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A Review of Nutrients and Compounds, Which Promote Or Inhibit Intestinal Iron Absorption: Making a Platform for Dietary Measures That Can Reduce Iron Uptake in Patients With

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A Review of Nutrients and Compounds, Which Promote Or Inhibit Intestinal Iron Absorption: Making a Platform for Dietary Measures That Can Reduce Iron Uptake in Patients With Hindawi Journal of Nutrition and Metabolism Volume 2020, Article ID 7373498, 15 pages https://doi.org/10.1155/2020/7373498 Research Article A Review of Nutrients and Compounds, Which Promote or Inhibit Intestinal Iron Absorption: Making a Platform for Dietary Measures That Can Reduce Iron Uptake in Patients with Genetic Haemochromatosis Nils Thorm Milman Department of Clinical Biochemistry, Næstved Hospital, University College Zealand, DK-4700 Næstved, Denmark Correspondence should be addressed to Nils orm Milman; [email protected] Received 29 May 2020; Revised 1 August 2020; Accepted 25 August 2020; Published 14 September 2020 Academic Editor: Stan Kubow Copyright © 2020 Nils orm Milman. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. To provide an overview of nutrients and compounds, which influence human intestinal iron absorption, thereby making a platform for elaboration of dietary recommendations that can reduce iron uptake in patients with genetic hae- mochromatosis. Design. Review. Setting. A literature search in PubMed and Google Scholar of papers dealing with iron absorption. Results. e most important promoters of iron absorption in foods are ascorbic acid, lactic acid (produced by fermentation), meat factors in animal meat, the presence of heme iron, and alcohol which stimulate iron uptake by inhibition of hepcidin expression. e most important inhibitors of iron uptake are phytic acid/phytates, polyphenols/tannins, proteins from soya beans, milk, eggs, and calcium. Oxalic acid/oxalate does not seem to influence iron uptake. Turmeric/curcumin may stimulate iron uptake through a decrease in hepcidin expression and inhibit uptake by complex formation with iron, but the net effect has not been clarified. Conclusions. In haemochromatosis, iron absorption is enhanced due to a decreased expression of hepcidin. Dietary modifications that lower iron intake and decrease iron bioavailability may provide additional measures to reduce iron uptake from the foods. is could stimulate the patients’ active cooperation in the treatment of their disorder and reduce the number of phlebotomies. 1. Introduction Homozygosity for a particular gene means that the two alleles of the gene present on both homologous chromo- Genetic haemochromatosis is characterized by an increased somes are identical. Homozygosity for the HFE-C282Y intestinal dietary iron uptake, of both nonheme and heme mutation (C282Y/C282Y) is the leading cause of preclinical iron [1–3], which in the long term may lead to the gradual and clinical haemochromatosis in ethnic Danes, where accumulation of excess iron in the body and clinical more than 95% of the patients have this mutation [7]. symptoms of iron overload. e various forms of genetic Heterozygosity for a particular gene means that the two haemochromatosis are caused by mutations on different alleles of the gene present on both homologous chromo- iron regulatory genes and are divided into two main groups: somes are not identical, i.e., the cells contain two different HFE-haemochromatosis being caused by mutations on the alleles, one mutant and one wild-type allele. Heterozygosity HFE-gene on chromosome 6 and non-HFE-haemochro- for the C282Y mutation (C282Y/wild type) is generally matosis. Among people of northwestern European descent, associated with a normal iron absorption pattern for both including ethnic Danes, HFE-haemochromatosis is the most nonheme and heme iron [8]. Population studies have common variant [4, 5], while non-HFE-haemochromatosis shown that among ethnic Danes, at least 0.4%, or one in occurs sporadically [6]. 250, are C282Y homozygous equivalent to more than 2 Journal of Nutrition and Metabolism 20,000 people in Denmark, and more than 500,000 people metabolism. Search terms included “iron absorption” and are heterozygous (C282Y/wild type) or compound het- “iron absorption [AND] ... name of the specific nutrient or erozygous (C282Y/H63D) for the HFE-mutations [9]. In compound”. Primarily, human studies on iron absorption comparison, the UK Biobank study examined more than have been included, but where necessary, some in vitro and 450,000 individuals of European descent and found a animal studies have been included for the purpose of prevalence of C282Y homozygosity of 0.6%, or one in 167 clarification. persons [10]. Hepcidin, which is produced in the liver, is considered to 2.1. Dietary Iron Intake. e composition of the diet con- be the “master regulator” of body iron homeostasis, and one cerning the content