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Prepublished online as a Blood First Edition Paper on January 9, 2003; DOI 10.1182/blood-2002-10-3071.
PLENARY PAPER
From the Department of Medicine, Kansas University
Medical Center, Kansas City, KS.
Current initiatives to reduce the high prevalence of nutritional
iron deficiency have highlighted the need for reliable epidemiologic methods to assess iron status. The present report describes a method
for estimating body iron based on the ratio of the serum transferrin
receptor to serum ferritin. Analysis showed a single normal
distribution of body iron stores in US men aged 20 to 65 years
(mean ± 1 SD, 9.82 ± 2.82 mg/kg). A single normal
distribution was also observed in pregnant Jamaican women (mean ± 1
SD, 0.09 ± 4.48 mg/kg). Distribution analysis in US women aged 20 to
45 years indicated 2 populations; 93% of women had body iron stores averaging 5.5 ± 3.35 mg/kg (mean ± 1 SD), whereas the remaining 7% of women had a mean tissue iron deficit of 3.87 ± 3.23 mg/kg. Calculations of body iron in trials of iron supplementation in Jamaica
and iron fortification in Vietnam demonstrated that the method can be
used to calculate absorption of the added iron. Quantitative estimates
of body iron greatly enhance the evaluation of iron status and the
sensitivity of iron intervention trials in populations in which
inflammation is uncommon or has been excluded by laboratory screening.
The method is useful clinically for monitoring iron status in those who
are highly susceptible to iron deficiency.
(Blood. 2003;101:3359-3363) Heightened awareness in recent years of the adverse consequences of iron
deficiency has prompted renewed efforts to reduce the prevalence of
this common micronutrient insufficiency. One of the main reasons for
the limited success of programs to combat iron deficiency is the
continuing uncertainty about the optimal epidemiologic approach for
identifying it and for measuring its severity. The inadequacy of anemia
surveys is reflected in the wide-ranging estimates by various expert
committees of the global prevalence of iron deficiency. In a 1985 World
Health Organization (WHO) report, it was estimated that 15% to 20% of
the world's population had iron deficiency anemia.1
Despite the lack of new prevalence data, estimates of the global
prevalence of iron deficiency anemia have increased to more than two
thirds of the world population.2 More reliable methods to
assess iron status are needed to determine the prevalence of iron
deficiency and the impact of iron supplementation and
fortification trials.
In the present article, a new method is described for assessing iron
status based on the quantitative measurement of body iron. The method
has been used to examine the iron status in a consensus sample of adult
men and women in the United States and of pregnant women in Jamaica.
The usefulness of the method has been further evaluated by measuring
the absorption of added iron in a supplementation trial in pregnant
women and a food fortification trial in anemic women.
Estimation of body iron
Surveys
The second study was performed in pregnant women living in Kingston,
Jamaica, West Indies, who participated in a trial of iron
supplementation.5 The selection criteria for participation in the study were maternal age of 16 to 35 years, gestational age of 14 to 22 weeks (mean, 135 days), and hemoglobin concentration between 80 and 110 g/L. After baseline specimens were obtained, the women were
randomly assigned to 1 of 3 groups: a control group given no additional
iron (n = 86), an FeSO4 group given a 50-mg FeSO4 tablet twice daily (n = 79), and a gastric delivery
system (GDS) group given a single 50-mg iron GDS capsule daily
(n = 83). Of the 376 women originally enrolled in the study, body
iron estimated from the R/F ratio was examined in 248 in whom blood
samples were available at baseline and after 6 and 12 weeks of study.
Baseline specimens were used to evaluate the frequency distribution of body iron in pregnancy, and values at 6 weeks and 12 weeks were used to
estimate iron absorption from the iron supplements.
The final set of data was obtained from specimens collected during a
double-blind, randomized trial of iron fortification in anemic
Vietnamese women.6,7 For 6 days each week, women were fed
a meal containing noodles or rice and served with 10 mL fish sauce
containing either no added iron (control) or 10 mg iron as NaFeEDTA
(sodium iron ethylenediaminetetraacetic acid) (fortified). Blood
samples were obtained at baseline and at 3 and 6 months later. Of the
136 women completing the study, the first 15 specimens received in our
laboratory from the control and fortified groups were selected to
assess the feasibility of using a reduced sample size to estimate
absorption of fortification iron.
