It is true that iron is essential to good health. Iron helps to form oxygen-carrying hemoglobin in our red blood cells, boosting brain function, producing energy, and giving us strong muscles and immune systems. For people who suffer from iron deficiency, anemia, or whose iron stores become diminished during pregnancy, iron supplementation is essential.
Normally, our bodies absorb only about 10 percent of the iron that we consume in food. Most iron circulates in the body in the form of hemoglobin, but some is also stored in the liver, bone marrow, and spleen. People with hemochromatosis, though, can absorb up to 20 percent or more of the iron they take in—twice as much as they need to replace iron lost from the body.
What Is Hemochromatosis?
Hemochromatosis is a condition characterized by excess iron accumulation in the liver and other vital organs. The excess iron is stored first in the liver, but also in the heart, pancreas, joints, pituitary gland, bone marrow, and spleen. Because the liver is the body’s primary location for storing iron, it suffers the most damage if the body stores too much of the mineral. If left untreated, iron buildup in any organ may cause it to stop working properly, and the patient becomes a candidate for cirrhosis, heart failure, diabetes, and liver cancer. Hemochromatosis is hereditary.
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Hereditary hemochromatosis is the most common genetic disease in the United States. It is particularly pervasive among individuals of northern European ancestry, including the Irish, Celtic, British, Scottish, or Nordic peoples, and occurs in 1 in 150 to 200 of this ethnic group. About 1.5 million Americans have the disease, and it is estimated that another 32 million are carriers.
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All of us have about 30,000 genes in our chromosomes that determine our development and characteristics. One of these, the HFE gene, controls the amount of iron we absorb from food. Carriers of hereditary hemochromatosis have a mutant or altered HFE gene in either a mutation called C282Y or one called H6oD. If you inherit a C282Y mutation from one parent, you will be a carrier of hereditary hemochromatosis and probably won’t develop the disease, though you may absorb some extra iron. In this country, about 10 percent of all Caucasians carry one mutant gene.
Most people with the clinical manifestations of hereditary hemochromatosis (HH), such as diabetes, cirrhosis, arthritis, and a type of heart failure, have inherited two copies of C282Y one from each parent—although not everyone who inherits two
C282Y genes goes on to develop the clinical form of HH. A few HH patients inherit the two types of mutated genes, one C2S2Y and one H63D. Lastly, quite a few people inherit two H63D genes, although they typically do not develop HH.
Complicating the hemochromatosis picture are other, rarer forms of the disease, including juvenile hemochromatosis-—-which carries a high risk of diabetes, irregular heartbeat, heart failure, and gonadal failure, leading to impotence and infertility—and neonatal hemochromatosis, in which iron accumulates in a baby’s liver so rapidly that he or she may be stillborn. These conditions, though, are comparatively rare.
Although the abnormal gene occurs equally in both sexes, men are at least twice as likely to have iron overload as women, probably because women lose so much iron during menstruation and pregnancy. However, the risk of developing hemochromatosis increases for women after menopause or a hysterectomy.
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