Sickle-cell anemia is a genetic condition characterized by a structural change in red blood cells. While normal red blood cells are round, those affected by this disorder take on an abnormal, crescent-like shape.

Comparison of Normal and Sickle-Shaped Red Blood Cells

Sickle-cell carriers are individuals who have inherited a single copy of the sickle-cell gene. Rather than experiencing the severe full-blown disease associated with having two gene copies, carriers usually only face minor health problems or symptoms triggered by extreme conditions like severe dehydration or oxygen deprivation. A crucial trait of these carriers is their natural protection against malaria, resulting from blood chemistry and immune alterations that suppress the parasite. This protective immunity is absent in individuals with full-blown sickle-cell anemia.

Characteristics of Sickle-Cell Carriers

A specific hereditary blood disorder involves red blood cells becoming rigid and crescent-shaped. While inheriting two copies of the responsible gene often leads to a severe, potentially lethal condition, inheriting only one copy makes a person largely asymptomatic and provides significant resistance to malaria. Evaluate the overall impact of this gene on human populations living in regions where malaria is widespread. In your evaluation, consider both the costs and benefits of the gene's presence in the population.

Evaluating a Genetic Trait's Impact

Although the genetic mutation that causes sickle-cell anemia often leads to early death, the gene remains relatively common among individuals of African descent. This persistence appears to contradict the notion of "survival of the fittest," which suggests that a disorder causing such severe negative evolutionary effects and low survival rates would naturally become less frequent in a population over time.

Evolutionary Paradox of the Sickle-Cell Gene

In sickle-cell anemia, the abnormal, crescent-like shape of the red blood cells impairs their typical function. These sickle-shaped cells can create blockages in blood vessels and restrict blood flow, which leads to physical consequences such as high fever, severe pain, swelling, and potential tissue damage.

Physical Implications of Sickle-cell Anemia

Sickle-cell anemia is a hereditary blood disorder where red blood cells become rigid and sickle-shaped, obstructing blood flow and causing serious health issues like severe pain and tissue damage. This condition is potentially lethal for individuals who are homozygous for the trait, meaning they have inherited two copies of the recessive gene. In contrast, heterozygous carriers, who have only one copy of the gene, are largely asymptomatic and exhibit resistance to malaria.

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Genetic disorders can be caused by the pairing of two recessive genes, meaning that an individual must inherit one copy of the recessive allele from each parent in order to develop the condition. Examples of such recessive genetic disorders include sickle-cell anemia and phenylketonuria (PKU).

Diseases Caused by Recessive Alleles

Spielman, R. M., Jenkins, W. J., & Lovett, M. D. (2020, April 22). Psychology (2nd ed.). OpenStax. https://openstax.org/books/psychology-2e/pages/1-introduction

OpenStax Psychology (2nd ed.) Textbook

Phenylketonuria (PKU) is a recessive hereditary disorder, meaning that two copies of the mutated gene implicated in PKU disease processes must be inherited in order for an individual to display symptoms of this disorder. It’s one of the most common inherited metabolic disorders. The mutated genes cannot produce the enzyme that normally metabolizes the compound phenylalanine, found in certain food products, into tyrosine. The build-up of phenylalanine in the brain can become toxic, leading to intellectual disability when the build-up interferes with myelination in the central nervous system. If a baby with PKU ingests food with phenylalanine, the build-up during the post-birh period stunts brain development. Because of its preventable nature, and because the test is inexpensive and accurate, many governments have passed laws for mandatory PKU testing shortly after birth, and this has prevented many cases of intellectual disability.
PKU can be prevented by regulating the level of phenylalanine intake, especially early in life. After the post-birth brain development period has passed, the low phenylalanine diet can be relaxed somewhat since the danger to brain development has passed. 
For pregnant women with PKU, however, this isn’t the case. When a fetus is in utero, it’s protected by its mother’s metabolism. For non-PKU having mothers, this means the baby is especially protected during this time. However, if the mother has PKU and ingests a diet with typical or high levels of phenylalanine - while it won’t damage HER brain - it will cause improper brain development in the fetus. 

Phenylketonuria (PKU)

Sickle-cell Anemia

Two individuals are both carriers for a genetic disorder that is caused by a recessive allele. They do not show any symptoms of the disorder themselves. What is the probability that their biological child will have the disorder?

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