Iron Storage Status Research Articles

Increased Iron Overload and Glycated Hemoglobin in Diabetes Mellitus-П Patients in Sulaimani city

The purpose of the current study was to assess the correlation between the iron
 overload and increased glycated hemoglobin (HbA1c) among some diabetic patients in
 Sulaimani outpatient clinics. The studied samples included 60 randomly selected patients
 diagnosed with diabetes mellitus-п, having mean age of 51 years. Oppositely, 20 nondiabetic persons (having normal blood glucose and HbA1c within the normal range (2- 6%) with mean age of (46) years; were enrolled as a control group. Serum ferritin (SF) was used for measuring iron storage status, correspondingly, blood glucose and mean
 values of glycemia, measured as glycated hemoglobin (HbA1c) are measured. The results
 of the current study revealed highly significant increasing of iron storage (P-value 0.001)
 and percentage of glycated hemoglobin (p 0.05) among the diabetic patients. Further
 studies with larger samples should be conducted to examine the possible role of iron overload in the emergence of diabetes.

Ferroportin1 in hepatocytes and macrophages is required for the efficient mobilization of body iron stores in mice

The liver is a major site of iron storage where sequestered iron can be actively mobilized for utilization when needed elsewhere in the body. Currently, hepatocyte iron efflux mechanisms and their relationships to macrophage iron recycling during the control of whole-body iron homeostasis are unclear. We hypothesized that the iron exporter, ferroportin1 (Fpn1), is critical for both iron mobilization from hepatocytes and iron recycling from macrophages. To test this, we generated hepatocyte-specific Fpn1 deletion mice (Fpn1(Alb/Alb) ) and mice that lacked Fpn1 in both hepatocytes and macrophages (Fpn1(Alb/Alb;LysM/LysM) ). When fed a standard diet, Fpn1(Alb/Alb) mice showed mild hepatocyte iron retention. However, red blood cell (RBC) counts and hemoglobin (Hb) levels were normal, indicating intact erythropoiesis. When fed an iron-deficient diet, Fpn1(Alb/Alb) mice showed impaired liver iron mobilization and anemia, with much lower RBC and Hb levels than Fpn1(flox/flox) mice on the same diet. Using a strategy where mice were preloaded with differing amounts of dietary iron before iron deprivation, we determined that erythropoiesis in Fpn1(Alb/Alb) and Fpn1(flox/flox) mice depended on the balance between storage iron and iron demands. On a standard diet, Fpn1(Alb/Alb;LysM/LysM) mice displayed substantial iron retention in hepatocytes and macrophages, yet maintained intact erythropoiesis, implying a compensatory role for intestinal iron absorption. In contrast, when Fpn1(Alb/Alb;LysM/LysM) mice were fed an iron-deficient diet, they developed severe iron-deficiency anemia, regardless of their iron storage status. Thus, Fpn1 is critical for both hepatocyte iron mobilization and macrophage iron recycling during conditions of dietary iron deficiency. Our data reveal new insights into the relationships between Fpn1-mediated iron mobilization, iron storage, and intestinal iron absorption and how these processes interact to maintain systemic iron homeostasis.

Ferroportin1 in hepatocytes and macrophages mediates systemic iron homeostasis

The liver is a major site for iron storage, but hepatocyte iron efflux mechanisms are unclear. To examine the hypothesis that Ferroportin1 (Fpn1) is a critical iron exporter in hepatocytes and macrophages, we generated both hepatocyte‐specific Fpn1 deletion mice (Fpn1Alb/Alb), and mice that lacked Fpn1 in hepatocytes and macrophages (Fpn1Alb/Alb;LysM/LysM). When fed a standard diet, Fpn1Alb/Albmice showed mild hepatocyte iron retention. However, RBC and hemoglobin levels were normal, indicating intact erythropoiesis. When fed an iron‐deficient diet, Fpn1Alb/Albmice showed impaired liver iron mobilization and anemia, with much lower RBC and hemoglobin, indicating that erythropoiesis depended upon both iron storage and iron demand status. Thus Fpn1 is critical for hepatocyte iron release. On standard diet, Fpn1Alb/Alb;LysM/LysM mice displayed substantially increased iron retention with intact erythropoiesis implying compensatory intestinal iron absorption. When fed an iron‐deficient diet, as iron mobilization from hepatocytes and iron recycling from macrophages were impaired, Fpn1Alb/Alb;LysM/LysM mice showed severe iron‐deficiency anemia regardless of their iron store status. Our data reveal new insights into the relationship among Fpn1‐mediated iron mobilization, iron storage, and iron absorption as these factors interact to maintain systemic iron homeostasis.Grant Funding Source: MOST of China (#2009CB941400, 2011CB966200); NSFC of China (# 10979071, 30970665, 31030039)

