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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Copper is known to be an essential nutrient for human beings, but a Recommended Dietary Allowance has not yet been established. A safe and adequate range of intake was established in 1980 for copper and five other trace elements. The range for copper, 2 to 3 mg/day, is higher than the usual dietary copper intake of many individuals in this country. On the basis of balance studies, a requirement of 1.3 mg/day has been suggested. Recent data on copper intake and bioavailability should aid in reevaluating the dietary copper requirement. Copper deficiency symptoms have seldom been observed in human beings. When copper deficiency has been recognized, it has been under unusual conditions, such as in patients receiving parenteral nutrition. Interactions between copper and other dietary components may alter copper status, but the impact of those interactions is not yet well understood. Dietary factors that may affect the bioavailability of copper include the levels of copper, zinc, and molybdenum in the diet; iron deficiency; ascorbic acid intake; intake of carbohydrates, including fructose, glucose, and starch; and fiber and phytate intakes. Some drugs may also affect copper bioavailability.
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PMID:Copper nutriture, bioavailability, and the influence of dietary factors. 327 98

During the last decade there has been considerable interest in the idea that dietary trace elements supplementation can result in an improvement in athletic performance. The current paper discusses this idea as it relates to 3 elements: iron, zinc and magnesium. Emphasis has been placed on examining the implicit assumptions underlying the idea that mineral supplements help the athlete. These assumptions include the beliefs that the athlete has a higher than normal requirement for minerals; that the athlete consumes a diet inadequate in these minerals; and that a marginal deficiency of these elements has a direct effect on athletic performance. Evidence is presented that both iron deficiency and magnesium deficiency can result in a significant reduction in exercise performance; however, the biochemical lesions underlying the reductions in exercise performance have not been identified. There is evidence that dietary magnesium intake may be suboptimal in some individuals, thus dietary supplementation of this element may be useful in some population groups. Excessive magnesium supplementation is not thought to be a serious health problem. Similar to magnesium dietary iron supplements can improve athletic performance in individuals severely deficient in this element. However, few studies have documented a need for iron supplements in healthy athletes. If iron supplements are used, it is important that the level of supplementation is not excessive, as excess iron in the diet can result in an induced zinc deficiency. In marked contrast to iron and magnesium, there is little evidence for the idea that zinc deficiency influences exercise performance in humans. Despite this fact, zinc supplements have been widely advocated for the athlete, as it is known that intense exercise can result in changes in zinc metabolism. If zinc supplements are used, it is important that they are not excessive, as excess zinc in the diet can result in a secondary copper deficiency.
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PMID:Iron, zinc and magnesium nutrition and athletic performance. 328 36

Copper deficiency was found in an adult patient who had received excessive daily oral zinc for 10 mo. The deficiency was characterized by hypochromic-microcytic anemia, leukopenia, and neutropenia. Although initially thought to be caused by iron deficiency, the anemia did not respond to oral or intravenous iron. Cessation of zinc tablets and ingestion of an oral copper preparation daily for 2 mo failed to correct the anemia or leukopenia. It was not until shortly after intravenous administration of a cupric chloride solution during a 5-day period, at a total dose of 10 mg, that serum copper and ceruloplasmin levels increased and the anemia, leukopenia, and neutropenia resolved. These data suggest that the elimination of excess zinc is slow and that, until such elimination occurs, the intestinal absorption of copper is blocked.
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PMID:Zinc-induced copper deficiency. 333 23

In Sweden a multicentre nutritional survey was performed in 1980-81 in four different parts of Sweden. The total number of children investigated was 1109, of whom 92 were two years old, 332 four years, 338 eight years and 347 thirteen years. The 24-hour recall method was used in all children. In addition 7-day record was used in the 2-, 4- and 8-year-olds and the dietary history method in the 13-year-olds. During the weekdays the 2-, 4-, 8- and 13-year-old children had 5.9, 5.8, 5.4 and 5.2 meals and snacks per day, respectively. During weekends these respective numbers decreased to 5.7, 5.6, 5.1 and 5.0. The mean number of light meals and snacks was almost the same on all days and varied between 2.4 and 3.3 in the different age groups. The part of the energy intake deriving from snacks has increased during the last 15 years. The mean daily energy intakes for the 2-, 4-, 8- and 13-year-old boys and girls were 5.8 and 5.6, 6.9 and 6.5, 8.9 and 7.9 and 12.1 and 9.7 MJ respectively. These values are below the recommendations for all age groups except the 2-year-old boys. The mean daily intakes of protein, retinol, ascorbic acid, thiamin, riboflavin, niacin, vitamin B12 and calcium were almost invariably higher or much higher than the recommendations, while those of vitamin D and zinc were below the recommended values. The iron intake fulfilled the recommendations except for the 2-year-olds and the 13-year-old girls. The intake of protein and fat expressed in per cent of the total energy intake was very similar in all age groups, about 14 per cent and 35-37 per cent respectively. The mean ratio between polyunsaturated and saturated fatty acids (P/S ratio) was also the same in all age groups, i.e. 0.22-0.23. This low ratio is explained by a high consumption of dairy products. Furthermore, the nutrient density of the food did not change appreciably with age. The only exception was found for the 2-year-old children, who had slightly higher nutrient density values on account of a relatively high consumption of fortified follow-up formula. In all age groups the mean nutrient densities of vitamins D and B6 and of iron were below the recommendations to varying degrees. No clinical signs of nutritional deficiencies, iron deficiency included, were found in any age group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Food habits and nutrient intake in childhood in relation to health and socio-economic conditions. A Swedish Multicentre Study 1980-81. 347 Oct 46