Measurement of serum ferritin and sTfR
The sTfR assay was standardized with transferrin-free receptor purified
from human placenta by the method of Turkewitz et al.10
Additional purification of the free receptor was accomplished by
passage of the transferrin-free receptor through a 100 × 2.5-cm HR-300 gel filtration column (Pharmacia, Uppsala, Sweden). After the
peak protein tubes, as measured by A280nm, were pooled and concentrated, the purity of the receptor was established on gel electrophoresis by demonstrating a single protein band at 190 000 Da
without reduction and 95 000 Da after reduction with
2-mercaptoethanol. The protein concentration was measured by the Lowry
assay.11 If a disparity greater than 5% was observed
between protein content and immunologic activity in the ELISA for sTfR,
the gel filtration step was repeated until less than 2% discrepancy
was obtained. The purified transferrin receptor was stored at 4°C,
conditions under which the purified receptor was shown in prior studies
to be stable for a minimum of 18 months. Fresh human placental receptor was prepared at the beginning of each study and was stored for no
longer than 1 year. The performance of all the serum ferritin and sTfR
assays reported here was further evaluated by including a minimum of 3 quality control sera that had been stored in aliquots at In the Jamaican and Vietnam surveys, in-house or field training was
provided to standardize the methods for collection and temperature-controlled transport of venous blood specimens to a
regional laboratory for processing on the day of collection. Blood was
centrifuged, and 0.5-mL aliquots of plasma were placed in
microfuge tubes for storage at Statistical analysis Frequency distributions of body iron were initially examined by graphic analysis. In the NHANES III specimens from adult women, there was a deviation from a Gaussian distribution in the lower portion of frequency distribution of body iron. An analytical method for identifying a mixture of frequency distributions was used to characterize a second normal distribution.12 Mixed distribution analysis has been used in several prior studies to estimate the prevalence of iron deficiency and other forms of anemia in population studies.13-16 In the present study, an iterative technique termed the "expectation-maximization algorithm" was used, as described previously, to estimate the means and standard deviations of 2 normal distributions.17 The program DISFIT18 was used for this calculation, by which the likelihood ratio statistic determines the best-fitting model, and 2 analysis is used to test the goodness-of-fit of the
best-fitting model.
Population studies The relationship between age and body iron was first examined in the convenience sample of males and females participating in the sTfR pilot study for NHANES III (Figure 2). Mean values in the 2 sexes were similar until late adolescence, when body iron in males increased abruptly to reach a plateau early in the third decade. This was followed by a slow, continued increase until the sixth decade, when body iron fell slightly. Because of the iron loss associated with menstruation and childbearing, there was no appreciable increase in body iron in women until the third decade. Body iron then remained relatively stable until the fifth decade, when it increased progressively, approaching values in men by the seventh decade. These findings are generally consistent with our knowledge of the effect of sex, growth, and menstruation on body iron.19
We next examined the frequency distributions of body iron in men and
women separately. In 649 men between 20 and 65 years of age, the
geometric mean ferritin concentration was 109 µg/L (± 1 SD; range,
66-285 µg/L), the mean sTfR concentration was 6.12 ± 2.73 mg/L,
and the geometric mean R/F ratio was 42 (± 1 SD; range, 19-93). Body
iron stores averaged 9.89 ± 2.82 mg/kg and were consistent with a
single normal distribution (Figure 3).
