Yes, white people can and do get sickle cell disease. While the condition disproportionately affects Black Americans, it is not exclusive to any single race. Sickle cell disease is an inherited blood disorder driven entirely by genetics, and the relevant gene variants exist in populations across the globe, including those of European descent.
Who Gets Sickle Cell Disease
About 100,000 people in the United States live with sickle cell disease. More than 90% are non-Hispanic Black or African American, and an estimated 3% to 9% are Hispanic or Latino. The remaining cases include people of Middle Eastern, South Asian, Mediterranean, and European backgrounds. The disease occurs in roughly 1 out of every 365 Black or African American births and about 1 out of every 16,300 Hispanic American births. Comparable nationwide birth-incidence figures for white Americans specifically are harder to pin down, but the gene is clearly present in that population: CDC data show that about 3 out of every 1,000 white newborns carry the sickle cell trait, meaning they have one copy of the gene variant.
Carrying the trait is not the same as having the disease. A person with one copy of the altered gene typically has no symptoms. But if both parents carry the trait, each pregnancy has a 25% chance of producing a child with sickle cell disease. That math applies regardless of race.
Why the Gene Is More Common in Certain Regions
The sickle cell gene variant didn’t spread randomly. It persisted in populations where malaria was historically endemic because carrying one copy offers significant protection against the parasite. People with the trait are less likely to develop severe malaria, so in regions where the disease was a leading killer, carriers survived and had children at higher rates. Over generations, this pushed the gene to relatively high frequencies.
Those regions include sub-Saharan Africa, but they also include parts of Southern Europe. Northern Greece, Sicily, and Southern Italy all have documented histories of both malaria and elevated sickle cell gene frequencies. The same is true of Southern Turkey, Saudi Arabia, large parts of India, and Spanish-speaking regions across the Caribbean, Central America, and South America. Researchers first noted the geographical overlap between sickle cell variants and malaria in Mediterranean areas as far back as the late 1940s, and extensive mapping studies have since confirmed a strong global link between the highest gene frequencies and areas of high malaria transmission.
This means a white American of Southern Italian or Greek descent, for example, may carry the sickle cell gene without any African ancestry. The same is true for people with roots in the Middle East or parts of Central Asia.
How Sickle Cell Disease Is Inherited
Sickle cell disease follows an autosomal recessive inheritance pattern. That means a child must inherit two altered copies of the HBB gene, one from each parent, to develop the disease. The HBB gene provides instructions for making a component of hemoglobin, the protein in red blood cells that carries oxygen. A specific variant of this gene produces an abnormal form called hemoglobin S, which causes red blood cells to become rigid and crescent-shaped instead of round and flexible.
The most common and typically most severe form, called HbSS, occurs when a person inherits hemoglobin S from both parents. But other combinations also cause sickle cell disease. A person can inherit hemoglobin S from one parent and a different abnormal hemoglobin variant (such as hemoglobin C) or a related condition called beta thalassemia from the other parent. These compound forms produce varying degrees of severity but are all classified as sickle cell disease.
Parents who each carry one copy of the altered gene are called carriers. They usually have no symptoms and may not know their status unless tested.
Every Newborn in the U.S. Is Screened
Since 2006, every state in the U.S. has mandated universal newborn screening for sickle cell disease. This was not always the case. The rollout began in the late 1980s after a landmark clinical trial showed that identifying affected infants early and starting preventive treatment dramatically reduced infant deaths. Most states adopted mandatory screening between 1987 and 1993, with the final state coming on board in 2006.
The word “universal” is important here. Screening is not limited to babies who appear to be of a particular racial or ethnic background. Every newborn gets a blood test, typically a heel prick within the first 48 hours of life, that can detect hemoglobin S and other abnormal hemoglobin types. This approach catches cases that targeted screening based on perceived ethnicity would miss.
In Europe, the picture is more uneven. A 2017 Pan European consensus conference recommended considering universal screening, but many countries still rely on targeted screening that restricts testing to babies from ethnic groups considered “at risk.” This approach can miss affected children from families that don’t fit the expected demographic profile.
The Cost of Racial Assumptions
The longstanding association between sickle cell disease and Black Americans has created real clinical blind spots. Historically, when sickle cell disease was identified in white patients, some physicians attributed it to “racial admixture” rather than accepting that the gene exists independently in multiple populations. The belief that sickle cell disease was exclusive to Black people was even used by some physicians as supposed evidence of biological differences between races.
These assumptions still have consequences. Bias toward patients with sickle cell disease has been documented to cause significant undertreatment of pain and missed diagnoses. For white or non-Black patients, the risk is a different kind of oversight: a doctor who doesn’t consider sickle cell disease in their differential diagnosis simply because of a patient’s appearance. A white patient showing up in an emergency room with severe pain episodes, chronic anemia, or organ damage might not be tested for sickle cell disease as quickly as a Black patient with identical symptoms.
If you have ancestry from any region where malaria was historically common, including parts of Southern Europe, the Middle East, India, or Latin America, and you experience unexplained anemia or recurring pain crises, sickle cell disease is worth considering and easy to test for. A hemoglobin electrophoresis test, which separates different types of hemoglobin in a blood sample using an electric current, can identify hemoglobin S and other variants. Results are typically interpreted alongside a complete blood count and a blood smear to confirm the diagnosis.
Sickle Cell Trait in White Populations
Even among white Americans without obvious Mediterranean or Middle Eastern ancestry, the sickle cell trait is not absent. CDC data from 13 states found an incidence of 3.0 cases of sickle cell trait per 1,000 white newborns. For comparison, the rate was 73.1 per 1,000 among Black newborns and 6.9 per 1,000 among Hispanic newborns. The white carrier rate is lower, but across millions of births per year, it adds up to a meaningful number of carriers.
Most people with sickle cell trait live entirely normal lives. The trait can occasionally cause problems under extreme conditions, such as intense physical exertion at high altitude or severe dehydration, but day-to-day it produces no symptoms. Its main significance is reproductive: two carriers can have a child with full sickle cell disease. Knowing your carrier status matters most when planning a family, particularly if your partner also has ancestry from a region where the gene is common.