Although hepcidin synthesis is stimulated by inflammation and inhibited by Fe deficiency, the strength of their opposing effects on serum hepcidin (SHep) in humans remains unclear. It was recently shown that an inflammatory stimulus in anaemic women did not increase SHep or decrease Fe absorption. The enhancing effect of ascorbic acid on Fe absorption may not be effective during inflammation because of increased SHep. Our study aim was to test whether reducing inflammation in Fe-depleted overweight (OW) women with low-grade inflammation would lower SHep and improve Fe absorption with and without ascorbic acid, compared with normal-weight (NW) women without inflammation. Before and after 14 d of anti-inflammatory treatment (3 × 600 mg ibuprofen daily) in OW and NW women (n 36; 19–46 years of age), we measured SHep and fractional Fe absorption (FIA) (erythrocyte Fe incorporation) from 57Fe- and 58Fe-labelled test meals with and without ascorbic acid. There were significant group effects on IL-6, C-reactive protein, serum ferritin and SHep (for all, P < 0·05). There was a significant treatment effect on SHep (P < 0·05): in OW women, treatment decreased IL-6 by approximately 30 % and SHep by approximately 45 %. However, there were no significant treatment or group effects on FIA. Body Fe stores (BIS) were a significant positive predictor of SHep before and after treatment (P < 0·001), but IL-6 was not. Reducing chronic inflammation in OW women halved SHep but did not affect Fe absorption with or without ascorbic acid, and the main predictor of Fe absorption was BIS.

Fe fortification of wheat flour was proposed in Haiti to combat Fe deficiency, but Fe bioavailability from fortificants has never been investigated in Haitian women or preschool children, two key target groups. We aimed to investigate the bioavailability of ferrous fumarate (FeFum), NaFeEDTA and their combination from fortified wheat flour. We recruited twenty-two healthy mother–child pairs in Port au Prince, Haiti, for an Fe-absorption study. We administered stable Fe isotopes as FeFum or NaFeEDTA individually in low-extraction wheat flour bread rolls consumed by all participants in a randomised, cross-over design. In a final, identical meal, consumed only by the women, FeFum+NaFeEDTA was administered. We measured Fe absorption by using erythrocyte incorporation of stable isotopes 14 d after consumption of each meal, and determined Fe status, inflammatory markers and Helicobacter pylori infection. Fe absorption (geometric mean was 9·24 (95 % CI 6·35, 13·44) and 9·26 (95 % CI 7·00, 12·31) from FeFum and 13·06 (95 % CI 9·23, 19·10) and 12·99 (95 % CI 9·18, 18·39) from NaFeEDTA in mothers and children, respectively (P<0·05 between compounds). Fe absorption from FeFum+NaFeEDTA was 11·09 (95 % CI 7·45, 17·34) and did not differ from the other two meals. H. pylori infection did not influence Fe absorption in children. In conclusion, in Haitian women and children, Fe absorption from NaFeEDTA was 40 % higher than from FeFum, and the combination FeFum+NaFeEDTA did not significantly increase Fe absorption compared with FeFum alone. In the context of Haiti, where the high costs of NaFeEDTA may not be affordable, the use of FeFum at 60 mg Fe/kg flour may be a preferable, cost-effective fortification strategy.

Different metabolic pathways of supplemental and fortification Fe, or inhibition of Zn absorption by Fe, may explain adverse effects of supplemental Fe in Fe-sufficient infants. We determined whether the mode of oral Fe administration or the amount habitually consumed affects Fe absorption and systemic Fe utilisation in infants, and assessed the effects of these interventions on Zn absorption, Fe and Zn status, and growth. Fe-sufficient 6-month-old infants (n 72) were randomly assigned to receive 6·6 mg Fe/d from a high-Fe formula, 1·3 mg Fe/d from a low-Fe formula or 6·6 mg Fe/d from Fe drops and a formula with no added Fe for 45 d. Fractional Fe absorption, Fe utilisation and fractional Zn absorption were measured with oral (57Fe and 67Zn) and intravenous (58Fe and 70Zn) isotopes. Fe and Zn status, infection and growth were measured. At 45 d, Hb was 6·3 g/l higher in the high-Fe formula group compared with the Fe drops group, whereas serum ferritin was 34 and 35 % higher, respectively, and serum transferrin 0·1 g/l lower in the high-Fe formula and Fe drops groups compared with the low-Fe formula group (all P<0·05). No intervention effects were observed on Fe absorption, Fe utilisation, Zn absorption, other Fe status indices, plasma Zn or growth. We concluded that neither supplemental or fortification Fe nor the amount of Fe habitually consumed altered Fe absorption, Fe utilisation, Zn absorption, Zn status or growth in Fe-sufficient infants. Consumption of low-Fe formula as the only source of Fe was insufficient to maintain Fe stores.

