Intake of iron

Secondary kemochromatosis can occur after repeated transfusions (eg, for treatment of sickle cell anemia), excessive oral intake of iron (eg, by African Banm peoples who consume alcoholic beverages fermented in containers made of iron), or a number of other condi-... 

Yu, S., C.E. West, and A.C. Beynen. 1994. Increasing intakes of iron reduce status, absorption and biliary excretion of copper in rats. Brit. Jour. Nutr. 71 887-895. 

However, it has been estimated that about 80% of the daily dietary intake of iron is in the form of non-heme iron and only about 20% from heme iron. Hence, any product added to the diet which causes a significant decrease in non-heme iron absorption is of concern. 

Adverse effects. The frequent gastrointestinal complaints (epigastric pain, diarrhea, constipation) necessitate intake of iron preparations with or after meals, although absorption is higher from the empty stomach. 

Absorption/Dlstrlbutlon - The average dietary intake of iron is 12 to 20 mg/day for males and 8 to 15 mg/day for females however, only about 10% of this iron is absorbed (1 to 2 mg/day) in individuals with adequate iron stores. Absorption is enhanced (20% to 30%) when storage iron is depleted or when erythropoiesis occurs at an increased rate. Iron is primarily absorbed from the duodenum and jejunum. The ferrous salt form is absorbed 3 times more readily than the ferric form. The common ferrous salts (ie, sulfate, gluconate, fumarate) are absorbed almost on a milligram-for-milligram basis but differ in the content of elemental iron. Sustained-release... 

As we have seen, the body has essentially no means of eliminating iron, so an excessive intake of iron causes various problems known as siderosis. Chelating agents are used to treat the excessive buildup of iron. In many cases (he chelates resemble or are identical to the analogous compounds used by bacteria to chelate iron. Thus desferrioxamine B is the drug of choice for African siderosis.1)7 The ideal chelating... 

Patients with iron deficiency anemia present with fatigue, weakness, and pallor, and possibly also with glossitis, headache, dysphagia, fingernail changes, gastric atrophy, and paresthesias. Inadequate intake of iron, malabsorption, and blood loss from any origin are the principal causes of iron deficiency anemia. 

The RNI (Recommended Nutrient Intake) of iron for women is listed as 14.8 mg per day. Ferrous gluconate, Fe(C6Hii07)2 is often used as an iron supplement for those who do not get enough iron in their diet because it is relatively easy for the body to absorb. Some iron-fortified breakfast cereals contain elemental iron metal as their source of iron. 

Q8 This is unlikely as Maria appears to have a well-balanced food intake and is not trying to diet. In iron-deficiency anaemia, whether caused by poor dietary intake of iron or haemorrhage, RBCs are small. New RBCs entering the circulation are microcytic and carry reduced amount of haemoglobin (hypochromic). The small cells can be visualized on a standard blood film. Premenopausal women are especially likely to suffer from iron-deficiency anaemia following menstrual blood loss and childbirth. However, the blood tests show that Maria s red cells are larger than normal, so she is not suffering from this form of anaemia. 

HANES 2 (1976 - 80) reports low intake of iron and ascorbic acid for large population segments, especially females below poverty line, e.g. at 10th percentile 4 mg iron and 7 mg ascorbic acid per day. 

Different diets also contained 8.5-20% protein (casein and/or mixed-grain protein) with or without supplements of copper and/or zinc. Zinc had no effect, but copper and protein had major effects as observed by measuring hemoglobin, hematocrit, red cell counts and liver iron. Most profound anemia was seen with 20% protein and low intakes of iron and copper. 

Nonpharmacologic therapy for anemia of CKD includes maintaining adequate dietary intake of iron. A relatively small amount of dietary iron, approximately 1 to 2 mg (or approximately 10%), is absorbed each day, primarily in the duodenum. While there is some debate as to whether GI absorption of iron is significantly altered in patients with severe CKD, it is clear that oral intake from dietary sources alone is generally not sufficient to meet the increased iron requirements that are necessitated by the initiation of erythropoietic therapy. ... 

The iron, zinc, iodine and selenium concentrations of the food dry matter consumed is only slightly higher than the normative requirements of these elements (see Table 4.8). The findings show that the intakes of iron, zinc, iodine and selenium in Germany and Europe do not always meet the normative requirements. 

Thomson ABR and Valbeeg LS (1972) Intestinal intake of iron, cobalt and manganese in the iron-dficient rat. Am J Physiol 223(6) 1327—1329. 

Iron-deficiency anemia results from dietary intake of iron that is inadequate to meet normal requirements (nutritional iron deficiency), blood loss, or interference with iron absorption. Most nutritional iron deficiency in the U.S. is mild. More severe iron deficiency is usually the result of blood loss, either from the GI tract, or in women, from the uterus. Impaired absorption of iron from food results most often from partial gastrectomy or malabsorption in the small intestine. Finally, erythropoietin therapy can result in a functional iron deficiency. 

The influence of different geographic locations could be documented on the mineral composition of edible red seaweed Porphyra vietmmensis from different localities of the central west coast India. The highest amount of Fe was observed in the wide range from 33.0 to 298.0 mg/ 100 g dry weight. Thanks to the high level of Fe, P. vietnamensis from these localities could be served as a food supplement to improve dietary intake of iron (Rao et al., 2007). 

Table 2. Suggested maximum intakes of iron as sodium iron EDTA (as compared with RDA values for iron) and corresponding maximum intakes of EDTA...

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