The influence of iron stores on cadmium body burden in a Thai population

Cadmium is a toxin of increasing public health concern due to its presence in most human foodstuffs and in cigarette smoke. Exposure to cadmium leads to tissue bioaccumulation and, in particular, has nephrotoxic effects. The aim of the present study was to investigate the association between cadmium body burden and iron stores in a Thai population. A total of 182 healthy adult Thai subjects of both genders (89 males, 93 females) aged between 18 and 57 years and weighing 40-95 kg were included in this study. The total amounts of cadmium excreted in urine over 2 h (microg/g creatinine) were used as an index of long-term cadmium exposure. Quantitation of cadmium was performed using electrothermal (graphite furnace) atomic absorption spectrometry. The urinary cadmium excreted displayed a normal frequency distribution. The average urinary cadmium level did not exceed the WHO maximum tolerable internal dose for the non-exposed population (2 microg/g creatinine). Body iron stores reflected by serum ferritin levels did not show any correlation with cadmium burden in both males and females, although a relatively stronger influence of body iron store status on cadmium burden was shown in females. When the levels of serum ferritin were stratified into five levels (<20, 20-100, 101-200, 201-300, and >300 microg/l), a significant difference in total cadmium body burden was observed between females and males only in the group with a low level of serum ferritin of <20 microg/l. The cadmium body burden in females was about twice that in males in this group.

High Prevalence of Iron Deficiency and Anemia in Female Military Recruits

Iron deficiency anemia has long been known to impair physical and mental performance. Iron deficiency itself, even without anemia, may also cause such an effect. Similar to female athletes, women in active military units may have increased risks for iron deficiency and its detrimental effects. Female recruits were screened for anemia and iron store status, and a questionnaire on lifestyle habits and menstruation was completed. Iron depletion (serum ferritin level of <20 microg/L) was found for 77% of study participants. Iron deficiency (ferritin level of <12 microg/L and transferrin saturation of <15%) was found for 15% of study participants. Anemia was found for 24% of subjects, and iron deficiency anemia was found for 10% of subjects. High prevalence of iron depletion, iron deficiency, anemia, and iron deficiency anemia was found among female recruits intended for active military duty. Therefore, a recommendation can be made to screen such female recruits for anemia and iron stores.

Rapid one-step immunofluorometric assay for measuring soluble transferrin receptor in whole blood.

Iron deficiency is common, and understanding of it is advancing (1). The clinical investigation of body iron metabolism now extends beyond the demonstration of iron deficiency (e.g., by bone marrow examination) and estimation of iron storage status (by, e.g., measurement of serum ferritin). An important aim now is to determine whether a patient would benefit from iron supplementation (2)(3)(4). Soluble transferrin receptor (sTfR) measurements (5)(6)(7)(8)(9)(10)(11)(12)(13)(14) have enabled efficient detection of early iron-deficiency anemia (IDA), the treatment of which is essential, especially during phases of psychomotor development, rapid growth, and pregnancy (15)(16)(17)(18). Furthermore, the distinction between IDA and anemia of chronic disease (ACD) has become less complicated, as has the characterization of functional iron deficiency (FID) in cases of multimorbidity in the elderly or in chronic or persisting inflammatory diseases (5)(6)(7)(8)(9)(10)(11)(12)(13)(14). sTfR is a broadly applicable tool to identify individuals who are likely to benefit from iron supplementation and, consequently, is a candidate for point-of-care (POC) testing. Although most of the above-mentioned conditions are highly relevant in the outpatient setting, the current commercially available sTfR methods are not suitable for extra-laboratory testing, and none use unprocessed whole blood as sample (7)(19)(20). We describe a novel, 5-min POC immunoassay for sTfR based on the all-in-one dry-reagent assay concept (21) and time-resolved fluorescence detection. The assays were performed in individual, assay-specific dry-reagent cups that were prepared similarly to the method described by von Lode et al. (22). In short, the monoclonal anti-sTfR capture antibody (HyTest Ltd.) was biotinylated and bound (200 ng/well) …

