The genetic 'mutation' (or phenotype/genotype) that causes sickle-cell anemia didn't originate as a response to malaria. It happened and happens randomly, by simple chance. As malaria epidemics would strike some area, the people who didn't have the mutation would be less likely to survive. Thus the percent of people that had the mutation would increase, and (since it is genetic/hereditary) the percentage would quickly increase. In places where malaria was a regular hazard, the people who lacked the mutation would be rapidly selected out as the percentage of those with the mutation would have so strong a survival advantage.
The advantage was and is profound. Granted, the disease comes with a truly dreadful down-side. Regrettably, since the mutation doesn't kill you off before reproductive age, the selective pressure is simply "positive" so it only grants what seems like a genetic advantage.
Sickle cell anemia could be adaptive in the way that it offers protection against malaria. Sickle cell anemia is dominant genetic disorder whereas if you inherit it from both parents (AA alleles) then you die early in life because your blood cells are unable to carry the required amount of oxygen. However if you only inherit it from one parent (Aa alleles), then only part of your blood cells shows the characteristic sickle shape while the other part is fully functional. We have not yet discovered the reason behind this, but it plays a part in protecting against the malaria parasite.
Some literature that may help you research this topic more thoroughly (some are free access at www.pubmed.com):
1. McKenzie, E; Killeen, G; Beier, J; Bossert, W. 2001. Seasonality, Parasite Diversity, and Local Extinctions in Plasmodium falciparum Malaria. Ecology 82(10) pp: 2673-2681.
2. Dajer, Tony. Blackwater Fever. 1992. Discover Magazine pp: 47-52.
3. Burns, E; Pollack, S. 1988. P. falciparum infected Erythrocytes are capable of Endocytosis. In Vitro Celular & Developmental Biology. 24(5). pp: 481-486. 4. O'Donnell, A; Weatheralla, D; Taylorc, A; Reederb, J; Allenab, A. 2005. Muscle cell injury, haemolysis and dark urine in children with falciparum malaria in Papua New Guinea 5. Suarez, C. 1985. Plasmodium Falciparum: Invasion and Development in highly Parasitized Cultures. 21(3). pp:161-164.
The heterozygous condition confers some resitance to malaria, especially in children. So, those who possed this condition would tend to survive more often in malaria country and live to have more children, some of which would inherit the trait.
Sickle cell anemia was discovered in the 1870's and carried many names, but 1922 it was officially named sickle cell anemia.
Yes, drepanocytosis(sickle cell anemia) is a type of poikilocytosis.
Sickle cell anemia is not sex linked.
ITS GOOD 4 UR SICKLE CELL! When you have sickle cell, your body looses cells. Folic acid helps to create new cells.
Anyone of any race can get sickle cell
because people in europe have not gotten used to sickle cell anemia because it is soo rare in europe
You get Sickle-Cell Anemia by Birth,it is a genetic disorder.
An example of point-mutation is sickle-cell anemia. Sickle-cell disease is hereditary.
Sickle cell anemia is an autosomal recessive disease. Carriers have sickle cell trait, which confers resistance to malaria.
Yes, Sickle Cell Anemia is in fact a genetic disorder.
An example of point-mutation is sickle-cell anemia. Sickle-cell disease is hereditary.
sickle cell anemia
Sickle cell anemia -yes it is hereditary
Sickle cell anemia was discovered in the 1870's and carried many names, but 1922 it was officially named sickle cell anemia.
It sounds like you are looking for Sickle Cell Anemia.
Sickle cell anemia is genetic. It is an autosomal recessive disease.
Yes, drepanocytosis(sickle cell anemia) is a type of poikilocytosis.