Evolution of a Defective Hemoglobin Gene

Evolution of a defective gene

Researchers believe the defective hemoglobin gene that causes sickle cell anemia evolved many years ago, among people living in parts of Africa, the Mediterranean, the Middle East and India. At that time, malaria epidemics killed many people in those regions.
But some people in those regions had a genetic mutation that caused some of their red blood cells to change shape - a condition now known as sickle cell trait. The sickle cells actually interfered with the growth of the parasite that causes malaria. So people with sickle cell trait often survived malaria outbreaks.

Over time, these survivors migrated and continued on with their lives. In some cases, two people with the sickle cell trait had children. And some of their children inherited two copies of the mutated gene, which results in sickle cell anemia. Today, millions of people all over the world have sickle cell anemia.

How defective hemoglobin causes anemia
Red blood cells with normal hemoglobin are smooth and round and glide through blood vessels. Red blood cells with defective hemoglobin may become hard, sticky and shaped like a sickle used to cut wheat. These crescent-shaped cells can get stuck in small blood vessels, blocking blood flow and causing episodes of pain and damage to organs.

Your bone marrow - the red, spongy material found within the cavities of many of your large bones - regularly produces red blood cells. Bone marrow also produces white blood cells to fight infections and platelets to help blood clot. These two types of blood cells aren't directly involved in sickle cell anemia.

Once red blood cells leave your bone marrow, they normally live for about 120 days before they die and need to be replaced. However, sickle cells die after only 10 to 20 days. So, it's difficult for your body to produce enough replacements. The result is a chronic shortage of red blood cells, known as anemia.

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