Prevalence of Iron Depletion and Anemia in Top-level Basketball Players

Iron depletion, with or without anemia, may have a negative effect on physical and mental performance. Even with current recognition of the problem, its incidence among athletes remains high. Most studies describe iron status in endurance athletes. This study examined the prevalence of iron depletion and anemia among male and female top-level basketball players. Adolescents and adults (N = 103) from 8 national basketball teams were screened for anemia and iron stores status, which included a complete blood count and levels of plasma ferritin, transferrin, and serum iron. Iron depletion, defined by a ferritin level below 20 microg/L, was found among 22% of study participants (15% in males vs. 35% in females, p = .019). Anemia was found among 25% of athletes (18% in males vs. 38% in females, p = .028). Iron deficiency anemia, defined by the presence of anemia, ferritin levels below 12 microg/L, and transferrin saturation below 16%, was found among 7% of players (3% in males vs. 14% in females, p = .043). In summary, a high prevalence of iron depletion, anemia, and iron deficiency anemia was found among basketball players of both genders. We recommend screening ballgame players for blood count and iron store status, and providing nutritional counseling and iron supplementation when necessary.

Influence of body iron store status and cigarette smoking on cadmium body burden of healthy Thai women and men

The influence of cigarette smoking, body iron store status and gender on cadmium (Cd) body burden was examined in a group of 197 healthy Thais with overall mean age of 30.5 year (19–47 year). The lowest, geometric mean, and the highest urinary Cd excretion rate was 0.04, 0.46 and 3.84 μg/g creatinine, respectively. The prevalence of low iron stores (serum ferritin <20 μg/l) was 16% and 2% in women and men, respectively. All women ( n=99) were non-smokers, but they had the same Cd body burden as did men ( n=47) who on average smoked 8.7 cigarettes per day for 9 years. These women and men had 1.9-fold greater body Cd burden than did non-smoking men ( t=4, P<0.001). In addition, the women Cd body burden was found to be inversely correlated with serum ferritin ( r=−0.39, P<0.001) and those with low iron stores showed a 3.4-fold greater Cd body burden than did women whose serum ferritin being between 101 and 200 μg/l ( F=6.2, P=0.003, one-way ANOVA). In contrast, men’s Cd body burden did not show a significant correlation with serum ferritin, but it did show a positive correlation with cumulative cigarette smoking index ( r=0.29, P=0.02). Thus, iron status and cigarette smoking were found to be determinants of Cd body burden in young adult Thai women and men.

Low body stores of iron and restless legs syndrome: a correctable cause of insomnia in adolescents and teenagers

Background: It has been shown that restless legs syndrome (RLS) in adults may be linked to abnormalities in iron stores. Whether reduced iron stores play a role in children is not clear. Methods: We evaluated the status of iron stores and sleep in three teenagers who presented with severe sleep onset insomnia, subjective sleep latency exceeding 60 min and excessive daytime sleepiness. Results: The three teenagers were found to have RLS and laboratory evaluation confirmed reduced body stores of iron with a low percent iron saturation (mean value 9.7%) and a low serum ferritin level (mean value 17 μg/l). None had marked anemia. The three patients were treated with oral iron for 4–5 months. As a group they had an increase in percent iron saturation (from a mean of 9.7 to 22.7%) and serum ferritin (from a mean of 17 to 27 μg/l) and a marked reduction of the symptoms of RLS, with mean subjective sleep latency decreasing from 143 to 23 min, sleep efficiency increasing from 75.7 to 84.0% and the number of periodic movements per hour of sleep decreasing from 20.5 to 10.5. Interpretation: These findings support the hypothesis that abnormal iron stores or metabolism may result in RLS causing insomnia in teenagers. We recommend evaluation of iron status including serum iron, total iron binding capacity and ferritin levels in teenagers with chronic insomnia of unexplained origin even when anemia is mild or absent.

