The sickle cell trait has been widely considered a classic example of human evolution in action because of the mutation’s ability to protect against malarial infections. Under normal physiological conditions, Plasmodium falciparum is capable of reproducing and spreading systemically, however individuals carrying the sickle cell trait possess sickled erythrocytes that excessively leak potassium, resulting in the inhibition of P. falciparum development. Recent studies have shown that the mutation responsible for the sickle cell trait – hemoglobin S (HbS) mutation – is higher in areas of the world where malaria is endemic. This indicates that the mutation is nonrandom in nature, driven by environmental pressure rather than random occurrence, countering a central criterion that the classic evolutionary theory postulates. Further research concludes that the sickle cell trait is the result of a de novo mutation because they often arise in individuals whose parents are both homozygous for HbA. A Master Bioengineer and Creator has anticipated the future of changing conditions and has provided humans the ability to adapt to one’s environment via epigenetics – the stimulation or suppression of a gene’s expression. Paralleling how the human body constantly engages in short-term physiological adaptions like reflexes and homeostasis to survive, the body can also promote the expression of certain beneficial mutations like the HbS mutation to modulate life-threatening malarial parasites (P. falciparum).
Gillen, Alan L.; Mast, Jared G.; and Mast, Nathan, "The Relationship between Sickle Cell Anemia and Falciparum Malaria: Is it Human Evolution in Action?" (2022). Faculty Publications and Presentations. 204.