HFE genotypes and dietary heme iron: No evidence of strong gene–nutrient interaction on serum ferritin concentrations in middle-aged women

A, Daphne L. van der; Peeters, Petra H.M.; Grobbee, Diederick E.; Roest, Mark; Voorbij, H. A. M.; Schouw, Yvonne T. van der

doi:10.1016/j.numecd.2005.07.008

Cited by 27 publications

(18 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Diet. A significant but weak correlation was found between serum ferritin levels and haem dietary intake in haemochromatotic subjects [51], especially in menopausal women [52]. In addition, the amount of iron to be removed annually in order to maintain low body iron stores has been shown to be slightly lower in haemochromatotic patients who regularly drink tea -which decreases iron absorption -than in those who do not [53].…”

Section: Environmental Modifiersmentioning

confidence: 99%

Iron and the liver: Update 2008

Deugnier¹,

Brissot²,

Loréal³

2008

Journal of Hepatology

View full text Add to dashboard Cite

The cross-talk which has taken place in recent years between clinicians and scientists has resulted in a greater understanding of iron metabolism with the discovery of new iron-related genes including the hepcidin gene which plays a critical role in regulating systemic iron homeostasis. Consequently, the distinction between (a) genetic iron-overload disorders including haemochromatosis related to mutations in the HFE, hemojuvelin, transferrin receptor 2 and hepcidin genes and (b) non-haemochromatotic conditions related to mutations in the ferroportin, ceruloplasmin, transferrin and di-metal transporter 1 genes, and (c) acquired iron-overload syndromes has become easier. However, major challenges still remain which include our understanding of the regulation of hepcidin production, the identification of environmental and genetic modifiers of iron burden and organ damage in iron-overload syndromes, especially HFE haemochromatosis, indications regarding the new oral chelator, deferasirox, and the development of new therapeutic tools interacting with the regulation of iron metabolism.

show abstract

Section: Environmental Modifiersmentioning

confidence: 99%

Iron and the liver: Update 2008

Deugnier¹,

Brissot²,

Loréal³

2008

Journal of Hepatology

View full text Add to dashboard Cite

show abstract

“…C282Y homozygotes and C282Y/H63D compound heterozygotes who consumed relatively high amounts of heme iron had the greatest SF concentrations. 71 It has been proposed that the high rate of expression of iron overload and associated manifestations in hemochromatosis homozygotes in Australia is caused by the high national rate of meat consumption. 72 Red meat consumption was positively associated with greater SF levels in adults in Busselton, Australia, regardless of HFE genotype.…”

Section: Ironmentioning

confidence: 99%

How I treat hemochromatosis

Adams

Barton

2010

Blood

160

167

View full text Add to dashboard Cite

Hemochromatosis is a common genetic disorder in which iron may progressively accumulate in the liver, heart, and other organs. The primary goal of therapy is iron depletion to normalize body iron stores and to prevent or decrease organ dysfunction. The primary therapy to normalize iron stores is phlebotomy. In this opinion article, we discuss the indications for and monitoring of phlebotomy therapy to achieve iron depletion, maintenance therapy, dietary and pharmacologic maneuvers that could reduce iron absorption, and the role of voluntary blood donation. (Blood. 2010;116(3):317-325)

show abstract

“…There is a weak, albeit significant correlation between serum ferritin levels and heme, but not non-heme dietary intake [45,46]. It seems reasonable to suppose that the dietary intake may have some small effect on the penetrance of the disorder, but there is no compelling evidence that would lead one to believe that it is a major factor in determining the degree of iron overload that occurs in patients homozygous for the C282Y mutation.…”

Section: Dietmentioning

confidence: 99%

Iron storage disease: Facts, fiction and progress

Beutler

2007

Blood Cells, Molecules, and Diseases

View full text Add to dashboard Cite

There are many forms of iron storage disease, some hereditary and some acquired. The most common of the hereditary forms is HFE-associated hemochromatosis, and it is this disorder that is the main focus of this presentation. The body iron content is regulated by controlling absorption, and studies in the past decade have clarified, in part, how this regulation functions. A 25 amino acid peptide hepcidin is upregulated by iron and by inflammation, and it inhibits iron absorption and traps iron in macrophages by binding to and causing degradation of the iron transport protein ferroportin. Most forms of hemochromatosis results from dysregulation of hepcidin or defects of hepcidin or ferroportin themselves.Hereditary hemochromatosis was once considered to be very rare, but in the 1970s and 1980s, with the introduction of better diagnostic tests, it became to be considered the most common disease of Europeans. Controlled epidemiologic studies carried out in the last decade have shown, however, the disease itself actually is rare, and it is only the genotype and associated biochemical changes that are common. We do not understand why only a few homozygotes develop severe disease. It now seems unlikely that there are important modifying genes, and although alcohol is known to have some effect, excess drinking probably plays only a modest role in determining the hemochromatosis phenotype.Hereditary hemochromatosis is readily treated by phlebotomy. Secondary forms of the disease require chelation therapy, and the recent introduction of effective oral chelating agents is an important step forward in treating patients with disorders in which iron overload often proves to be fatal, such as thalassemia, myelodysplastic anemias, and dyserythropoietic anemias.While much has been learned about the regulation of iron homeostasis in the past decade, many mysteries remain and represent challenges that will keep us occupied for years to come.It is a great honor for me to present this lecture in memory of my good friend Bracha Ramot. It is because this lecture is in honor of Bracha that I do not feel the least bit uncomfortable speaking about iron storage diseases in a symposium entitled "Genomics and Molecular Biology of Hematopoietic Malignancies". I know that had it been possible to ask her whether this might be appropriate Bracha would have said: "Of course, Ernie. Talk about whatever you want to". That was her way. And, of course, Bracha was no stranger to iron metabolism. She was scientifically broad, a Renaissance hematologist. A MEDLINE search reveals 261 publications by Bracha and eight of those deal with iron --iron in thalassemia, iron in sideroblastic anemia, and iron in iron deficiency anemia.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable...

show abstract

HFE genotypes and dietary heme iron: No evidence of strong gene–nutrient interaction on serum ferritin concentrations in middle-aged women

Cited by 27 publications

References 47 publications

Iron and the liver: Update 2008

Iron and the liver: Update 2008

How I treat hemochromatosis

Iron storage disease: Facts, fiction and progress

Contact Info

Product

Resources

About