Determination of Iron Metabolism-related Reference Values in a Healthy Adult Population

Although iron evaluation on bone marrow aspirates remains the gold standard for assessing iron status, several other methods have been implemented that are less invasive and more practical. Serum iron, percentage of saturation, and total iron-binding capacity, however, lack sensitivity and are too labile to be of value as single determiners (1). Indirect measures of the functional iron compartment, such as mean cell volume and red cell distribution width, have the disadvantage of becoming indicators relatively late in the development of iron deficiency (2). Serum ferritin can be used as a marker of the iron storage compartment because it is the earliest marker to decrease with iron depletion. However, because ferritin is an acute-phase reactant in serum, its concentration may rise disproportionately to the iron storage status during inflammation, infection, or neoplasia (3), an occurrence that limits utility of ferritin in the differential diagnosis between anemia from iron deficiency and anemia from chronic disease (4). Because the soluble transferrin receptor (sTfR) concentration is not influenced by acute-phase reactions, it remains within reference values in patients with anemia of chronic disease. sTfR, therefore, can be used as a more reliable index of iron deficiency anemia (5)(6). The correlation between sTfR and bone marrow erythropoetic activity allows the use of sTfR for monitoring erythropoetin therapy, with sTfR increasing 4 weeks before the first increase of hemoglobin (7). However, conditions associated with erythroid hyperplasia can also lead to an increase of sTfR in the absence of iron deficiency (8). The sTfR/log ferritin ratio (sTfR/ferritin ratio) is reported to be even more sensitive in the presence of borderline normal ferritin and/or sTfR concentrations. This index may also be useful in distinguishing iron deficiency from conditions with hyperplastic erythropoiesis (2). Because of the lack of international standardization, different reference values for sTfR …

Iron overload is a determinant of morbidity and mortality in adult patients with sickle cell disease

Patients with sickle cell disease (SCD) often require blood transfusion starting in early childhood. Multiple blood transfusions on a chronic basis lead to excessive accumulation of iron, especially in adults with sickle cell anemia (SS) that is progressively increasing in size. Blood exchange transfusion and the use of iron chelation therapy may prevent or delay the onset of iron overload. The majority of adults with SS, however, require episodic blood transfusions on a chronic basis and, hence, are at risk to develop iron overload. Recent reports suggest an association between iron overload and organ failure in chronically transfused patients. Patients with SCD and iron overload may thus be at increased risk to develop organ failure compared to those with normal iron stores. In order to clarify this issue we have prospectively collected the following data on our adult patients with SCD between 1978 and 1998: (1) the amount of blood transfused; and (2) the status of iron stores determined with serum ferritin, serum iron, total iron binding capacity (TIBC), and percent transferrin saturation (% Sat). Between 1987 and 1998, 247 adult patients with SS were regularly followed in our sickle cell center. Of these, 152 (62%) were transfused with 4,875 units of red blood cells (RBCs). Transfused patients received an average of 10 units of RBCs per year, which is equivalent to about 2.0 g of iron per year. This does not include transfusions at other institutions or before 1987. About one third of the adult patients with SS had % Sat greater than 50 in the steady state, suggesting iron overload. During painful episodes serum ferritin increased significantly in paired observations. Serum iron and TIBC decreased during painful episode disproportionately so that there was a significant net decrease in % Sat in paired observations. Patients with low values of serum ferritin and % Sat had lower incidence of acute painful episodes (38% v 64%) and organ failure (19% v 71%) than those who had iron overload, respectively. Mortality was significantly higher in the iron overload group: 64% versus 5%, respectively. Taken together, the data indicate that (1) the status of iron stores in adults with SS is best determined by keeping accurate records of the amount of blood transfused and serial determinations of ferritin levels in the steady state; (2) a significant number of adults with SS have iron overload; and (3) iron overload seems to be a predisposing factor of disease severity.

Serum Transferrin Receptor and Erythrocyte Zinc Protoporphyrin in Patients with Anemia