In 409 women between 20 and 45 years of age, the geometric mean serum
ferritin was 34 µg/L (± 1 SD; range, 12-94 µg/L), the mean sTfR
concentration was 6.3 ± 2.57 mg/L, and the geometric mean R/F ratio
was 172 (± 1 SD; range, 54-544). Body iron stores in the total sample
averaged 4.87 ± 4.14 mg/kg. However, unlike the distribution in men,
the frequency distribution deviated from linearity in the lower portion
of the curve, indicating a minor population of women with iron
deficiency. Mixed distribution analysis indicated 2 normally
distributed populations. The main population, representing 92.7% of
women, had mean iron stores of 5.5 ± 3.35 mg/kg (± 1 SD), whereas
a second population of 7.3% had a mean deficit in tissue iron of
Baseline estimates of body iron are shown for 246 pregnant women
between 16 and 35 years of age living in Kingston,
Jamaica5 (Figure 3). All women were anemic, as defined by
a hemoglobin concentration below 110 g/L. The geometric mean serum
ferritin was 11 µg/L (± 1 SD; range, 4-32 µg/L), the mean sTfR
was 7.87 ± 3.4 mg/L (± 1 SD), and the geometric mean R/F was 650 (± 1 SD; range, 187-2258). Body iron averaged only 0.085 ± 4.48
mg/kg, indicating that half the women had tissue iron deficiency. The goodness-of-fit Intervention trials The advantages of using body iron measurements were apparent when a trial of iron supplementation in pregnant Jamaican women was re-examined. In the original publication, both groups of women given an iron supplement had a significant increase in hemoglobin concentration and a decline in sTfR compared with the control subjects.5 However, there was no apparent difference between the FeSO4 group given 100 mg iron daily and the GDS group given 50 mg iron daily. When body iron estimates were used, a difference between the iron groups was readily apparent (Figure 4). More important, body iron measurements provided a measure of iron absorption. During the 3-month trial, the mean body iron count in the control group fell from 68 mg to 111 mg, or an overall decline of 179 mg. This average daily iron loss of 2 mg reflects the iron requirements of the fetus. Women in the FeSO4 group had increases in
storage iron from an average of 0 to 141 mg iron, whereas women in the GDS group had increases from 47 mg to 36 mg for a gain of 83 mg body
iron. Compared with the control group, women in the FeSO4 group gained 320 mg body iron, representing absorption of 3.5 mg daily
or 3.5% of the iron supplement provided. The GDS group gained 262 mg
iron, or 2.9 mg iron daily, indicating a higher absorption of 5.8%.
The latter demonstrates the physiologic advantage of the GDS
formulation that was designed to delay the release of iron in the
stomach and thereby reduce the inhibiting effect of food on the
absorption of elemental iron.
The usefulness of body iron determinations were next examined in an
iron fortification trial in which changes in iron status are less
pronounced and occur more slowly than with iron supplementation. The
changes in body iron in 15 anemic Vietnamese women given either no iron
or 10 mg fortification iron daily are shown in Figure 5.
In the control group, the mean baseline tissue iron deficit of
Despite the continuing widespread use of anemia screening to assess iron status of populations, isolated measurements of the hemoglobin concentration or hematocrit level are unsuitable as the sole indicator of iron status. The sensitivity of hemoglobin measurements is poor because anemia associated with nutritional iron deficiency is relatively mild, resulting in extensive overlap in hemoglobin values between healthy and iron-deficient persons.13,15,20 The problem is magnified by the near universal acceptance of the WHO criteria of anemia, despite evidence of significant racial differences in normal hemoglobin values.21-24 Low specificity is an even greater limitation of hemoglobin screening for iron deficiency in developing countries where poverty, malnutrition, and infection are associated with a high prevalence of the anemia of chronic disease, which often exceeds that caused by iron-deficiency anemia. In the NHANES in the United States, multiple laboratory measurements have been used to identify iron deficiency more precisely,4 but most of these additional parameters are influenced similarly by iron-deficiency anemia and the anemia of chronic disease. Moreover, the cost and inconvenience of this approach is prohibitive in countries in which the prevalence of anemia is highest. Body iron estimates in the present study using the R/F ratio are similar to values obtained with an earlier, more complex approach using several laboratory measurements and 3 separate algorithms.25 Body iron stores averaged 776 ± 313 mg (± 1 SD) in men and 309 ± 346 mg in women according to the original method compared with 752 mg and 297 mg, respectively, after the data in the present report were converted to absolute values for body iron using average weights for US men and women.26 The earlier method was used to advantage in the analysis of a 2-year trial of iron fortification in South Africa27 and a 36-month trial of sugar fortification in semirural Guatemala.28 In both these studies, the changes in body iron resulting from fortification agreed with prestudy absorption measurements using radioisotopes of iron. It should be noted that a minor population of women with lower body iron was not detected in the original study but could have been missed because of the empirical algorithms used to estimate body iron. This minor population could represent women with the Gly227Ser transferrin mutation, which has been reported to increase the risk for iron deficiency.29 Estimation of body iron using the R/F ratio has several advantages over the original method,25 which required 5 laboratory value measurements (hemoglobin, serum ferritin, erythrocyte protoporphyrin, and serum iron levels and total iron-binding capacity) compared with 2 with the present method. Moreover, by eliminating the need for the transferrin saturation value, body iron can be determined with the R/F ratio from a small capillary blood specimen. This is an important advance in field studies, particularly in developing countries in which permission for venous sampling is often difficult to obtain. Another advantage of the present method is