of iron and the content of inhibitors/ of its main tasks is to inactivate ferroportin, which regulates promoters of iron absorption may have a significant influence iron transport out of the cells (efflux) through the cell on the development of clinically overt haemochromatosis. membrane in enterocytes, hepatocytes, and macrophages e recommended intake of dietary iron in healthy men [11]. Normal HFE- and transferrin receptor-2 complexes on in the Western World varies from 8 to 11 mg/day, depending the cell membrane of the hepatocytes stimulate the pro- on country-specific recommendations [18–20]. Danish men duction/activation of hepcidin, which subsequently inhibits have a median dietary iron intake of 12.7 mg/day (10–90 intestinal iron uptake [11, 12]. In haemochromatosis, be- percentile 8.3–18.0) [21], indicating that the majority have cause of a defective HFE-complex, the production/activation an intake which is above the recommended intake. In the of hepcidin is reduced, resulting in an increased intestinal USA, the “estimated” mean iron intake is even higher, iron uptake, which by and large is independent of the body’s 16.1 mg/day [22]. iron status. HFE-haemochromatosis and several other forms In addition, men have a distinctly higher intake of meat of genetic haemochromatosis are characterized by a low [21, 23] and alcohol [21] than women, both factors, which plasma concentration of hepcidin and a condition termed increase iron uptake (see below) and the rate of body iron “hepcidin insufficiency” [11, 12]. accumulation in men with genetic haemochromatosis. e standard treatment of HFE-haemochromatosis In healthy women of reproductive age, the recom- consists of repeated lettings of 400–500 ml of whole blood mended iron intake varies from 15 to18 mg/day [18–20]. A (phlebotomy) where excess body iron is gradually removed review of dietary iron intake in women in Europe has re- [4, 13]. Treatment is divided into the induction phase, where cently been published [24]. Danish women in the repro- patients are phlebotomized weekly or every other week until ductive age have a median iron intake of 9.7 mg/day (5–95 serum ferritin has declined to 50–100 µg/L. In the following percentile 5.6–14.5) [21, 24], indicating that all women have maintenance phase, phlebotomy is performed two to four an intake below the recommended intake. In the USA, the times a year maintaining ferritin around 50–100 µg/L [4]. “estimated” mean iron intake is higher, 12.3 mg/day [22]. In haemochromatosis, body iron overload is gradually e majority of healthy women of reproductive age have increasing over time due to excessive absorption of iron from an iron intake which is markedly below the recommended the food. Consuming a diet void of iron or with a low iron intake [24]. In addition, women of reproductive age have content will downregulate the body iron accumulation. physiological iron losses by menstruations [25] and preg- Another important factor is the bioavailability of the iron in nancies [26], exerting an inhibitory effect on body iron the food as well as the presence of promoters versus inhibitors accumulation in women with haemochromatosis, thereby of iron absorption. ere exists only scarce literature con- delaying or preventing the onset of clinical disease. cerning the significance of dietary iron intake in haemo- Although the HFE-mutations occur with the same fre- chromatosis, and the effect of dietary intervention has not quencies in men and women, preclinical and clinical hae- been sufficiently investigated [3] However, the focus on mochromatosis is much more prevalent in men than in population groups with specific dietary habits has provided us women and presents at a younger age in men compared to with valuable data showing that the content and the chemical women [4]. is gender difference is partly explained by a form of iron in the diet have a definite influence on body iron higher dietary iron intake in men, combined with a higher status. Vegetarians/vegans have a low body iron status and intake of absorption promoters, e.g., meat and alcohol, many, especially women in the reproductive age, develop iron compared to women. deficiency [14, 15]. In a cross-over study, total and fractional iron absorption was significantly lower in a vegetarian than in a meat-rich diet [16]. A Western-type vegetarian diet has a 2.2. Different Forms of Dietary Iron. An overview of the low bioavailability ranging from 5 to 12% [17]. intestinal absorption of nonheme and heme iron is shown in e purpose of this paper is to review the existing Figure 1. knowledge on the different nutrients and compounds that Iron in the foods exists in two forms: (i) inorganic influence iron uptake from the diet. iron � nonheme iron consisting of mostly ferric iron (Fe3+) and some ferrous iron (Fe2+) and (ii) organic iron consisting 2. Methods of heme iron from animals and ferritin iron from
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