In addition to phytate, polyphenols (PP) might contribute to low Fe bioavailability from sorghum-based foods. To investigate the inhibitory effects of sorghum PP on Fe absorption and the potential enhancing effects of ascorbic acid (AA), NaFeEDTA and the PP oxidase enzyme laccase, we carried out three Fe absorption studies in fifty young women consuming dephytinised Fe-fortified test meals based on white and brown sorghum varieties with different PP concentrations. Fe absorption was measured as the incorporation of stable Fe isotopes into erythrocytes. In study 1, Fe absorption from meals with 17 mg PP (8·5 %) was higher than that from meals with 73 mg PP (3·2 %) and 167 mg PP (2·7 %; P< 0·001). Fe absorption from meals containing 73 and 167 mg PP did not differ (P= 0·9). In study 2, Fe absorption from NaFeEDTA-fortified meals (167 mg PP) was higher than that from the same meals fortified with FeSO4 (4·6 v. 2·7 %; P< 0·001), but still it was lower than that from FeSO4-fortified meals with 17 mg PP (10·7 %; P< 0·001). In study 3, laccase treatment decreased the levels of PP from 167 to 42 mg, but it did not improve absorption compared with that from meals with 167 mg PP (4·8 v. 4·6 %; P= 0·4), whereas adding AA increased absorption to 13·6 % (P< 0·001). These findings suggest that PP from brown sorghum contribute to low Fe bioavailability from sorghum foods and that AA and, to a lesser extent, NaFeEDTA, but not laccase, have the potential to overcome the inhibitory effect of PP and improve Fe absorption from sorghum foods.

Fe bioavailability can be manipulated by the nutritional composition of a meal. Ascorbic acid and unidentified components of meat, fish and poultry, but particularly beef, all appear to enhance the absorption of non-haem Fe. The aim of the present study is to identify whether extracts of green-lipped mussels (GLM; Perna canaliculus) enhance non-haem Fe absorption in Caco-2 cells and to compare the effect with that of beef. Raw GLM and raw beef homogenates were digested in vitro with pepsin at pH 2, and pancreatin and bile salts at pH 7. Tracer 55Fe was used to measure cellular Fe uptake. Ascorbic acid was used as a positive control and egg albumin, exposed to the same in vitro digestion process, was used as a negative control. Caco-2 cell monolayers were incubated with treatments for 60 min. All values were standardised per μg of GLM, egg albumin, beef or ascorbic acid. The results showed that ascorbic acid enhanced non-haem Fe absorption to the highest degree. Beef and GLM digestates both significantly enhanced Fe absorption compared with egg albumin. In conclusion, GLM digestate significantly enhances non-haem Fe uptake in Caco-2 cells with a similar magnitude to that of beef.

Fe deficiency and Fe-deficiency anaemia are common in patients with inflammatory bowel disease (IBD). Traditional clinical markers of Fe status can be skewed in the presence of inflammation, meaning that a patient's Fe status can be misinterpreted. Additionally, Fe absorption is known to be down-regulated in patients with active IBD. However, whether this is the case for quiescent or mildly active disease has not been formally assessed. The present study aimed to investigate the relationship between Fe absorption, Fe requirements and standard haematological indices in IBD patients without active disease. A group of twenty-nine patients with quiescent or mildly active IBD and twenty-eight control subjects undertook an Fe absorption test that measured sequential rises in serum Fe over 4 h following ingestion of 200 mg ferrous sulphate. At baseline, serum Fe, transferrin saturation, non-transferrin-bound Fe (NTBI), ferritin and soluble transferrin receptor were all measured. Thereafter (30–240 min), only serum Fe and NTBI were measured. Fe absorption did not differ between the two groups (P = 0·9; repeated-measures ANOVA). In control subjects, baseline haematological parameters predicted Fe absorption (i.e. Fe requirements), but this was not the case for patients with IBD. Fe absorption is normal in quiescent or mildly active IBD patients but standard haematological parameters do not accurately predict Fe requirements.