the expression of body iron on the basis of body weight rather than absolute values used in the original method and in much of the published literature on iron status. In addition to eliminating the effect of differences in body weight, expressing body iron per kilogram permits extrapolation to younger persons. The extent to which the algorithm using the R/F ratio can be applied to school-aged and preschool-aged children is uncertain, but the age relationships shown in Figure 2 are plausible. It will be difficult to validate the relationship between the R/F ratio and body iron in children and pregnant women because of the constraints in performing quantitative phlebotomy. Body iron measurements using the R/F ratio provide a measure of iron status in each person surveyed rather than the current epidemiologic approaches based on arbitrary cutoff points of laboratory indices. The ability to examine the distribution of iron status in different segments of a population can provide important insights into the optimal design of public health strategies to reduce iron deficiency. Existing intervention programs often provide iron only to those with anemia, an approach that implies 2 separate populations of iron-deficient and healthy persons. The single distribution of body iron observed in pregnant Jamaican women using the R/F ratio indicates that it is better to target the entire population using food fortification. Another advantage of determining body iron individually is that small subsets of the population can be examined to assess the effect of various determinants of iron nutrition, such as racial or ethnic background, socioeconomic status, dietary patterns, iron supplements, and certain drugs such as aspirin. Limited interim surveys can also be used to detect temporal changes in iron status in the direction of either increasing or declining body iron. Body iron measurements are independent of hemoglobin determinations and
thereby shift the focus of screening programs from anemia to iron
deficiency, the only cause of anemia than can be alleviated readily by
public health measures. Capillary measurements of hemoglobin can be
obtained when determining the R/F ratio, but anemia can also be
determined from the deficit in tissue iron measured with the R/F ratio.
In an iron-replete person, the development of anemia corresponds to a
decrease in hemoglobin level of 20 g/L or a tissue iron deficit of
approximately The use of the R/F ratio to estimate body iron has certain limitations. The most important one is the influence of inflammation or liver disease on the serum ferritin level independent of body iron stores. In view of the large and expanding list of laboratory markers of inflammation, it is conceivable that an algorithm can be developed in the future that corrects for the effect of inflammation on the serum ferritin value, thereby permitting its use for the calculation of body iron. At present, the only practical approach is to use a screening test such as C-reactive protein to exclude persons with inflammation from calculations of body iron. The sTfR can still be used to detect concurrent iron deficiency in persons with inflammation.30,31 Another significant obstacle to wider use of the R/F ratio in population studies is the variable range of reported values for the sTfR with different commercial assays. Most of the disparities between assays could probably be eliminated by using a common reference material for standardization. At present, the manufacturers of different commercial assays provide no details about the source and method of purification of transferrin receptor used in their assay. Although the need for standardization of the sTfR is commonly mentioned,32,33 there has been no effort by industry to develop a reference material, presumably because of proprietary concerns. Until the standardization issue is resolved, the R/F ratio must be calibrated by quantitative phlebotomy measurements before it is used to estimate body iron. The clinical application of body iron measurements is limited by the numerous disorders that affect serum ferritin and sTfR levels independently of iron status, although the most important ones can be detected by elevated levels of C-reactive protein. The main clinical application is the monitoring of iron status in those who are highly susceptible to iron deficiency, such as infants, preschool children, and pregnant women. At present, clinicians rely on the serum ferritin level to determine the adequacy of iron stores and on the hemoglobin concentration to identify advanced iron deficiency at the other end of the iron spectrum. However, there is no reliable laboratory method at present for detecting tissue iron deficiency before the onset of anemia. Iron deficiency without anemia can represent up to 30% of a susceptible population, such as pregnant Jamaican women (Figure 2). There is substantial evidence of the deleterious effect of iron deficiency during infancy on subsequent intellectual performance and learning capacity34,35 and a continuing concern about the adverse effects of iron deficiency during gestation. Body iron measurements provide a method for investigators to assess more precisely the relevance of tissue iron deficiency without anemia and for clinicians to detect it. The most important immediate application of body iron measurements is the assessment of intervention trials to improve iron status. Given the dismal long-term success of iron supplementation programs, the major focus of programs to alleviate iron deficiency in recent years is food iron fortification.36,37 Most of the fortification strategies now under investigation are based on isotopic measurements of iron absorption from meals fed to fasting subjects in a laboratory setting, but this approach does not assess the many others factors that determine the success or failure of a given strategy when implemented in a population. Fortification trials have traditionally required hundreds of participants and years to conduct.27,28,34,35 In the Vietnam study, measurements in 30 subjects for 3 months were sufficient to define the efficacy of the fortification strategy (Figure 5). Body iron measurements can greatly accelerate the development and implementation of programs to reduce the prevalence of iron deficiency.
