Thousands of years ago a child was born in west Africa with genetic mutation that altered the shape of his/her hemoglobin. This mutation wasn’t harmful because each person has two copies of every gene and the other gene was normal and so they lived and passed on their mutated gene that would save millions of lives.
The gene spread across all of Africa and into parts of southern Europe and India. Every so often two people with the gene would make a child that had two copies of the gene. The child would no longer be able to produce normal hemoglobin. As a result, their red cells became defective and clogged their blood vessels. The condition, now known as sickle cell anemia, leads to extreme pain, difficulty with breathing, kidney failure and even strokes. Most people with this disease die before 40.
In the early 1900s doctors in the U.S first noticed this disease and called its sickle cell anemia because of the way the cells look. Most cases were found in African Americans and studies showed that 8 percent of African Americans had some sickle-shaped blood cells, yet the vast majority had no symptoms at all.
By 1950 doctors had discovered that sickle cell anemia was an incomplete dominance trait and the people who had one copy of the mutated and one of the normal gene showed no symptoms. They soon found out the sickle cell anemia was not unique to the U.S in fact the gene turned up in high rates across Africa, southern Europe and into India. Genetically speaking this made no sense because having two copies of the trait was so deadly it would be most likely that the mutation would have become rarer with each generation.
In 1954 a geneticists Anthony C. Allison observed that people in Uganda who carried a copy of the sickle cell mutation had lower rates of getting malaria. Later research confirmed Dr. Allison’s findings. It seems that the sickle cells defend against malaria by starving the single-celled parasite that causes the disease. The parasite feeds on hemoglobin, and so it’s likely that it can’t grow on the sickle cell version of the molecule.