Phytates iron absorption

Inhibitors of non-haem iron absorption include polyphenols and phytates. The former, secondary plant metabolites rich in phenolic hydroxyl groups, are found... 

Gillooly et al. (42J observed that iron absorptions were markedly decreased by the additon of sodium phytate to test meals while similarly marked decreases in zinc absorption have been observed (36,43 Table II). Contradictory results were recently reported (23.44). Addition of high levels (1.5 to 2.9g/day) of sodium phytate did not significantly affect the apparent absorption of iron, manganese, copper or zinc. 

Hallberg, L. (1987). Wheat fiber, phytates and iron absorption. Scand. J. Gastroenterol. Suppl. 129, 73-79. 

Iron absorption occurs predominantly in the duodenum and upper jejunum. The physical state of iron entering the duodenum greatly influences its absorption. At physiological pH, ferrous iron is rapidly oxidized to the insoluble ferric form. Gastric acid lowers the pH in the proximal duodenum, enhancing the solubility and uptake of ferric iron. When gastric acid production is impaired, iron absorption is reduced substantially. Ascorbic acid enhances iron absorption. Ascorbic acid mobilizes iron from iron-binding proteins in vivo, which in turn could catalyze lipid peroxidation. Iron absorption is inhibited by antacids, phytates, phosphates and tetracyclines. 

Iron absorption takes place predominantly in the duodenum where the acid environment enhances solubility, but also throughout the gut, allowing sustained-release preparations to be used. Most iron in food is present as ferric hydroxide, ferric-protein complexes or haem-protein complexes. Ferrous (Fe " ) iron is more readily absorbed than ferric (Fe ). Thus the simultaneous ingestion of a reducing agent, such as ascorbic acid, increases the amount of the ferrous form ascorbic acid 50 mg increases iron absorption from a meal by 2-3 times. Food reduces iron absorption due to inhibition by phytates, taimates and phosphates. 

Iron deficiency anemia occurs mainly in infants, children, and fertile women. For this reason, a variety of foods, including infant formula and infant cereals, is fortified with iron. Ferrous sulfate is a form of iron that is most readily absorbed by the gut, but when added to dry cereals it can promote their spoilage and rancidity. For this reason, dry cereals are fortified with elemental iron particles, ferric pyrophosphate, or ferrous fumarate (Davidsson et ah, 1997). Ascorbic add may also be added to the cereal to enhance iron absorption. To view some of the numbers, infant cereals may contain 75 mg iron/kg cereal (1.3 mmol iron/kg), 1 mmol phytic acid/kg, and 2.6 mmol ascorbic acid/kg (Davidsson et cd., 1997). Although phytic acid impairs iron absorption, the added ascorbate serves to prevent this effect. An alternate method for preventing phytate from impairing iron absorption is to treat the food with the enzyme phytase. A parent interested in enhancing a child s iron absorption can easily feed a child some orange juice, but it would not be practical to pretreat the child s cereal with phytase. A typical availability of ferrous sulfate in infants is about 3-5% (with no ascorbate), and 6-10% (with ascorbate). Ascorbate is effective when present in a twofold molar excess over the iron. 

Other organic acids which have been tested for their impact on iron absorption include oxalic, succinic, fumaric and lactic acid (Table V). The iron from iron phytates was bioavailable only in the soluble monoferric form, whereas the less soluble diand tetra-ferric phytates were very poor iron sources (37,... 

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. 

Despite this drawback, a number of studies based almost entirely upon the use of rats have shown that dietary fibers from various sources may impair iron absorption (Table 1). The fiber sources examined most often were fiber-rich mill fractions of wheat, generally bran. The use of isolated fiber components is confined largely to cellulose. Although wheat bran is rich in phytate, the work of Morris and Ellis (34) supported by subsequent publications from the same source, indicates that interference by phytate with iron absorption is not appreciable, and can be disregarded. Liebman and Driskell (35) and Hunter (36) have also found no interference by phytate with iron metabolism, confirming the earlier report of Cowan et al (22). However, Simpson et al (61) very recently recently reported that a phosphate-rich extract of dephy-tinized bran inhibited iron absorption. Thus, it is not permissible to equate bran with fiber completely. 

On the other hand, Morris et al. (7) recently pointed out that naturally occuring iron in wheat is predominantly present in the form of monoferric phytate, which (unlike phytate complexed with two or more iron atoms) is soluble at pH 7.0 and above and may therefore be a relatively available form of dietary iron. Conflicting reports in the literature on the effect of phytate on iron absorption might be due to the use of different ferric phytate complexes in the various studies. 

Phytate-bound iron may or may not constitute available forms of iron to the human as discussed in several other chapters of this book. Earlier work sugests that phytates inhibit iron absorption. Since phytates and oxalates are provided by cereal/ plant products, an Increase in the plant components of diet is likely to increase the intake of these inhibitors. 

Absorption of iron is never very efficient and is influenced by many factors. Hydrochloric acid, pepsin, proteins and their digestion products, and ascorbic acid appear to be concerned in the reduction of iron to the ferrous state in which form it is absorbed. Absorption takes place largely in the duodenum (Chapter 20). Iron absorption may be increased by administration of ascorbic acid and decreased by phosphates and perhaps by phytates. 

Iron absorption is inhibited by the following phytates (whole grains, bran), oxalates (Spinach and rhubarb), raw... 

Heme-iron, only present in animal foods, is more bioavailable compared to other sources contained in grains and vegetables. The consumption of animal products enhances iron absorption associated with grains. Another important enhancer of iron absorption is vitamin C because it chelates nonheme-iron under stomach acidic conditions, and keeps it soluble under the relatively neutral pH conditions of the duodenum. Vitamin C reduces ferric iron (Fe+ ) into ferrous iron (Fe+ ) in the stomach. The ferrous form is more efficiently absorbed by the duodenum epithelial cells. Heme-iron enters the epithelial cells complexed to porphyrin myoglobin and hemoglobin. The absorbed iron is stored in ferritin molecules located inside the intestinal cells and transported bound to transferrin. There are known inhibitors of iron absorption, the most important being phytates and fiber. 

Non-heme iron exists in plant products and its bioavailability is compromised by the concurrent ingestion of tannins, phytates, soy, and other plant constituents, that decrease its solubility in the intestinal lumen. Bioavailability of non-heme iron is increased by concurrent ingestion of ascorbic acid and meat products. Nonheme iron is reduced from the ferric to the ferrous form in the intestinal lumen and transported into enterocytes via the divalent metal transporter (DMT-1). Once inside the enterocyte, iron from heme and nonheme sources is similarly transported through the cell and across the basolateral membrane by the ferroportin transporter in conjunction with the ferroxidase hephaestin after which it can be taken up by transferrin into the circulation. The regulation of iron across the basolateral membrane of the enterocyte is considered the most important aspect of iron absorption. 

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