We thank Dr Pham Van Thuy for permission to use preliminary data from the iron fortification trial in Vietnamese women. The study was supported by the Nippon Foundation and the International Life Sciences Institute Center for Health Promotion (Atlanta, GA), and it was conducted by the National Institute of Nutrition (Hanoi, Vietnam), the Institute of Research Development (Montpellier, France), and the Laboratory for Human Nutrition, Institute of Food Science, Swiss Federal Institute of Technology (Ruschlikon, Switzerland).
Submitted October 9, 2002; accepted November 15, 2002.
Prepublished online as Blood First Edition Paper, January 9, 2003; DOI 10.1182/blood- 2002-10-3071.
Reprints: James D. Cook, Department of Medicine, Kansas University Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160-7233; e-mail: jcook1{at}kumc.edu. The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked "advertisement" in accordance with 18 U.S.C. section 1734.
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S. Muthayya, A. Eilander, C. Transler, T. Thomas, H. C. van der Knaap, K. Srinivasan, B J. W. van Klinken, S. J. Osendarp, and A. V Kurpad Effect of fortification with multiple micronutrients and n-3 fatty acids on growth and cognitive performance in Indian schoolchildren: the CHAMPION (Children's Health and Mental Performance Influenced by Optimal Nutrition) Study Am. J. Clinical Nutrition, June 1, 2009; 89(6): 1766 - 1775. [Abstract] [Full Text] [PDF]
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J. R Hunt, C. A. Zito, and L. K Johnson Body iron excretion by healthy men and women Am. J. Clinical Nutrition, June 1, 2009; 89(6): 1792 - 1798. [Abstract] [Full Text] [PDF]
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M. E Cogswell, A. C Looker, C. M Pfeiffer, J. D Cook, D. A Lacher, J. L Beard, S. R Lynch, and L. M Grummer-Strawn Assessment of iron deficiency in US preschool children and nonpregnant females of childbearing age: National Health and Nutrition Examination Survey 2003-2006 Am. J. Clinical Nutrition, May 1, 2009; 89(5): 1334 - 1342. [Abstract] [Full Text] [PDF]
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M. F Young, R. P Glahn, M. Ariza-Nieto, J. Inglis, G. Olbina, M. Westerman, and K. O O'Brien Serum hepcidin is significantly associated with iron absorption from food and supplemental sources in healthy young women Am. J. Clinical Nutrition, February 1, 2009; 89(2): 533 - 538. [Abstract] [Full Text] [PDF]
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M. Andersson, P. Thankachan, S. Muthayya, R. B Goud, A. V Kurpad, R. F Hurrell, and M. B Zimmermann Dual fortification of salt with iodine and iron: a randomized, double-blind, controlled trial of micronized ferric pyrophosphate and encapsulated ferrous fumarate in southern India Am. J. Clinical Nutrition, November 1, 2008; 88(5): 1378 - 1387. [Abstract] [Full Text] [PDF]
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M. B Zimmermann, S. Fucharoen, P. Winichagoon, P. Sirankapracha, C. Zeder, S. Gowachirapant, K. Judprasong, T. Tanno, J. L Miller, and R. F Hurrell Iron metabolism in heterozygotes for hemoglobin E (HbE), {alpha}-thalassemia 1, or {beta}-thalassemia and in compound heterozygotes for HbE/{beta}-thalassemia Am. J. Clinical Nutrition, October 1, 2008; 88(4): 1026 - 1031. [Abstract] [Full Text] [PDF]
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 C. Sala, M. Ciullo, C. Lanzara, T. Nutile, S. Bione, R. Massacane, P. d'Adamo, P. Gasparini, D. Toniolo, and C. Camaschella Variation of hemoglobin levels in normal Italian populations from genetic isolates Haematologica, September 1, 2008; 93(9): 1372 - 1375. [Abstract] [Full Text] [PDF]