The present study was designed to investigate the effect of pectin on Fe bioavailability in ileorectomised rats or caecectomised rats. In Expt 1, rats were divided into the following two groups: ileorectomised rats fed a fibre-free diet (FF diet) and ileorectomised rats fed a FF diet supplemented with 5 % (w/w) pectin (pectin diet). Apparent Fe absorption in ileorectomised rats fed the pectin diet was significantly lower compared with ileorectomised rats fed the FF diet. In Expt 2, caecectomised rats and sham-operated rats were given one of the following diets for 3 weeks: diet containing ferrous iron (FeII diet), diet containing pectin at 50 g/kg diet (pectin diet) and diet containing a mixture of FeII and product prepared by the enzymatic degradation of pectin (FeII–OGA diet), which were presumed to be oligomers of galacturonic acid. The Fe content of these diets was 7·6, 8·1 and 7·7 mg/kg diet, respectively. The bioavailability of Fe in rats fed the FeII diet was not affected by caecectomy. In contrast, in rats fed the pectin diet, where Fe bound to pectin was the only Fe source, Hb gain and Hb regeneration efficiency were significantly decreased by caecectomy. The bioavailability of Fe from the FeII–OGA complex was not affected by caecectomy. These results suggest that Fe in pectin might be released by microbial degradation and subsequently made available for absorption in the large intestine, although pectin might decrease Fe absorption in the small intestine.

In the present in vitro study, the effects of pH and ionic strength on the release of iron from pectin and the ability of pectin to reduce ferric iron to ferrous iron were examined. The bioavailability of Fe bound to pectin was evaluated in rats. The amount of Fe released from pectin was at a maximum at pH 2·0 and decreased as the pH value increased. At pH 2·0, the amount of Fe released from pectin increased as the ion length increased; at pH 5·0, ion length had no effect on pectin release. Pectin effectively reduced Fe from the ferric form to the ferrous form. In rats fed a pectin diet, where Fe bound to pectin was the only Fe source, the final Hb concentration using diets containing 4·4–5·7, 7·2 or 11·5 mg Fe/kg diet was equal to the concentration in rats fed diets containing 4·5, 7·6 or 13·5 mg ferrous iron/kg diet, respectively. Hb regeneration efficiencies in rats fed pectin diets were significantly different from rats fed a diet containing 13·5 mg ferrous iron/kg diet. In rats fed a diet with or without pectin, where ferric iron was the only Fe source, pectin increased the final Hb concentration. These results suggest that Fe bound to pectin is utilised by rats.

Hepcidin, the Fe-regulatory peptide, has been shown to inhibit Fe absorption and reticuloendothelial Fe recycling. The present study was conducted to explore the mechanism of in vivo Fe regulation through genetic disruption of hepcidin1 and acute effects of hepcidin treatment in hepcidin1 knockout (Hepc1− / − ) and heterozygous mice. Hepcidin1 disruption resulted in significantly increased intestinal Fe uptake. Hepcidin injection inhibited Fe absorption in both genotypes, but the effects were more evident in the knockout mice. Hepcidin administration was also associated with decreased membrane localisation of ferroportin in the duodenum, liver and, most significantly, in the spleen of Hepc1− / −  mice. Hypoferraemia was induced in heterozygous mice by hepcidin treatment, but not in Hepc1− / −  mice, 4 h after injection. Interestingly, Fe absorption and serum Fe levels in Hepc1− / −  and heterozygous mice fed a low-Fe diet were not affected by hepcidin injection. The present study demonstrates that hepcidin deficiency causes increased Fe absorption. The effects of hepcidin were abolished by dietary Fe deficiency, indicating that the response to hepcidin may be influenced by dietary Fe level or Fe status.

