Genetic Disorders: Iron Overload (HH)

There are two types of hemochromatosis, primary and secondary. Primary hemochromatosis is a genetic disorder passed down through families. It occurs at birth. People with this condition absorb too much iron through their digestive tract. Iron builds up in the body, especially the liver. You are more likely to get this disease if someone else in your family has or had the condition. Secondary hemochromatosis is due to other blood-related disorders such as thalassemia or certain anemia’s. Sometimes it occurs in people with long-term alcoholism and other health conditions.

Iron deficiency anemia, one of the most common types of anemia, is a blood disorder where

Hemochromatosis is a deadly disease in which the body believes that it never has enough iron. The body, as a result is that iron is not filtered out through the intestines, it is always entering the body. This iron runs out of places to be stored, and is spread throughout the body. These iron stores eventually end up changing the body and causing damage to major organs and joints. Hemochromatosis can lead to cancer, heart failure, and a plethora of other problems.

Iron is an important nutrient because it helps carry oxygen in the hemoglobin in red blood cells around the human body. When a healthy iron supply is reached, the body immediately stops absorbing the nutrient, and just lets it past through the digestive system. However, people with hemochromatosis absorb all the iron from the food consumed, past healthy levels.­­­­­­ All the extra iron spreads throughout the body, and unevitably causes great damage to major organs and almost all other parts of the body. According to Survival of the Sickest, "hemochromatosis can lead to liver failure, heart failure, diabetes, arthritis, infertility, psychiatric disorders,... cancer," and other diseases if left untreated (Maulem

Hemochromatosis is when there is excess iron in the body. It is a genetic disorder that is passed down each generation and is inherited by the offspring. Iron overload directly affects the circulatory system but eventually the complications can affect the whole body and many major organs. In addition, hemochromatosis can show no symptoms but the body sometimes shows

Therefore, the amount of hemoglobin in blood is critical to a runner’s capacity to compete. As hemoglobin levels drop, so does an athlete’s ability to perform. Without this knowledge, many runners can potentially suffer from symptoms of an iron deficiency without understanding how or why they can no longer perform as they once could. The directly proportional relationship between the amount of hemoglobin, and therefore iron, and a runner’s ability to compete is important for athletes to understand. Information provided by the medical community can help to ultimately prevent a deficiency from occurring. However, through iron supplementation, athletes can return their levels to the healthy standard to decrease the effect of iron deficiency symptoms on their ability to compete. The authors summarize their findings in the study of treating fatigue in nonanemic female patients with low serum ferritin concentration by providing intravenous iron

Essentially, iron is what allows almost every form of life to metabolize and function. In fact, our bodies body has several mechanisms that prevent access to iron to pathogens and other infectious bacteria thrive on iron that may harm our bodies known as the acute phase response. The author describes this as he states “the bloodstream is flooded with illness-fighting proteins, and, at the same time, iron is locked away to prevent biological invaders from using it against us (7).” So us readers can take away the idea that iron is crucial for our bodies. So how could potentially accumulating too much iron affect our health? That 's when hemochromatosis comes along. Our bodies assumes that the person is lacking iron in their system so they continually absorb the iron in the intestine. Not only that, don’t forget that bacteria and diseases also rely on iron to grow and accumulate.This can cause cancer cells to grow and spread continuously without stopping if it consumes our iron.

Iron is an essential element in the human body. It can be found in the hemoglobin and transferrin of the bloodstream, and in myoglobin in muscle tissue. The main purpose of iron is to transfer oxygen within the body. To gain iron, humans must consume a diet that consist abundantly of iron such as leaf vegetables, fish, beans, etc. Absorption of iron is especially important because less than 15% of iron in daily diets are absorbed and used (Jacobs 1971). The formation of iron (II) occurs in the stomach because of its low

The Hemochromatosis mutation occurs in 25-33% of people of Western European descent. However, only 0.5% (1 in 200) people of Western European ancestry actually has developed the disease. This makes the disease have a very low penetrance level, meaning that for all of the people with the mutation; only very few actually develop the disease. It is believed that the disease was originally evolved by populations living in harsh environments to offset iron deficiencies that were caused by highly iron-deficient diets. Viking populations were the first to develop the disease and spread it around Northern

Hereditary hemochromatosis also known as HH and classic hereditary hemochromatosis is an inherited disorder that absorbs an abundant amount of iron in the body. The increased intake causes damage to the organs, which leads to many symptoms.

Iron deficiency is the most common type of anemia, along with the most advanced stage of iron deficiency. Iron deficiency anemia occurs when there is low amount of iron in the body, and without iron the bone marrow cannot make hemoglobin for the red blood cells. Iron deficiency occurs mostly in women and children, but can also affect the elderly. Regardless of gender or age, anemia has been identified in numerous studies as an independent risk factor for morbidity

Hereditary hemochromatosis (HHC), the accumulation of iron overload in body tissues. This overload of iron usually occurs because of a genetic predisposition to absorb iron in excess. It can also occur as a complication of hematologic disorders, hepatitis, excessive of iron intake, repeated transfusion therapy and injections of iron dextram. Since there is no physiologic mechanism, the only way for excretion of excess iron is blood loss. Iron is transported in the body via transferrin and stored in ferritin molecules. Once the absorption of iron exceeds its storage capacity in the ferritin molecules, all the excess and unbounded iron promotes free-radical formation in cells, which then results in the peroxidation of membrane lipids and injury of cells. The deposition of iron occurs in many organs, such as, liver, pancreas, and heart.

Hemochromsatosis- A disorder in which the body absorbs more iron than needed. There are two types primary which is genetic or secondary which is from repeated blood transfusions. It mostly comes from the diet you consume. The excess iron is stored in the organs and leads to organ toxicity. It can also lead to serious illnesses such as liver disease, heart problems and diabetes.

Hemochromatosis is the most common form of iron overload disease. This disease causes the body to absorb more iron then what it needs; too much iron results in an iron overload or hemochromatosis. Although the body needs iron, too much of it becomes dangerous to the body. The body doesn’t remove iron naturally; instead it stores it in organs which cause damages to them if left untreated. Organs included are the liver, the heart and the pancreas. There are three types if hemochromatosis; primary hemochromatosis, secondary hemochromatosis and neonatal hemochromatosis.

The protein transferrin receptor 2 (Tfr2) is partly responsible for regulation of hepcidin in the liver and is affiliated with erythropoietin receptor (Epor) in erythroid cells (1, 2). A mutation in Tfr2 leads to an iron overload disease known as haemochromatosis (Hfe) type 3, without any apparent erythroid irregularities (1). Tfr2 is a constituent of an atypical iron-sensing pathway that adapts erythrocyte production, according to iron accessibility, achievable by modulating the erythroblast erythropoietin sensitivity (1). The red blood cell (RBC) specific hormone erythropoietin (Epo) accounts for the proliferation and differentiation of J2E erythroid cells (3, 4). Although, J2E cells mature at a different morphological