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E. H.J.M. Kemna, H. Tjalsma, H. L. Willems, and D. W. Swinkels Reply to: [Comment to: Hepcidin: from discovery to differential diagnosis. Haematologica 2008; 93:90-7] Haematologica, June 1, 2008; 93(6): e52 - e52. [Full Text] [PDF]
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 S. M. King, C. M. Donangelo, M. D. Knutson, P. B. Walter, B. N. Ames, F. E. Viteri, and J. C. King Daily Supplementation with Iron Increases Lipid Peroxidation in Young Women with Low Iron Stores Experimental Biology and Medicine, June 1, 2008; 233(6): 701 - 707. [Abstract] [Full Text] [PDF]
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 J. M. Brotanek, J. Gosz, M. Weitzman, and G. Flores Secular Trends in the Prevalence of Iron Deficiency Among US Toddlers, 1976-2002 Arch Pediatr Adolesc Med, April 1, 2008; 162(4): 374 - 381. [Abstract] [Full Text] [PDF]
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A. S. W. Mburu, D. I. Thurnham, D. L. Mwaniki, E. M. Muniu, F. Alumasa, and A. de Wagt The Influence and Benefits of Controlling for Inflammation on Plasma Ferritin and Hemoglobin Responses following a Multi-Micronutrient Supplement in Apparently Healthy, HIV+ Kenyan Adults J. Nutr., March 1, 2008; 138(3): 613 - 619. [Abstract] [Full Text] [PDF]
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 S. E. Cusick, A. C. Looker, M. E. Cogswell, C. M. Pfeiffer, and L. Grummer-Strawn Iron-Status Indicators Pediatrics, March 1, 2008; 121(3): 651 - 652. [Full Text] [PDF]
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J. M. Brotanek, G. Flores, and M. Weitzman Iron-Status Indicators: In Reply Pediatrics, March 1, 2008; 121(3): 652 - 652. [Full Text] [PDF]
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 C. A Northrop-Clewes Interpreting indicators of iron status during an acute phase response - lessons from malaria and human immunodeficiency virus Ann Clin Biochem, January 1, 2008; 45(1): 18 - 32. [Abstract] [Full Text] [PDF]
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M. Wijaya-Erhardt, J. G Erhardt, J. Untoro, E. Karyadi, L. Wibowo, and R. Gross Effect of daily or weekly multiple-micronutrient and iron foodlike tablets on body iron stores of Indonesian infants aged 6 12 mo: a double-blind, randomized, placebo-controlled trial Am. J. Clinical Nutrition, December 1, 2007; 86(6): 1680 - 1686. [Abstract] [Full Text] [PDF]
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M. Arredondo, D. Jorquera, E. Carrasco, C. Albala, and E. Hertrampf Microsatellite polymorphism in the heme oxygenase-1 gene promoter is associated with iron status in persons with type 2 diabetes mellitus Am. J. Clinical Nutrition, November 1, 2007; 86(5): 1347 - 1353. [Abstract] [Full Text] [PDF]
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The NEMO Study Group Effect of a 12-mo micronutrient intervention on learning and memory in well-nourished and marginally nourished school-aged children: 2 parallel, randomized, placebo-controlled studies in Australia and Indonesia Am. J. Clinical Nutrition, October 1, 2007; 86(4): 1082 - 1093. [Abstract] [Full Text] [PDF]
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 M. B. Zimmermann, H. Burgi, and R. F. Hurrell Iron Deficiency Predicts Poor Maternal Thyroid Status during Pregnancy J. Clin. Endocrinol. Metab., September 1, 2007; 92(9): 3436 - 3440. [Abstract] [Full Text] [PDF]
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L. E Murray-Kolb and J. L Beard Iron treatment normalizes cognitive functioning in young women Am. J. Clinical Nutrition, March 1, 2007; 85(3): 778 - 787. [Abstract] [Full Text] [PDF]
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J. H. Swain, L. K. Johnson, and J. R. Hunt Electrolytic Iron or Ferrous Sulfate Increase Body Iron in Women with Moderate to Low Iron Stores J. Nutr., March 1, 2007; 137(3): 620 - 627. [Abstract] [Full Text] [PDF]