There is concern regarding the possible negative effects of ingestion of dietary fibre on growth and intestinal Fe absorption in infants. The aim of the present study was to compare the effect of a fibre mixture on the growth and the intestinal absorption of Fe in rats with Fe-deficiency anaemia with that of a diet without fibres. Faecal weight and caecal pH were also evaluated. According to the Hb depletion–repletion model, twenty-two male weaned Wistar rats were fed the AIN93-G diet without Fe until Fe-deficiency anaemia was induced with Hb < 70 g/l. The anaemic rats were divided into two groups: (1) fibre mixture group – fed 100 g of fibre mixture/kg of diet (soya polysaccharide, inulin, resistant starch, Arabic gum, fructo-oligossaccharide and cellulose) (n 11); (2) control group – fed without fibres (n 11). All diets had 157 mg of ferric citrate (30 mg of elemental Fe) added to lead to recovery from anaemia. Fe intestinal absorption was measured by Hb repletion efficiency (HRE) and apparent Fe intestinal absorption. The HRE was 44·8 (sd 9·5) % in the fibre mixture group and 43·0 (sd 9·5) % in the control group (P = 0·664). The apparent Fe absorption was 46·2 (sd 16·5) and 47·2 (sd 10·2) % (P = 0·861) in the fibre mixture and control groups, respectively. The faecal weight median was 6·17 g in the fibre mixture group and 2·11 g in the control group (P < 0·001). The caecal pH was in the same order: 6·11 (sd 0·59) and 7·07 (sd 0·34) (P < 0·001). Both the groups consumed similar quantities of diet, and growth was similar in both the groups. The fibre mixture had no influence either on growth or on Fe intestinal absorption in rats recovering from anaemia. This mixture favoured an increase in faecal weight and a decrease in caecal pH.

The Thriposha programme is a community-level nutrition intervention in Sri Lanka that provides a combination of energy, protein and micronutrients as a ‘ready-to-eat’ cereal-based food. We measured the bioavailability of Fe and Zn from Thriposha formula at two different molar ratios of Zn:Fe in order to determine the effect on Fe and Zn absorption. Children 4–7 years (n 53) were given a meal prepared with 50 g Thriposha containing 1·5 mg Zn as zinc sulphate and either 9 mg (high Fe concentration (HiFe)) or 4·5 mg (low Fe concentration (LoFe)) Fe as ferrous fumarate. Zn and Fe percent absorption were measured using stable isotopes by tracer:tracee ratio and by incorporation of erythrocytes, respectively. Percent Fe absorption from the two meals was similar (6·6 % (4·8) v. 4·8 % (2·6); P = 0·15), but total Fe absorption was significantly higher from the HiFe meal (0·59 (0·43) mg) than the LoFe meal (0·20 (0·12) mg; P = 0·01). There was no significant difference between the two groups in Zn absorption (10·7 % (0·9) v. 8·8 % (1·4), P = 0·13, respectively). Decreasing the amount of Fe in Thriposha did not cause a significant change in the percent absorption of Fe and Zn, but significantly lowered the total amount of absorbed Fe. These results demonstrate the utility of maintaining a higher Fe content in this supplement. Further studies to increase Zn content are warranted while maintaining a HiFe.

We measured non-haem Fe absorption with and without added Ca in a short-term feeding study, in thirteen women with marginal Fe status, by the use of a double stable isotope technique. Supplementing 500 mg Ca as calcium carbonate significantly (P = 0·0009) reduced Fe absorption from a single meal from 10·2 % (range 2·2–40·6) to 4·8 % (range 0·7–18·9). A significant inverse correlation in the absence ( − 0·67, P = 0·010) and presence ( − 0·58, P = 0·037) of Ca, respectively, was found between Fe absorption and Fe stores measured by serum ferritin (SF). Wide variation in Fe absorption was observed between individuals in the absence and in the presence of Ca, despite pre-selection of participants within a relatively narrow range of iron stores (SF concentrations). Correction of Fe absorption data based on group mean SF was not found to be useful in reducing the inter-individual variability in iron absorption. It appears that selecting a study group with a narrow initial range of Fe stores does not necessarily reduce the inter-individual variability in Fe bioavailability measurements. These results support the hypothesis that body Fe stores, although an important determinant of dietary Fe absorption, are not the main factor that determines Fe absorption under conditions of identical dietary intake in subjects with low Fe stores.

