|Malaria and Sickle Cell Anemia
Pauling's concern about the spread of sickle cell hemoglobin arose from its relatively high frequency in the human population.
By drawing on work performed by other investigators, Pauling stated that the mutation perpetuated because it protected individuals
from contracting malaria. Thus, he noted that while some molecular mutations are detrimental, sickle cell trait protected
against malaria and benefited these individuals living in malarial areas.
He described three genetic possibilities and translated what each meant for the individual's health as well as explained the
genetic make-up of a population procreating in a region with high incidences of malaria. First, people with normal hemoglobin
are homozygous dominant and do not exhibit crescent shaped hemoglobin; therefore, they do not have sickle cell trait or sickle
cell anemia and additionally are not protected against malaria. Most likely, the majority of these people would die from malaria
and therefore stop procreating. Secondly, those born homozygous recessive for sickle cell hemoglobin suffer from sickle cell
anemia and typically die young, usually without procreating. Thirdly, those with heterozygous hemoglobin have sickle cell
trait and withstand infection from the malaria parasite. These people benefit most in an area with high mortality rates from
malaria because they do not contract either disease full-blown.
In areas where malaria is not endemic, Pauling confidently averred that the sickle cell mutation was being removed from the
human germ plasma. However, Pauling thought that the natural rate of removal happened too slowly in comparison to the introduction
of new mutations. Thus, he promoted eugenic practices as a way to decrease the number of mutations that passed to future generations.