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D. Moretti, M. B Zimmermann, S. Muthayya, P. Thankachan, T.-C. Lee, A. V Kurpad, and R. F Hurrell Extruded rice fortified with micronized ground ferric pyrophosphate reduces iron deficiency in Indian schoolchildren: a double-blind randomized controlled trial. Am. J. Clinical Nutrition, October 1, 2006; 84(4): 822 - 829. [Abstract] [Full Text] [PDF]
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M. B Zimmermann, R. Biebinger, F. Rohner, A. Dib, C. Zeder, R. F Hurrell, and N. Chaouki Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron. Am. J. Clinical Nutrition, September 1, 2006; 84(3): 580 - 586. [Abstract] [Full Text] [PDF]
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K. B Hadley, L. K Johnson, and J. R Hunt Iron absorption by healthy women is not associated with either serum or urinary prohepcidin Am. J. Clinical Nutrition, July 1, 2006; 84(1): 150 - 155. [Abstract] [Full Text] [PDF]
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R. Wegmuller, F. Camara, M. B. Zimmermann, P. Adou, and R. F. Hurrell Salt Dual-Fortified with Iodine and Micronized Ground Ferric Pyrophosphate Affects Iron Status but Not Hemoglobin in Children in Cote d'Ivoire J. Nutr., July 1, 2006; 136(7): 1814 - 1820. [Abstract] [Full Text] [PDF]
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 D. W. Swinkels, M. C.H. Janssen, J. Bergmans, and J. J.M. Marx Hereditary Hemochromatosis: Genetic Complexity and New Diagnostic Approaches Clin. Chem., June 1, 2006; 52(6): 950 - 968. [Abstract] [Full Text] [PDF]
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L. H. Allen New Approaches for Designing and Evaluating Food Fortification Programs J. Nutr., April 1, 2006; 136(4): 1055 - 1058. [Abstract] [Full Text] [PDF]
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 E. Beutler and J. Waalen The definition of anemia: what is the lower limit of normal of the blood hemoglobin concentration? Blood, March 1, 2006; 107(5): 1747 - 1750. [Abstract] [Full Text] [PDF]
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 K. Dassler, M. Zydek, K. Wandzik, M. Kaup, and H. Fuchs Release of the Soluble Transferrin Receptor Is Directly Regulated by Binding of Its Ligand Ferritransferrin J. Biol. Chem., February 10, 2006; 281(6): 3297 - 3304. [Abstract] [Full Text] [PDF]
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M. B Zimmermann, P. Winichagoon, S. Gowachirapant, S. Y Hess, M. Harrington, V. Chavasit, S. R Lynch, and R. F Hurrell Comparison of the efficacy of wheat-based snacks fortified with ferrous sulfate, electrolytic iron, or hydrogen-reduced elemental iron: randomized, double-blind, controlled trial in Thai women Am. J. Clinical Nutrition, December 1, 2005; 82(6): 1276 - 1282. [Abstract] [Full Text] [PDF]
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J. D. Haas, J. L. Beard, L. E. Murray-Kolb, A. M. del Mundo, A. Felix, and G. B. Gregorio Iron-Biofortified Rice Improves the Iron Stores of Nonanemic Filipino Women J. Nutr., December 1, 2005; 135(12): 2823 - 2830. [Abstract] [Full Text] [PDF]
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F. T Wieringa and M. A Dijkhuizen Validity of the dose-response tests for the determination of vitamin A status Am. J. Clinical Nutrition, November 1, 2005; 82(5): 1138 - 1139. [Full Text] [PDF]
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L. L. Iannotti, K. O. O'Brien, S.-C. Chang, J. Mancini, M. Schulman-Nathanson, S. Liu, Z. L. Harris, and F. R. Witter Iron Deficiency Anemia and Depleted Body Iron Reserves Are Prevalent among Pregnant African-American Adolescents J. Nutr., November 1, 2005; 135(11): 2572 - 2577. [Abstract] [Full Text] [PDF]
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P. Van Thuy, J. Berger, Y. Nakanishi, N. C. Khan, S. Lynch, and P. Dixon The Use of NaFeEDTA-Fortified Fish Sauce Is an Effective Tool for Controlling Iron Deficiency in Women of Childbearing Age in Rural Vietnam J. Nutr., November 1, 2005; 135(11): 2596 - 2601. [Abstract] [Full Text] [PDF]