The conventional laboratory test for diagnosing iron deficiency anemia (IDA) is the measurement of serum ferritin. In healthy persons, serum ferritin is directly proportional to body iron stores. In the presence of anemia, a value <20 μg/L is regarded as evidence of IDA (1). In patients with anemia of chronic disease (ACD), an increase in serum ferritin, unrelated to iron storage status, occurs. Serum ferritin concentrations usually exceed 100 μg/L when iron stores are adequate, but they may still be within the reference interval in the presence of coexisting iron deficiency (1). The assay lacks sensitivity in diagnosing IDA in patients with ACD, as well as in patients with acute infections and with liver diseases. The best established method for evaluating iron stores is examination of bone marrow iron, but this test is cumbersome and expensive. Since the early 1970s, measurement of the zinc protoporphyrin concentration (ZPP) in erythrocytes has been used as test for iron deficiency. When there is insufficient iron for incorporation into protoporphyrin IX to form heme, ZPP increases, indicating iron-deficient erythropoiesis (2). Most authors have reported a high sensitivity in diagnosing IDA, irrespective of the presence of complicating diseases (3)(4)(5). However, disturbed incorporation of iron into protoporphyrin IX can also occur in other diseases, such as ACD, hemolytic anemias, bone marrow diseases, and lead intoxication. The specificity of ZPP in diagnosing IDA is limited (6)(7). In recent years, the measurement of soluble transferrin receptor (sTfR) fragments has been introduced for the identification of iron deficiency (8). The concentration of sTfR is directly proportional to the number of red cell precursors. An exception to this rule is in patients with IDA. A reduction in iron supply leads to up-regulation of transferrin receptor synthesis, producing an increase in sTfR concentration. Several …

Dogfish (Squalus acanthias) and dogfish silage as feed-stuffs in growing-furring diets for mink (Mustela vison)

A production trial was carried out with 120 mink (Mustela vison) of standard genotype to demonstrate the effects of dogfish (DF) and dogfish silage (DFS) on growth and fur development from weaning until pelting. The experimental treatments were 1) Control, 2) DF15%, 3) DF30%, 4) DF45%, 5) DFS15%, and 6) DFS30%. The test ingredients were used to replace the haddock-herring (35%:10%) mixture in the Control diet at percentage levels indicated by the diet group designation. The rest of the diet was compounded of 10% beef tripe and lungs, 8% poultry offal, 10% cereal, 5% corn gluten meal, 0–2% vegetable oil, 0.4% vitamin-mineral premix and water. All diets guaranteed the females normal body weight gain during the trial. The males receiving the dogfish test diets had significantly poorer growth compared with the males in the Control group. Two males of the DF30% group also developed rickets. The incidence of cotton fur syndrome in the experimental groups was: Control, 0/20; DF15%, 6/20; DF30%, 7/17; DF45%, 0/19; DFS15%, 2/18; and DFS30%, 3/17 pelts produced. Acid ensiling of dogfish was shown to reduce the incidence of cotton fur in the mink but also produced an increased trend in the occurrence of enteritis in the females. Based on the haematology results and tissue iron store analysis, impaired iron metabolism was demonstrated in the DF15-30% and DFS15-30% groups. It can be concluded that the anti-nutritional factor, trimethylamine oxide (TMAO), present in dogfish reduced iron absorption in most of the experimental groups and resulted in disturbances in the fur development of the mink. The absence of cotton fur in the DF45% group is likely due to greater ammonia formation in the feed thus preventing TMAO degradation by triamine oxidase. The improved iron store status in the mink fed the DF45% diet compared with the Control and other dogfish test groups may be explained by the chelating effect of polyamines on iron consequently enhancing its absorption. Key words: Anaemia, cotton fur, trimethylamine oxide, TMAO, nutrition

Deliberations and Evaluations of the Approaches, Endpoints and Paradigms for Iron Dietary Recommendations

Iron deficiency severe enough to cause anemia is associated with significant morbidity while uncontrolled iron absorption which occurs in disorders such as hereditary hemochromatosis causes multiorgan failure and early death. Preliminary data from the Third National Health and Nutrition Examination Survey demonstrate that the prevalence of iron deficiency anemia in the United States is now very low. This implies that the current iron consumption is adequate for most individuals. An important unresolved question relates to the necessity for further reducing the prevalence of iron deficiency without anemia. More information is required to determine whether this lesser degree of iron deficiency is harmful. Recent survey data indicate that concomitantly with the reduced prevalence of iron deficiency there has been a rise in serum ferritin concentrations in American men and postmenopausal women. These findings have led to concern about the effectiveness of the physiological mechanisms for limiting storage accumulation in normal individuals and carriers of the hemochromatosis gene when dietary iron content is high. Furthermore, recent epidemiological observations suggest that a modest increase in iron stores (in a range previously considered safe) is a possible risk factor for ischemic heart disease and cancer; however, a causal relationship remains to be proven. Nonetheless, because there is no known benefit of high iron storage status, it seems prudent to avoid further increases in and possibly to reduce the dietary iron intake of men and postmenopausal women. Mean intake in these groups exceeds the current RDA by a significant margin. Therefore, the sources of dietary iron as well as other factors contributing to high serum ferritin values have to be defined. Also, efforts should be made to increase the awareness of professionals and the public about the possible risks of excessive dietary iron. The complexity of the Western diet and an incomplete understanding of all of the factors affecting serum ferritin concentrations make it very difficult to specify a safe upper range for daily iron intake at the present time.

