What causes hemochromatosis?

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Hemochromatosis is a condition characterized by excessive absorption of iron from the diet, leading to iron overload in various organs, particularly the liver, heart, and pancreas. If untreated, this can cause damage to these organs and lead to serious health problems. There are two main types of hemochromatosis: primary (hereditary) and secondary (acquired). The causes vary depending on the type.

1. Primary (Hereditary) Hemochromatosis

Hereditary hemochromatosis is the most common form and is caused by genetic mutations that affect the regulation of iron absorption. It is an inherited disorder, passed down from parents to their children.

Genetic Mutation in the HFE Gene:
- The most common cause of hereditary hemochromatosis is a mutation in the HFE gene. The HFE gene helps regulate iron absorption in the body.
- The two most common mutations of the HFE gene are:
  - C282Y Mutation: This is the most common mutation associated with hemochromatosis. People who inherit two copies of the C282Y mutation (one from each parent) have a high risk of developing iron overload.
  - H63D Mutation: This mutation is less common and usually causes a milder form of hemochromatosis. A person who inherits one C282Y mutation and one H63D mutation may also be at risk for iron overload, but typically to a lesser extent.
Inheritance Pattern:
- Hereditary hemochromatosis follows an autosomal recessive inheritance pattern, meaning a person must inherit two abnormal copies of the HFE gene (one from each parent) to be at high risk of developing the condition.
- People who inherit one abnormal gene and one normal gene (carriers) typically do not develop iron overload but may pass the gene on to their children.
Iron Overload Mechanism:
- In individuals with the HFE gene mutation, the body absorbs too much iron from food. Normally, the body regulates iron absorption, ensuring that only the amount needed is taken up. In hemochromatosis, this regulation is impaired, leading to iron buildup in tissues and organs over time.
Risk Factors:
- Family history of hemochromatosis increases the likelihood of inheriting the condition.
- Gender: Men are more likely to develop symptoms of iron overload at an earlier age, often between 30-50 years, while women may not show symptoms until after menopause because menstruation naturally reduces iron levels.

2. Secondary (Acquired) Hemochromatosis

Secondary hemochromatosis is not inherited but develops as a result of another condition or external factors that lead to excessive iron accumulation in the body. Common causes include:

Chronic Blood Transfusions:
- People who receive regular blood transfusions, such as those with anemia (e.g., thalassemia or sickle cell anemia), can develop iron overload. Each transfusion introduces more iron into the body, and the body lacks a mechanism to effectively remove excess iron.
Iron Overload from Supplements or Diet:
- In rare cases, consuming too much iron through supplements or a diet extremely high in iron can cause secondary hemochromatosis. This typically only occurs in individuals predisposed to iron absorption issues or those who have pre-existing conditions that affect iron metabolism.
Chronic Liver Diseases:
- Conditions like chronic hepatitis, alcoholic liver disease, or nonalcoholic fatty liver disease (NAFLD) can impair the liver’s ability to store and regulate iron, leading to secondary iron overload.
Certain Blood Disorders:
- Diseases that cause increased red blood cell turnover or destruction, such as thalassemia major or hereditary spherocytosis, can cause secondary hemochromatosis because iron released from destroyed red blood cells is reabsorbed and accumulates over time.
Iron-Loading Anemias:
- In conditions like ineffective erythropoiesis (impaired production of red blood cells), such as thalassemia or myelodysplastic syndrome, the body absorbs more iron to compensate for the anemia, but it cannot use all the iron, leading to iron buildup.

3. Other Less Common Genetic Forms

In addition to HFE-related hereditary hemochromatosis, there are other, rarer genetic causes of iron overload:

Juvenile Hemochromatosis:
- Caused by mutations in the HJV (hemojuvelin) or HAMP (hepcidin) genes, juvenile hemochromatosis leads to early-onset iron overload, typically appearing before age 30. It is more aggressive and can cause severe damage to the heart, liver, and endocrine glands.
TFR2-Related Hemochromatosis:
- Mutations in the TFR2 gene can also cause a less common form of hereditary hemochromatosis. This form behaves similarly to HFE-related hemochromatosis but tends to appear later in life.
Ferroportin Disease:
- Caused by mutations in the SLC40A1 (ferroportin) gene, this disorder leads to iron overload that is typically more prominent in macrophages (immune cells) rather than in the liver and other organs. Symptoms can vary from mild to severe.

Conclusion:

The main cause of primary hemochromatosis is genetic mutations, primarily in the HFE gene, leading to excessive iron absorption and storage. The most common mutations are C282Y and H63D, and the condition is inherited in an autosomal recessive pattern. Secondary hemochromatosis results from other medical conditions, such as chronic blood transfusions, liver diseases, or iron-loading anemias. Understanding the cause of hemochromatosis is important for determining the appropriate treatment, which may involve managing iron levels through dietary changes, phlebotomy (blood removal), or medications.

Ironbound™ A Strategy For The Management Of Hemochromatosis