Haem carrier protein 1 (HCP1) was originally identified and characterised as a mammalian haem transporter. However, recent evidence has shown that it is also a proton-coupled folate transporter (PCFT) and mutations in the gene cause hereditary folate deficiency in humans. We therefore investigated haem and folate transport characteristics of PCFT/HCP1 both in vivo and in vitro in CD-1 mice and in the presence or absence of a blocking antibody for PCFT/HCP1, and also in cultured cells (which express PCFT/HCP1 endogenously) to elucidate the specificity and selectivity of PCFT/HCP1. The in vivo study showed that the addition of folic acid inhibited 59Fe-labelled haem transport in hypoxic mice but had no effect in normal mice. Using in vitro methods, the results showed increased [3H]folate uptake into everted duodenum from hypoxic mice but uptake was reduced by the addition of haem or PCFT/HCP1 antibodies to the medium. Caco-2 cells transiently transfected with small interfering RNA (siRNA) PCFT/HCP1 duplex oligos resulted in a 69 % reduction in PCFT/HCP1 mRNA when compared with the control siRNA. Both haem and folate uptake were significantly (P < 0·05) reduced in cells transfected with PCFT/HCP1 siRNA; however, the magnitude of reduction with folic acid uptake was greater (48 %) than that of haem (22·5 %). Overall the data support PCFT/HCP1 as a primary folate transporter with a lower affinity for haem. PCFT/HCP1 could therefore play a physiological role in Fe nutrition and the data highlight the potential for the interaction of folate and haem at the level of intestinal absorption.

Fe homeostasis is maintained by regulation of Fe absorption to balance largely unregulated body Fe losses. The majority of human subjects maintain relatively constant Fe stores; however, Fe deficiency and Fe overload are common conditions. Fe overload is frequently associated with mutations in genes of Fe metabolism. The present paper summarises present knowledge of these mutations as well as indicating other genes that animal studies have implicated as candidates for influencing body Fe stores.

Hepcidin plays a major role in iron homeostasis, but understanding its role has been hampered by the absence of analytical methods for quantification in blood. A commercial ELISA has been developed for serum prohepcidin, a hepcidin precursor, and there is interest in its potential use in the clinical and research arena. We investigated the association between serum prohepcidin concentration and iron absorption in healthy men, and its relationship with iron status in men carrying HFE mutations, hereditary haemochromatosis patients, and pregnant women. Iron absorption was determined in thirty healthy men (fifteen wild-type, fifteen C282Y heterozygote) using the stable isotope red cell incorporation technique. Iron status was measured in 138 healthy men (ninety-one wild-type, forty-seven C282Y heterozygote), six hereditary haemochromatosis patients, and thirteen pregnant women. Mean serum prohepcidin concentrations were 214 (sd 118) ng/ml [208 (sd 122) ng/ml in wild-type and 225 (sd 109) ng/ml in C282Y heterozygotes] in healthy men, 177 (sd 36) ng/ml in haemochromatosis patients, and 159 (sd 59) ng/ml in pregnant women. There was no relationship between serum prohepcidin concentration and serum ferritin in any subject groups, nor was it associated with efficiency of iron absorption. Serum prohepcidin is not a useful biomarker for clinical or research purposes.

An in vitro digestion/Caco-2 cell model was applied to explore the impact of lactic acid (LA) fermentation by Lactobacillus pentosus FSC1 and Leuconostoc mesenteroides FSC2 on the Fe bioavailability of carrot juice. The redox state of Fe in fermented carrot juice was also assessed as a crucial factor for absorption. LA fermentation was shown to improve mineral solubility to different extents at simulated physiological conditions: Mn (2-fold); Fe (1·5–1·7-fold); Zn (1·2-fold); Cu (1-fold). Soluble Fe2+ was increased about 16-fold by LA fermentation, and about one third of the Fe2+ remained soluble after in vitro digestion (about 4–5-fold higher than in fresh juice). Data on cell-line studies showed a 4-fold increase in the efficiency of Fe uptake, but not in transepithelial transfer by Caco2 cells, as a result of fermentation. The increases in Fe2+ level and the efficiency of cellular Fe uptake were strain-dependent. To sum up the effect on both Fe solubility and cellular uptake efficiency, the amount of cellularly absorbed Fe from Ln. mesenteroides FSC2-fermented juice was about 20 % higher than that from L. pentosus FSC1-fermented juice (22·7 v. 19·2 μg/l juice per mg protein). To conclude, LA fermentation enhanced Fe absorption by Caco-2 cells from carrot juice because of increases in not only Fe solubility after digestion, but also the efficiency of cellular Fe uptake. The fermentation-improved efficiency of Fe uptake was possibly due to the increased level of soluble Fe2+ rather than a being a strain-specific event.

