Hemochromatosis risk factors
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Risk Factors
People who inherit the HFE gene mutation from both parents are at the greatest risk for developing hemochromatosis. Although both men and women can inherit the gene defect, men are more likely to be diagnosed with the effects of hemochromatosis than women. Other factors that increase risk are:[1][2]
- Ethnic Background: White people of northern European descent (for example, families from England, Ireland, Scotland, Denmark, France, and Scandinavia) have a higher chance of having the HFE gene mutation.
- Family History: People with a close relative (grandparent, mother, father, sibling, niece, nephew) who has hemochromatosis have a higher chance of having the HFE gene mutation.
There are other factors which influence the rate at which iron is absorbed by the body:
- Dietary supplements: Taking iron supplements or multivitamins with iron can speed up the rate at which iron builds up in the body. Persons with hemochromatosis should not take pills containing iron. Eating foods that contain iron is fine. Taking vitamin C supplements may cause the body to absorb more iron. Persons with hemochromatosis should not take pills with more than 500 milligrams of vitamin C per day. Eating foods that contain vitamin C is fine.
- Blood loss: Losing iron by giving blood and losing iron through menstruation and unrecognized bleeding may slow the start of hemochromatosis. Therefore, men at risk for hemochromatosis usually develop the disease and its symptoms at a younger age than women who are at risk.
References
- ↑ Benyamin B, Esko T, Ried JS, Radhakrishnan A, Vermeulen SH, Traglia M; et al. (2014). "Novel loci affecting iron homeostasis and their effects in individuals at risk for hemochromatosis". Nat Commun. 5: 4926. doi:10.1038/ncomms5926. PMC 4215164. PMID 25352340.
- ↑ Peculis R, Lace B, Putnina A, Nikitina-Zake L, Klovins J (2015). "HFE-related hemochromatosis risk mutations in Latvian population". Ann Hematol. 94 (2): 343–4. doi:10.1007/s00277-014-2157-2. PMID 25015053.