Sickle cell anemia (SCA) is an inherited blood disorder affecting hemoglobin, the protein responsible for carrying oxygen within red blood cells. The disease causes normally flexible, disc-shaped red blood cells to become rigid, sticky, and crescent-shaped, resembling a sickle. This abnormal shape leads to blockages in small blood vessels, causing pain and organ damage throughout the body. While SCA is widely associated with people of African descent, the underlying genetic mechanism reveals a far more complex picture of its global reach, clarifying how a person who identifies as white can indeed be affected by or carry the trait.
How Sickle Cell Anemia is Inherited
Sickle cell anemia is caused by a specific point mutation in the HBB gene, which provides instructions for making beta-globin, a component of the hemoglobin protein. This mutation results in the creation of an abnormal type of hemoglobin known as hemoglobin S (HbS). The inheritance pattern for SCA is autosomal recessive, meaning a child must inherit two copies of the mutated HBB gene—one from each parent—to develop the full disease.
If a person inherits only one copy of the HbS gene and one normal copy, they are said to have the sickle cell trait. Individuals with the sickle cell trait are typically healthy and do not experience the severe symptoms of the disease, but they are carriers who can pass the gene to their children. When two parents are both carriers of the sickle cell trait, there is a 25 percent chance with each pregnancy that their child will inherit two copies of the HbS gene and be born with sickle cell anemia.
The presence of the HbS gene is a molecular reality, not a matter of visual appearance. For the disease to manifest, both biological parents must contribute the gene, forming the homozygous (HbSS) condition. Understanding this genetic foundation is key to recognizing the disorder’s distribution across diverse populations.
The Global Genetic Footprint of the Sickle Cell Trait
The uneven distribution of the sickle cell gene across the globe is directly related to a historical evolutionary advantage it offered. The sickle cell trait provides a degree of protection against severe illness from malaria. Consequently, the gene became concentrated in regions where malaria was historically endemic, including parts of Africa.
Crucially, these malaria-endemic zones also extended far beyond the African continent, leading to a significant prevalence of the sickle cell gene in non-African populations. High frequencies of the trait are found in areas of the Mediterranean basin, such as Greece, Italy, and Turkey. This includes southern European populations who are often categorized as white.
The sickle cell gene is also widely distributed across the Middle East, including countries like Saudi Arabia and Lebanon, and in certain tribal groups in India. The presence of the HbS gene in these regions can sometimes lead to a milder form of the disease. Therefore, individuals whose ancestry traces back to these Mediterranean, Middle Eastern, or South Asian regions carry a risk of inheriting the gene.
Why Ancestry, Not Race, Determines Risk
The question of whether a white person can get sickle cell anemia is answered by looking at ancestry rather than race. A person identifying as white can inherit the HbS gene and develop the disease if their genetic heritage includes ancestors from high-prevalence areas. These regions include Southern Europe and the Middle East, where the gene has been established for centuries due to the selective pressure of malaria.
Race is a social construct based on external appearances, while genetic risk follows the biological paths of family history and ancestral migration patterns. The gene does not recognize social categories, only the opportunity to be passed from one generation to the next. Migration has further dispersed the gene, meaning an individual’s appearance may not reflect their deeper genetic roots.
For this reason, genetic screening and counseling are recommended based on a thorough family history that investigates ties to all high-prevalence areas, not just the common association with African descent. Focusing solely on perceived race overlooks the significant number of people of Mediterranean, Middle Eastern, or Indian ancestry who are carriers and are therefore at risk of passing the condition to their children.