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C. Hershko Iron and high living Blood, August 15, 2005; 106(4): 1142 - 1142. [Full Text] [PDF]
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J. D. Cook, E. Boy, C. Flowers, and M. del Carmen Daroca The influence of high-altitude living on body iron Blood, August 15, 2005; 106(4): 1441 - 1446. [Abstract] [Full Text] [PDF]
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Z. Mei, M. E. Cogswell, I. Parvanta, S. Lynch, J. L. Beard, R. J. Stoltzfus, and L. M. Grummer-Strawn Hemoglobin and Ferritin Are Currently the Most Efficient Indicators of Population Response to Iron Interventions: an Analysis of Nine Randomized Controlled Trials J. Nutr., August 1, 2005; 135(8): 1974 - 1980. [Abstract] [Full Text] [PDF]
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C. Molgaard, P. Kaestel, and K. F Michaelsen Long-term calcium supplementation does not affect the iron status of 12-14-y-old girls Am. J. Clinical Nutrition, July 1, 2005; 82(1): 98 - 102. [Abstract] [Full Text] [PDF]
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 A. T. Chan, J. Ma, G. J. Tranah, E. L. Giovannucci, N. Rifai, D. J. Hunter, and C. S. Fuchs Hemochromatosis Gene Mutations, Body Iron Stores, Dietary Iron, and Risk of Colorectal Adenoma in Women J Natl Cancer Inst, June 15, 2005; 97(12): 917 - 926. [Abstract] [Full Text] [PDF]
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M. B Zimmermann, N. Chaouki, and R. F Hurrell Iron deficiency due to consumption of a habitual diet low in bioavailable iron: a longitudinal cohort study in Moroccan children Am. J. Clinical Nutrition, January 1, 2005; 81(1): 115 - 121. [Abstract] [Full Text] [PDF]
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M. B Zimmermann, R. Wegmueller, C. Zeder, N. Chaouki, R. Biebinger, R. F Hurrell, and E. Windhab Triple fortification of salt with microcapsules of iodine, iron, and vitamin A Am. J. Clinical Nutrition, November 1, 2004; 80(5): 1283 - 1290. [Abstract] [Full Text] [PDF]
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J. G. Erhardt, J. E. Estes, C. M. Pfeiffer, H. K. Biesalski, and N. E. Craft Combined Measurement of Ferritin, Soluble Transferrin Receptor, Retinol Binding Protein, and C-Reactive Protein by an Inexpensive, Sensitive, and Simple Sandwich Enzyme-Linked Immunosorbent Assay Technique J. Nutr., November 1, 2004; 134(11): 3127 - 3132. [Abstract] [Full Text] [PDF]
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M. B Zimmermann, R. Wegmueller, C. Zeder, N. Chaouki, F. Rohner, M. Saissi, T. Torresani, and R. F Hurrell Dual fortification of salt with iodine and micronized ferric pyrophosphate: a randomized, double-blind, controlled trial Am. J. Clinical Nutrition, October 1, 2004; 80(4): 952 - 959. [Abstract] [Full Text] [PDF]
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C. Brugnara Iron Deficiency and Erythropoiesis: New Diagnostic Approaches Clin. Chem., October 1, 2003; 49(10): 1573 - 1578. [Abstract] [Full Text] [PDF]
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P. V. Thuy, J. Berger, L. Davidsson, N. C. Khan, N. T. Lam, J. D Cook, R. F Hurrell, and H. H. Khoi Regular consumption of NaFeEDTA-fortified fish sauce improves iron status and reduces the prevalence of anemia in anemic Vietnamese women Am. J. Clinical Nutrition, August 1, 2003; 78(2): 284 - 290. [Abstract] [Full Text] [PDF]
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 E. Beutler, A. V. Hoffbrand, and J. D. Cook Iron Deficiency and Overload Hematology, January 1, 2003; 2003(1): 40 - 61. [Abstract] [Full Text] [PDF]
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Abstract
Introduction
