Human dietary iron absorption

Intestinal absorption of is low, ranging from 0.4% to 2.5%, so fecal output is mainly unabsorbed dietary chromium. Absorption is increased marginally by ascorbic acid, amino adds, oxalate, and other dietary factors. After absorption, chromium binds to plasma transferrin with an affinity similar to that of iron. It then concentrates in human liver, spleen, other soft tissue, and bone. Urine chromium output is around 0.2 to 0.3 U,g/day, the amount excreted being to some extent dependent upon intake. Paradoxically, urine output appears to be relatively increased at low dietary levels. Thus 2% is lost in urine at an intake of lOpg/day, but only 0.5% at an intake of 40pg/day. Both running and resistive exercise increases urine chromium excretion. 

This reference dose of ferrous sulfate ascorbic acid was absorbed at a higher rate in iron deficient subjects than in iron replete subjects a ratio of the absorption of the test meal to the reference dose allowed comparisons to be made between individual subjects. As these early studies were limited to study of single food items an effort was made to extend the technique by developing designs utilizing extrinslcally tagged test meals (3,4). Utilization of these techniques has given evidence that dietary iron forms two separate pools in the gut, one a pool of heme iron and the other a pool of nonheme iron. The predominate source of iron in human diets is in the form of nonheme iron (5),... 

Extensive research on the absorption of iron from various types of meals has allowed guidelines to be developed by which the amount of dietary iron available for absorption may be estimated. Iron is the first trace mineral to be thus treated and thus serves as a model for other nutrients (19). The model for estimating bioavailable iron is based on the concept that iron forms a) a pool of heme iron which is readily available to humans and is uneffected by other dietary components and b) a pool of nonheme iron which is of low bioavailability unless enhancing factors are present concommitantly (20). 

Other factors in the diet have also been found to modify the effect of phosphorus on iron and zinc metabolism. One such factor is ascorbic acid. Peters, et al. (35) observed that when human subjects were fed a solution of iron chloride, they absorbed very little iron if ascorbic acid was not present in the solution (Table IV). In fact, if ascorbic acid was not present, absorption of iron was so low it was difficult to tell whether dietary factors, such as phosphorus, affected the absorption of iron. However, ascorbic acid may also counteract the effect of dietary phosphorus on the absorption of nonheme iron. Investigators have demonstrated that the addition of ascorbic acid to a diet counteracted the effect of the phosphoprotein in egg yolk on iron absorption (17. 18). 

Monoferric phytate is the major fraction of iron in wheat bran, and is a highly bioavailable form of dietary iron in contrast to insoluble di- or tetra-ferric phytate. Monoferric phytate equilibrates with the miscible nonheme iron pool of a meal in extrinsic label iron absorption tests. Whole wheat bran depressed absorption by humans of nonheme iron in a meal. Dephytinized wheat bran also inhibited nonheme iron absorption by humans and the inhibition could not be clearly attributed to either the insoluble or soluble fractions of the dephytinized bran. Adult men who consumed 36 g of wheat bran per day had positive iron balances. Iron balance was not increased when dephytinized bran was consumed. The form of ferric phytate must be known to properly explain the effect of phytic acid on iron absorption. The overall meal composition must be considered to evaluate the effect of wheat bran on iron nutrition of humans. 

Table V. Dephytinized Wheat Bran and Absorption of Nonheme Dietary Iron by Humans ...

A common baby food, strained pears, inhibited iron absorption in the presence of human milk according to Oski and Landau (55). Although the authors did not attribute the action to dietary fiber, it is a possible suspect. 

Ferritin also occurs in the cells of the intestinal mucosa where it has been thought to play some role in regulating the amount of dietary iron absorbed from the gut. From evidence of increased absorption of radioactive iron in humans with iron deficiency compared with normal subjects, who absorb very little, the idea of a mucosal block was... 

Flanagan PR, Hamilton DL, Haist J, Valberg LS (1979) Interrelationships between iron and lead absorption in iron-deficient mice. Gastroenterology 77 1074-1081 Flanagan PR, McLellan JS, Haist J, Cherian MG, Chamberlain JJ, Valberg LS (1978) Increased dietary cadmium absorption in mice and human subjects with iron deficiency. Gastroenterology 74 841-846... 

Even if we had accurate and comprehensive information on the trace element content of human milk, we are still faced with the enormous problem of probably large, but poorly quantitated differences in bioavailability for at least some specific trace elements between human milk and the various formulas used in infant feeding. This problem is of great importance in the young infant because of his dependence on one major dietary staple. For example, the iron status of breast fed infants is known to be relatively favorable during the first six months despite a very low iron intake from human milk and iron absorption has been shown to be especially high when given with human milk [13]. The same appears to be true for zinc [14]. 

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