Prof. Dr. Barbara True Felt

E-Mail Website
Guest Editor
Department of Pediatrics, University of Michigan, Ann Arbor, MI, USA
Interests: developmental pediatrics; disorders of elimination; parent–child interaction difficulties; sleep problems; school problems and attention deficit disorder
Dr. Yue Chen

E-Mail Website
Guest Editor
Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota at Twin Cities, Minneapolis, MN 55455, USA
Interests: functional proteomics; epigenetics; cell signaling; cancer biology; metabolic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Increasing evidence indicates that early life exposures (e.g., malnutrition, toxins, stress) can have a lasting impact on physiological and mental health—a central concept of the developmental origins of health and disease (DOHaD). These lasting effects are a burden to society. Iron deficiency (ID) is the foremost micronutrient deficiency, affecting 40–50% of pregnant women and preschool-aged children worldwide. There are a multitude of both controllable and uncontrollable factors that contribute to poor iron status during fetal and early childhood periods, including anemia, maternal obesity, maternal diabetes, placental dysfunction, intrauterine growth restriction, and socioeconomic status. ID during the fetal and early childhood periods (developmental ID) has a significant effect on neurodevelopment, resulting in cognitive, socio-emotional, and learning and memory deficits that continue into adulthood despite prompt iron therapy after diagnosis. Developmental ID also carries long-term health risks including increased risk for neuropsychiatric disorders, such as autism and schizophrenia. Parallel studies in pre-clinical models have shown that early-life ID results in abnormal brain structure, function, and gene expression, occurring acutely during rapid neurodevelopment then continuing persistently through to adulthood. The persistent and widespread changes in gene networks implicated in psychopathologies are a likely major cause of adult neurobehavioral abnormalities.

This Special Issue will publish original research and reviews of developmental ID on health outcomes and risks, as well as mechanisms (e.g., iron trafficking and metabolism, maternal-fetal/infant iron transport, microbiota, epigenetics, iron-dependent gene regulation and post-translational modifications), by which developmental ID determines the long-term health outcomes.

Dr. Phu V. Tran
Prof. Dr. Barbara True Felt
Dr. Yue Chen
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • iron deficiency
  • iron metabolism
  • neurodevelopment
  • behavior
  • cognition
  • learning and memory
  • microbiota
  • iron-trafficking
  • epigenetics
  • maternal–fetal iron

Published Papers (6 papers)

