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The near equivalence of haem and non-haem iron bioavailability and the need for reconsidering dietary iron recommendations

Associating haem and non-haem iron intake with ‘iron status’ and the risk for anaemia, Vandevijvere et al.1 recently suggested in this Journal that adolescent girls may be a group at risk for iron deficiency. In our view, their work deserves some additional and important comments.

From assessed dietary intake and by using average bioavailability values of 25 and 10% for haem and non-haem iron, respectively, the authors concluded that the estimated requirement for bioavailable iron intake was only met by about 14% of the girls followed-up, a figure determined to a large extent by the proportion of haem and non-haem intake. This conclusion is not in accordance with low estimates of iron depletion (21%) and iron-deficient anaemia (4.7%) reported earlier by the same group.2 This discrepancy coincides with the absence of significant relations between iron intakes and iron status values reflected in serum-soluble transferrin receptor and ferritin levels. Although the authors recognize the complex relationships between iron intake and iron status parameters, subject to interindividual variation of iron absorption and factors other than only iron intake, a reference to recent insights on factors determining iron availability and anaemia is missing.

Indeed, it has been recognized that iron status and other host factors have a key role in dietary iron bioavailability and have a greater effect than diet composition, as established for obesity and pregnancy.3 Evaluation of iron status is traditionally based on serum values of total iron and ferritin as well as percent transferrin saturation. It is now clear that these values are the reflection of homeostatic mechanisms aiming to ensure that absorption of dietary iron is up- or downregulated in response to low and high iron status. The synthesis of ferroportin and transporter proteins appears to be the cornerstone in this iron homeostatic mechanism, mainly effective for non-haem iron, and is controlled by hepcidin, a key peptide synthesized in the liver and inducing the degradation of ferroportin.4 Synthesis of this hormone varies with the production of multiple cytokines, affected by physiological states such as obesity and pregnancy and is increased by inflammation associated, for example, with infectious disease, autoimmune diseases and some cancers. The latter mechanism is recognized as the basis for the widespread lack of response of anaemia to iron supplementation in developing countries5 and the downregulation of hepcidin production may explain the similar occurrence of anaemia in both vegetarians and non-vegetarians as reported by Millward and Garnett.6 Individual variability in hepcidin production may thus be more important than the variable diet-related bioavailability values of 5, 10, 12 and 15% used for the estimation of dietary iron requirements.7 Uncertainty and variability of bioavailability values for iron absorption explain the variability of dietary recommendations, ranging, for example, for young girls between 11 and 21 mg per day as listed by Vandevijvere et al.1 Apart from this, the lack of clear functional disabilities reported for intakes below recommended values has led to the conclusion that existing dietary iron recommendations may be too high and should be reviewed as reported for the United Kingdom.8 In line with this, Harvey et al.9 recently concluded that ‘suitable data were also unavailable that would currently allow reference values to be based on selected health outcomes associated with iron intake or status’ and underlined the need for ‘investigations into the potential impact of genetic polymorphisms in iron status and metabolism in healthy individuals’. It is clear that serum hepcidin could be used as a biomarker in such studies as proposed for the evaluation of iron supplementation in iron-deficient anaemia.6,10 Apart from hepcidin, an ever-increasing number of identified genetic polymorphisms of other proteins related to iron uptake from the gastrointestinal tract, such as ferritin and transferrin, should indeed be recognized.3 Furthermore, although the latter authors report estimates for iron bioavailability to be in the range of 14–18% for mixed diets and 5–12% for vegetarian diets in subjects with no iron stores, Millward and Garnett6 refer to ‘considerable scientific uncertainty about the extent of the superiority of Fe from meat as a dietary source’ and ‘an explicit equivalence of iron from meat and from non-meat sources’ for Western diets.

We hope that these arguments confirm that dietary iron requirements as well as bioavailabilities are mainly determined by the individual iron homeostatic status, affected by physiological conditions and reflected to a large extent in serum hepcidin levels. More than the amount and nature of food iron intake, the latter also determines the risk for iron deficient anaemia. These arguments should also be considered in relation to recommendations on the consumption of meat and meat products, recognized as the major sources of haem iron.2,6

References

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Acknowledgements

This reaction summarizes part of the contents of a scientific advice on Red meat, processed red meats and the prevention of colorectal cancer’ by the Belgian Superior Health Council. The authors were members of the ad hoc work group, and sincerely thank the other members of this work group (G De Backer, S De Henauw, N Delzenne, L Herman, G Maghuin-Rogister, B Mertens, N Paquot, M Peeters and J Van Camp).

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Demeyer, D., De Smet, S. & Ulens, M. The near equivalence of haem and non-haem iron bioavailability and the need for reconsidering dietary iron recommendations. Eur J Clin Nutr 68, 750–751 (2014). https://doi.org/10.1038/ejcn.2014.58

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