The production of the immunotransmitter, interleukin 1 (IL-1), by peritoneal exudate cells (PEC) was examined in iron-deficient and control rats. Three groups of weanling male Sprague-Dawley rats were fed a purified diet containing 6, 12, or 35 ppm iron for 6 wk to produce severe iron deficiency, moderate iron deficiency, or adequate iron status. Crude IL-1 samples were prepared from acute PEC and assayed for activity. IL-1 preparations from severely and moderately iron-deficient rats enhanced mouse thymocyte proliferation in vitro less than half as much as IL-1 preparations from control rats. In a rabbit bioassay, injection of IL-1 prepared with PEC from either group of iron-deficient rats had little effect on body temperature or plasma minerals, while IL-1 from iron-adequate source PEC produced a febrile response and markedly lowered plasma iron and zinc in recipient rabbits. Severe or moderate iron deficiency, then, clearly impairs IL-1 production by rat PEC.
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PMID:Iron deficiency and interleukin 1 production by rat leukocytes. 349 73

The role of protein and calorie deficiency in sickle cell disease remains poorly defined. While such features as growth retardation, impaired immune function, and delayed menarche do suggest a relationship between sickle cell disease and undernutrition, measurement of more direct nutritional parameters in these patients have yielded mixed results. Anthropometric measurements such as skinfold thickness are subnormal in many but not all reports. Serum protein levels are normal, but low values for serum lipids have been reported. Finally, one small study shows an improvement in both growth parameters and clinical course following caloric supplementation. A variety of micronutrient deficiencies have been suggested in sickle cell disease. Numerous case reports describing an exacerbation of the chronic anemia that was reversed by folic acid therapy led to routine folate supplementation. More recent studies have shown, however, that clinically significant folic acid deficiency occurs only in a small minority of sickle cell patients. Clearly, more work is necessary to define the cost/benefit ratio of routine folic acid supplementation. Pharmacological amounts of vitamin B6 and certain of its derivatives possess in vitro antisickling activities. Nevertheless, a small clinical trial failed to demonstrate any consistent hematologic effects of B6 supplementation. Several reports indicate that vitamin E levels are low in sickle erythrocytes. Since these abnormal red cells both generate excessive oxidation products and are more sensitive to oxidant stress, and because oxidants appear to play a role in ISC formation, vitamin E deficiency could well be linked to ISC formation and hemolysis. Small clinical trials, however, have again failed to produce a clear hematological response in sickle cell anemia. The role of zinc in sickle cell disease has received considerable attention. Though studies are generally small, most do support a relationship between sickle cell disease and zinc deficiency. Etiologic associations between zinc deficiency and such complications of sickle cell disease as poor ulcer healing, growth retardation, delays in sexual development, immune deficiencies, and high ISC counts have all been suggested. Most of these studies need further corroboration. Iron deficiency is now known to be a relatively common occurrence in sickle cell anemia, especially in children and pregnant women. The theoretical benefits of concomitant iron deficiency and sickle cell anemia remain to be proven in a controlled clinical trial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and sickle cell disease. 355 92

Reference serum copper, ceruloplasmin and zinc values were established for 100 healthy white nulliparous students aged 18-23 years resident in Cape Town who had been taking low-dosage triphasic contraceptives for a minimum period of 3 months, and in 100 female students not taking contraceptives. The mean serum copper values were 26.5 +/- 4.2 mumol/l and 16.9 +/- 2.7 mumol/l for those taking and not taking oral contraceptives respectively; corresponding values for ceruloplasmin were 181 +/- 43.9 IU/ml and 110 +/- 22.7 IU/ml respectively. Both differences were statistically significant. Serum zinc values for those on contraceptives were 14.1 +/- 2.1 mumol/l and for the others 14.7 +/- 2.0 mumol/l. There were no differences in the haematological parameters except for a significantly higher mean corpuscular volume in females taking oral contraceptives. Of possible clinical significance in this student population are prevalence rates of 2.2% for anaemia (haemoglobin value less than 11.5 g/dl), 7% for iron deficiency (serum ferritin less than 12 micrograms/l) and 6.6% for iron depletion (serum ferritin 12-20 micrograms/l).
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PMID:Reference values for serum copper, ceruloplasmin and zinc and haematological indices for healthy nulliparous females. 366 Jan 57