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Research

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20 pages, 3504 KiB  
Article
Maternal Iron Deficiency and Environmental Lead (Pb) Exposure Alter the Predictive Value of Blood Pb Levels on Brain Pb Burden in the Offspring in a Dietary Mouse Model: An Important Consideration for Cumulative Risk in Development
by Janine Cubello, Derick R. Peterson, Lu Wang and Margot Mayer-Proschel
Nutrients 2023, 15(19), 4101; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15194101 - 22 Sep 2023
Cited by 1 | Viewed by 1235
Abstract
Maternal iron deficiency (ID) and environmental lead (Pb) exposure are co-occurring insults that both affect the neurodevelopment of offspring. Few studies have investigated how ID affects brain-region-specific Pb accumulations using human-relevant Pb concentrations. Furthermore, how these Pb exposures impact blood and brain Fe [...] Read more.
Maternal iron deficiency (ID) and environmental lead (Pb) exposure are co-occurring insults that both affect the neurodevelopment of offspring. Few studies have investigated how ID affects brain-region-specific Pb accumulations using human-relevant Pb concentrations. Furthermore, how these Pb exposures impact blood and brain Fe levels remains unclear. Importantly, we also wanted to determine whether the use of blood Pb levels as a surrogate for the brain Pb burden is affected by underlying iron status. We exposed virgin Swiss Webster female mice to one of six conditions differing by iron diet and Pb water concentration (0 ppm, 19 ppm, or 50 ppm lead acetate) and used Inductively Coupled Plasma Mass Spectrometry to measure the maternal and offspring circulating, stored, and brain Pb levels. We found that maternal ID rendered the offspring iron-deficient anemic and led to a region-specific depletion of brain Fe that was exacerbated by Pb in a dose-specific manner. The postnatal iron deficiency anemia also exacerbated cortical and hippocampal Pb accumulation. Interestingly, BPb levels only correlated with the brain Pb burden in ID pups but not in IN offspring. We conclude that ID significantly increases the brain Pb burden and that BPb levels alone are insufficient as a clinical surrogate to make extrapolations on the brain Pb burden. Full article
(This article belongs to the Special Issue Iron Deficiency and Iron-Related Disorders)
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13 pages, 289 KiB  
Article
Examining the Double Burden of Underweight, Overweight/Obesity and Iron Deficiency among Young Children in a Canadian Primary Care Setting
by Sean A. Borkhoff, Patricia C. Parkin, Catherine S. Birken, Jonathon L. Maguire, Colin Macarthur and Cornelia M. Borkhoff
Nutrients 2023, 15(16), 3635; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15163635 - 18 Aug 2023
Cited by 1 | Viewed by 1098
Abstract
There is little evidence on the prevalence of the double burden and association between body mass index (BMI) and iron deficiency among young children living in high-income countries. We conducted a cross-sectional study of healthy children, 12–29 months of age, recruited during health [...] Read more.
There is little evidence on the prevalence of the double burden and association between body mass index (BMI) and iron deficiency among young children living in high-income countries. We conducted a cross-sectional study of healthy children, 12–29 months of age, recruited during health supervision visits in Toronto, Canada, and concurrently measured BMI and serum ferritin. The prevalence of a double burden of underweight (zBMI < −2) and iron deficiency or overweight/obesity (zBMI > 2) and iron deficiency was calculated. Regression models examined BMI and serum ferritin as continuous and categorical variables, adjusted for covariates. We found the following in terms of prevalence among 1953 children (mean age 18.3 months): underweight 2.6%, overweight/obesity 4.9%, iron deficiency 13.8%, iron-deficiency anemia 5.4%, underweight and iron deficiency 0.4%, overweight/obesity and iron deficiency 1.0%. The change in median serum ferritin for each unit of zBMI was −1.31 µg/L (95% CI −1.93, −0.68, p < 0.001). Compared with normal weight, we found no association between underweight and iron deficiency; meanwhile, overweight/obesity was associated with a higher odds of iron deficiency (OR 2.15, 95% CI 1.22, 3.78, p = 0.008). A double burden of overweight/obesity and iron deficiency occurs in about 1.0% of young children in this high-income setting. For risk stratification and targeted screening in young children, overweight/obesity should be added to the list of important risk factors. Full article
(This article belongs to the Special Issue Iron Deficiency and Iron-Related Disorders)
15 pages, 5775 KiB  
Article
Sex-Specific Effects of Early-Life Iron Deficiency and Prenatal Choline Treatment on Adult Rat Hippocampal Transcriptome
by Shirelle X. Liu, Tenille K. Fredrickson, Natalia Calixto Mancipe, Michael K. Georgieff and Phu V. Tran
Nutrients 2023, 15(6), 1316; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15061316 - 07 Mar 2023
Cited by 1 | Viewed by 1482
Abstract
Background: Fetal-neonatal iron deficiency (ID) causes long-term neurocognitive and affective dysfunctions. Clinical and preclinical studies have shown that early-life ID produces sex-specific effects. However, little is known about the molecular mechanisms underlying these early-life ID-induced sex-specific effects on neural gene regulation. Objective: To [...] Read more.
Background: Fetal-neonatal iron deficiency (ID) causes long-term neurocognitive and affective dysfunctions. Clinical and preclinical studies have shown that early-life ID produces sex-specific effects. However, little is known about the molecular mechanisms underlying these early-life ID-induced sex-specific effects on neural gene regulation. Objective: To illustrate sex-specific transcriptome alterations in adult rat hippocampus induced by fetal-neonatal ID and prenatal choline treatment. Methods: Pregnant rats were fed an iron-deficient (4 mg/kg Fe) or iron-sufficient (200 mg/kg Fe) diet from gestational day (G) 2 to postnatal day (P) 7 with or without choline supplementation (5 g/kg choline) from G11–18. Hippocampi were collected from P65 offspring of both sexes and analyzed for changes in gene expression. Results: Both early-life ID and choline treatment induced transcriptional changes in adult female and male rat hippocampi. Both sexes showed ID-induced alterations in gene networks leading to enhanced neuroinflammation. In females, ID-induced changes indicated enhanced activity of oxidative phosphorylation and fatty acid metabolism, which were contrary to the ID effects in males. Prenatal choline supplementation induced the most robust changes in gene expression, particularly in iron-deficient animals where it partially rescued ID-induced dysregulation. Choline supplementation also altered hippocampal transcriptome in iron-sufficient rats with indications for both beneficial and adverse effects. Conclusions: This study provided unbiased global assessments of gene expression regulated by iron and choline in a sex-specific manner, with greater effects in female than male rats. Our new findings highlight potential sex-specific gene networks regulated by iron and choline for further investigation. Full article
(This article belongs to the Special Issue Iron Deficiency and Iron-Related Disorders)
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Review

