Scientist claim sickle-cell anemia started in one person in West Africa some 7,300 years ago who was born with the genetic mutation that altered his hemoglobin.
This child had survived in the Sahara which was not a desert at the time but a green belt of savannas with lakes and rivers in which hunter-gatherers caught fish and speared hippos.
His genetic mutation was not harmful as he had two copies of the hemoglobin gene and one was normal. He passed it on to future generations who had moved to other parts of Africa and became cattle-herders and farmers when the desertification of the Sahara began.
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This research was carried out by scientist Daniel Shriner and Charles N. Rotimi, the director of the Center for Research on Genomics and Global Health in the United States where the research was conducted.
The findings published last Thursday in the American Journal of Human Genetics indicated that people who carried one mutated gene were protected against malaria which was a threat in the region.
However, some of the descendants inherited two copies of the mutant hemoglobin gene instead of one and could no longer produce normal hemoglobin.
This resulted in defective red cells that clogged their blood vessels causing the condition known as sickle cell anemia which has killed many children and caused extreme pain, difficulty with breathing, kidney failure and even strokes.
Dr. Shriner and Dr. Rotimi analyzed the genomes of nearly 3,000 people to reconstruct the genetic history of the disease which has spread throughout Africa, southern Europe, the Near East and India with about 300,000 children each year born with sickle cell anemia.
Dr. Rotimi explained that they carried out the research because an improved understanding of the history of sickle cell anemia could lead to better medical care. It might allow researchers to predict who will suffer severe symptoms and who will only experience mild ones, reports the New York Times.
The research found that sickle cell mutation seemed to defend against malaria by starving the single-celled parasite that causes the disease. The parasite feeds on hemoglobin, and so it’s possible that it can’t grow on the sickle cell version of the molecule.
“It would definitely help physicians to treat patients at a global level,” says Dr Rotimi who believes the mutation which was discovered in the 1900s can be treated with inspiration from their findings.