The Effect of Recombinant Erythropoietin on the Early Hematocrit Rise after Capd Initiation

To determine if the simultaneous initiation of continuous ambulatory peritoneal dialysis (CAPD) and Erythropoietin therapy masks the hematocrit (Hct) rise that frequently follows the initiation of CAPD alone. Single-center retrospective analysis. University multidisciplinary dialysis program. All adult CAPD patients with a Hct less than or equal to 28% whose nephrologist felt they would benefit from Erythropoietin therapy and who did not have technical reasons for exclusion (N = 25). Eight patients began CAPD and Erythropoietin alfa subcutaneously, at a dose of 128 +/- 9 (X +/- SEM) units/kg/week at the same time. Seventeen patients already on CAPD for 8.7 +/- 1.5 months received Erythropoietin alfa subcutaneously at a dose of 124 +/- 7 units/kg/week. Pre-epoetin Hct's were similar. Hematocrit changes, status of iron stores, incidence of peritonitis, and dosage of Erythropoietin. In 1 month, the group initiating both therapies simultaneously demonstrated a mean Hct rise of 7.6 +/- 0.5% while established CAPD patients receiving Erythropoietin increased their Hct by only 4.7 +/- 1.0% (p less than .03). Iron status could not explain this difference. Peritonitis did not appear to dampen the Hct rise following Erythropoietin in either CAPD group. By 2 months after Erythropoietin, the differences were less apparent. The early rapid increase in Hct is probably the combined effect of CAPD and Erythropoietin and should not be attributed to Erythropoietin alone. When comparing responses to Erythropoietin from patients on different therapies, the timing of dialysis initiation and Erythropoietin initiation must be considered.

Monocyte ferritin in idiopathic haemochromatosis, thalassaemia and liver disease.

Monocyte ferritin (MF) content was measured in normal subjects and patients with a variety of disorders of iron storage. MF was above the normal range in 4 patients with idiopathic haemochromatosis (IHC). However, in 4 patients with transfusion siderosis (TS), secondary to aplastic anaemia, who had similar elevations in serum ferritin, MF was highly elevated. 10 patients with thalassaemia intermedia and thalassaemia major with no previous history of transfusions, but with elevated serum ferritin, also had significantly elevated MF. Disproportionately low MF in IHC could reflect defective ferritin metabolism in reticuloendothelial cells in this disorder. Finally, in 3 patients with acute rises in serum ferritin caused by acute hepatitis, MF was not increased. This suggests that MF is not directly affected by high circulating levels of serum ferritin raised acutely, but rather reflects iron storage status in conditions not associated with primary disorders of iron metabolism.

Effect of Iron Saturation of Transferrin on Hepatic Iron Uptake: An in Vitro Study

Studies were performed to delineate the effect of percentage of saturation of transferrin and total iron concentration on the rate of uptake of iron by the perfused rat liver. Normal and iron-deficient rat livers were perfused with sera that contained varying concentrations of 59Fe-labeled iron and transferrin saturation. Varying the percentage of saturation of transferrin while maintaining a constant concentration of iron did not influence the hepatic uptake of iron. However, raising the concentration of iron in the perfusate while maintaining a constant saturation of transferrin did increase the uptake of iron by the liver. At similar concentrations of iron and transferrin saturation, iron-deficient livers took up greater amounts of iron than did normal livers. In our experiments, the hepatic uptake of transferrin-bound iron is determined by (1) the concentration of iron in perfusate and (2) the status of iron stores in the liver being perfused.

Relationship of Maternal and Infant Iron Stores as Assessed by Determination of Plasma Ferritin

Using plasma ferritin derminations, iron stores have been evaluated at the end of pregnancy in 26 women and followed sequentially in their healthy, full-term infants. It has been shown that the iron storage status of the mother does not affect the iron status of the infant. Determinations of plasma ferritin in the infants have demonstrated that by 6 months of age the iron status of the infant reflects the adequacy of the dietary intake of iron. In the absence of effective iron supplementation during the first six months, plasma ferritin levels fall to low levels, indicating the depletion of iron stores in the infant.