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16 pages, 771 KiB  
Review
Biomarkers of Brain Dysfunction in Perinatal Iron Deficiency
by Raghavendra B. Rao
Nutrients 2024, 16(7), 1092; https://0-doi-org.brum.beds.ac.uk/10.3390/nu16071092 - 08 Apr 2024
Viewed by 755
Abstract
Iron deficiency in the fetal and neonatal period (perinatal iron deficiency) bodes poorly for neurodevelopment. Given its common occurrence and the negative impact on brain development, a screening and treatment strategy that is focused on optimizing brain development in perinatal iron deficiency is [...] Read more.
Iron deficiency in the fetal and neonatal period (perinatal iron deficiency) bodes poorly for neurodevelopment. Given its common occurrence and the negative impact on brain development, a screening and treatment strategy that is focused on optimizing brain development in perinatal iron deficiency is necessary. Pediatric societies currently recommend a universal iron supplementation strategy for full-term and preterm infants that does not consider individual variation in body iron status and thus could lead to undertreatment or overtreatment. Moreover, the focus is on hematological normalcy and not optimal brain development. Several serum iron indices and hematological parameters in the perinatal period are associated with a risk of abnormal neurodevelopment, suggesting their potential use as biomarkers for screening and monitoring treatment in infants at risk for perinatal iron deficiency. A biomarker-based screening and treatment strategy that is focused on optimizing brain development will likely improve outcomes in perinatal iron deficiency. Full article
(This article belongs to the Special Issue Iron Deficiency and Iron-Related Disorders)
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15 pages, 774 KiB  
Review
The Interaction between Psychological Stress and Iron Status on Early-Life Neurodevelopmental Outcomes
by Brie M. Reid and Michael K. Georgieff
Nutrients 2023, 15(17), 3798; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15173798 - 30 Aug 2023
Cited by 3 | Viewed by 2339
Abstract
This review presents evidence from animal and human studies demonstrating the possible connection and significant impact of poor iron status and psychological distress on neurocognitive development during pregnancy and the neonatal period, with implications for long-term cognition. Stress and iron deficiency are independently [...] Read more.
This review presents evidence from animal and human studies demonstrating the possible connection and significant impact of poor iron status and psychological distress on neurocognitive development during pregnancy and the neonatal period, with implications for long-term cognition. Stress and iron deficiency are independently prevalent and thus are frequently comorbid. While iron deficiency and early-life stress independently contribute to long-term neurodevelopmental alterations, their combined effects remain underexplored. Psychological stress responses may engage similar pathways as infectious stress, which alters fundamental iron metabolism processes and cause functional tissue-level iron deficiency. Psychological stress, analogous to but to a lesser degree than infectious stress, activates the hypothalamic–pituitary–adrenocortical (HPA) axis and increases proinflammatory cytokines. Chronic or severe stress is associated with dysregulated HPA axis functioning and a proinflammatory state. This dysregulation may disrupt iron absorption and utilization, likely mediated by the IL-6 activation of hepcidin, a molecule that impedes iron absorption and redistributes total body iron. This narrative review highlights suggestive studies investigating the relationship between psychological stress and iron status and outlines hypothesized mechanistic pathways connecting psychological stress exposure and iron metabolism. We examine findings regarding the overlapping impacts of early stress exposure to iron deficiency and children’s neurocognitive development. We propose that studying the influence of psychological stress on iron metabolism is crucial for comprehending neurocognitive development in children exposed to prenatal and early postnatal stressors and for children at risk of early iron insufficiency. We recommend future directions for dual-exposure studies exploring iron as a potential mediating pathway between early stress and offspring neurodevelopment, offering opportunities for targeted interventions. Full article
(This article belongs to the Special Issue Iron Deficiency and Iron-Related Disorders)
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Other

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8 pages, 948 KiB  
Brief Report
LRG1 Associates with Iron Deficiency Anemia Markers in Adolescents
by Rashed Alhammad, Mohamed Abu-Farha, Abdur Rahman, Thangavel Alphonse Thanaraj, Lemia Shaban, Reem Alsabah, Samar Hamad, Maha M. Hammad, Arshad Channanath, Fahd Al-Mulla and Jehad Abubaker
Nutrients 2023, 15(14), 3100; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15143100 - 11 Jul 2023
Viewed by 1111
Abstract
Leucine-rich α-2 glycoprotein1 (LRG1) has been shown to be associated with several health conditions; however, its association with iron deficiency anemia, especially in children, has not been previously explored. In this study, we investigated the association between LRG1 and several iron deficiency anemia [...] Read more.
Leucine-rich α-2 glycoprotein1 (LRG1) has been shown to be associated with several health conditions; however, its association with iron deficiency anemia, especially in children, has not been previously explored. In this study, we investigated the association between LRG1 and several iron deficiency anemia markers, including hemoglobin (Hb), albumin, red cell distribution width (RDW), iron, ferritin, and Hb transferrin saturation. A total of 431 participants were included in this analysis aged between 11 and 14 years. Higher LRG1 levels were observed in children diagnosed with anemia [31.1 (24.6, 43.2) µg/mL] compared to non-anemic children [29.2 (22.7–35.95) µg/mL]. Statistically significant differences of LRG1 level across the three groups (tertiles) of Hb, iron, transferrin saturation, albumin, RDW, ferritin, and WBC were observed. Strong negative correlations were observed between LRG1 and Hb (Spearman’s rho = −0.11, p = 0.021), albumin (Spearman’s rho = −0.24, p < 0.001), iron (Spearman’s rho = −0.25, p < 0.001), and Hb transferrin saturation (Spearman’s rho = −0.24, p < 0.001), whereas circulating LRG1 levels were positively associated with RDW (Spearman’s rho = 0.21, p < 0.001). In conclusion, our findings demonstrate for the first time the strong association between iron deficiency anemia markers and LRG1 in otherwise healthy school-aged children. However, further studies are needed to corroborate those results and to look for similar associations in other population subgroups. Full article
(This article belongs to the Special Issue Iron Deficiency and Iron-Related Disorders)
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