The objectives of the present study were to study the correlation between the change in serum Fe and Fe absorption when administering 100 mg Fe (as FeSO4) orally, and to study the correlation between the absorption from a 3 mg and a 100 mg Fe (as FeSO4) dose. The study was conducted in a group of eleven male blood donors, without any evident infection, who had given blood 8 weeks before the study. On three consecutive mornings the subjects were served a wheat roll fortified with Fe. On the first 2 d the roll was fortified with 3 mg Fe labelled with 59Fe; on day 3 the roll was fortified with 100 mg Fe labelled with 55Fe. The serum Fe response to the 100 mg dose was followed for 6 h. Fe absorption was measured by whole-body counting. High correlations were seen between the absorption of Fe and the change in serum Fe after 100 mg Fe (r2 0·94, P>0·001), between the absorption from 3 mg and 100 mg Fe (r2 0·88, P>0·001), and between the absorption from 3 mg Fe and change in serum Fe after 100 mg Fe (r2 0·90, P>0·001). This strengthens the evidence that it is possible to use the change in serum Fe as a measure of Fe absorption, e.g. when establishing the relative bioavailability for Fe powders. The results also imply that the induced serum Fe increase following 100 mg Fe added to a food could predict the Fe absorption of a small dose of Fe added to the same meal.

Ferric pyrophosphate is a water-insoluble Fe compound used to fortify infant cereals and chocolate-drink powders as it causes no organoleptic changes to the food vehicle. However, it is only of low absorption in man. Recently, an innovative ferric pyrophosphate has been developed (Sunactive Fe™) based on small-particle-size ferric pyrophosphate (average size 0·3 μm) mixed with emulsifiers, so that it remains in suspension in liquid products. The aim of the present studies was to compare Fe absorption of micronised, dispersible ferric pyrophosphate (Sunactive Fe™) with that of ferrous sulfate in an infant cereal and a yoghurt drink. Two separate Fe absorption studies were made in adult women (ten women/study). Fe absorption was based on the erythrocyte incorporation of stable isotopes (57Fe and 58Fe) 14 d after the intake of labelled test meals of infant cereal (study 1) or yoghurt drink (study 2). Each test meal was fortified with 5 mg Fe as ferrous sulfate or micronised, dispersible ferric pyrophosphate. Results are presented as geometric means. There was no statistically significant difference between Fe absorption from micronised, dispersible ferric pyrophosphate- and ferrous sulfate-fortified infant cereal (3·4 and 4·1 % respectively; P=0·24) and yoghurt drink (3·9 and 4·2 % respectively; P=0·72). The results of the present studies show that micronised, dispersible ferric pyrophosphate is as well absorbed as ferrous sulfate in adults. The high relative Fe bioavailability of micronised, dispersible ferric pyrophosphate indicates the potential usefulness of this compound for food fortification.

The aim of the present study was to compare Fe absorption from industrially-manufactured and home-cooked cereal foods. Fe absorption was measured using the radiolabelled Fe extrinsic tag technique in thirty-nine adult human subjects from cereal porridges manufactured by extrusion cooking or roller-drying, and from the same cereal flours after home cooking to produce pancakes, chappattis or bread. One series of cereal porridges was amylase-treated in addition before roller-drying. Fe absorption was relatively low from all products, ranging from 1·8–5·5% for rice, 2·5–3·5% for maize, 4·9–13·6 % for low-extraction wheat, and <1% for high-extraction wheat foods. The phytic acid content remained high after drying of the cereal porridges being about 1·20, 1·70, 3·20, 3·30 mg/g in low-extraction wheat, rice, high-extraction wheat and maize products respectively, and could explain the low Fe absorption. There were little or no differences in Fe absorption between the extruded and roller-dried cereals, although amylase pre-treatment increased Fe absorption from the roller-dried rice cereal 3-fold. This was not due to phytate degradation but possibly because of the more liquid nature of the cereal meal as fed. There were similarly few or no differences in Fe absorption between the industrially-processed cereals and home-cooked cereals made into pancakes or chappattis. Bread-making, however, degraded phytic acid to zero in the low-extraction wheat flour and Fe absorption increased to 13·6%, the greatest from all cereal foods tested. It is concluded that Fe absorption from extruded, roller-dried or home-cooked cereal foods is similarly low and that only those cooking procedures such as bread-making, which extensively degrades phytic acid, or amylase pre-treatment, which substantially liquifies cereal porridges, improve Fe absorption.