Iron status, including hemoglobin, S-ferritin, S-iron, S-transferrin, transferrin saturation and the erythrocyte zinc protoporphyrin/hemoglobin (ZPP:Hb) ratio, was evaluated in 85 healthy iron-supplemented mothers at parturition and in 74 of their term newborn infants. Of the mothers, 17% had a S-ferritin level less than 15 micrograms/l (i.e. depleted iron stores), 9.9% had S-ferritin less than 15 micrograms/l and transferrin saturation less than 15% (i.e. latent iron deficiency), and 2.4% had S-ferritin less than 15 micrograms/l, transferrin saturation less than 15% and Hb less than 120 g/l (i.e. iron deficiency anemia). Newborn infants had higher S-ferritin than mothers: median 128 micrograms/l versus 21 micrograms/l (p less than 0.0001), higher transferrin saturation: 48% vs. 21% (p less than 0.0001), and higher ZPP:Hb ratio: 74 mumol/mol Hb vs. 41 mumol/mol Hb (p less than 0.0001). During the first 5 post-natal days, median S-ferritin rose from 128 to 236 micrograms/l (p less than 0.0001). S-ferritin appeared to be the best single indicator of maternal iron status. Ferritin levels in newborn infants were correlated to levels in mothers (rs = 0.36, p less than 0.01), indicating that fetal iron reserves are dependent on maternal iron stores.
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PMID:Serum ferritin and iron status in mothers and newborn infants. 366 Nov 27

One hundred and forty five Asian children born at Sorrento Maternity Hospital, Birmingham, were reviewed at the age of 22 months. A significant association of iron deficiency and poor vitamin D state was found. Two fifths of the children were anaemic, two fifths had a low plasma concentration of vitamin D, and one fifth had both features. This was more than simple overlap of the two deficiencies; the children with low plasma vitamin D concentrations had significantly lower concentrations of haemoglobin and serum iron. On the other hand, the deficiencies were not merely individual features of generally poor nutrition; growth and other measures of protein energy nutrition were slightly better in these children, and their plasma zinc concentration was no lower than in the children without deficiencies. It seems, therefore, that child health surveillance as currently practised--for example, growth monitoring, clinical signs, etc--will not detect these problems unless a haemoglobin determination is included. In view of the association of poor iron and vitamin D state combined prophylaxis is desirable. At present, strategies for preventing rickets in this country are not combined with attempts to detect or prevent iron deficiency. In our opinion they should be and the options are discussed.
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PMID:Combined deficiency of iron and vitamin D in Asian toddlers. 376 13

The effects of iron deficiency and iron overloading on the mitochondrial enzymes involved in heme synthesis were studied in rat livers. The in vitro activities of several of the enzymes in this pathway were differentially influenced by the in vivo iron status of the animals. delta-Aminolevulinic acid synthase was slightly increased in iron-overloaded animals, but remained normal in iron-deficient animals (0.58 +/- 0.09, 0.91 +/- 0.19 and 0.61 +/- 0.12 nmol delta-aminolevulinic acid/mg per h). Copro- and protoporphyrinogen oxidase activities were increased (20 and 60% above controls) in iron-deficient animals. In contrast, coproporphyrinogen oxidase was decreased by 20%, while protoporphyrinogen oxidase remained unchanged in iron-overloaded rats. These variations of activities were not due to changes in the affinity of these enzymes toward their substrates, as coporphyrinogen had the same Km in each case (0.62 +/- 0.05 M) as did protoporphyrinogen (0.22 +/- 0.035 M). Thus, the Km did not vary with the treatment received by the animals. Ferrochelatase activity was measured by both the pyridine hemochromogen method and by measurement of zinc protoporphyrin with endogenous zinc as substrate. In all cases, ferrochelatase was found to be able to synthesize zinc protoporphyrin with endogenous zinc as substrate. However, the apparent Km of zinc chelatase for protoporphyrin was significantly different in the three groups of animals with Km,appProto, app = 2.4 +/- 0.1 10(-7), 4 +/- 0.3 10(-7) and 9.10 +/- 0.05 10(-7) M in iron-overloaded, control and iron-deficient animals, respectively. When ferrochelatase activity was measured by pyridine hemochromogen, identical results were observed in iron-deficient and control animals but decreased by 45% in iron-overloaded animals. The mitochondrial heme content was also decreased by 40% in iron-overloaded rats but unchanged in either iron-deficient or control rats.
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PMID:Effects of iron deficiency and chronic iron overloading on mitochondrial heme biosynthetic enzymes in rat liver. 395 59


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