Frequency of Blood Types Across Populations

Blood type frequencies vary enormously from one population to the next, shaped by tens of thousands of years of migration, genetic drift, and natural selection by infectious diseases. Type O is the most common blood group worldwide, but its prevalence ranges from roughly 40–45 percent in many European and Asian populations to near 100 percent in some Indigenous American groups. The Rh-negative trait, meanwhile, peaks above 25 percent in parts of western Europe and North Africa but falls below 1 percent across much of East Asia. These are not small statistical wrinkles; they create real consequences for transfusion supply chains, organ transplant access, and maternal-fetal medicine in ethnically diverse societies.

The Global Picture for ABO

Across most of the world’s populations, all four ABO types are present, but in markedly different proportions. Type O tends to be the single most common group globally, followed by A, then B, with AB the rarest almost everywhere. In populations of European descent, type A runs close to or slightly above O in frequency, typically in the range of 35–40 percent each. In sub-Saharan Africa, type O tends to dominate more strongly, often making up half or more of the population. South and Southeast Asian populations tend to carry higher proportions of type B than Europeans, with B frequencies reaching 25–30 percent in parts of the Indian subcontinent and Central Asia.

The 1000 Genomes Project, which sequenced the genomes of over 2,500 individuals from five continental superpopulations, helped clarify how blood group genetic variants are distributed geographically, identifying variants of clinical significance that differ sharply by region.¹ These are not just academic curiosities. A hospital serving a predominantly South Asian community faces different blood supply challenges than one in Scandinavia or West Africa, and the genetic data increasingly shapes how regional blood banks plan their inventories.

Rh Factor and Its Dramatic Geographic Skew

The Rh system, and specifically the D antigen that determines whether you are “positive” or “negative,” shows an even more striking geographic split than ABO. In populations of European descent, roughly 15–17 percent of individuals are Rh-negative. In the United States overall, the figure is around 15 percent. But outside Europe and its diaspora populations, Rh-negative frequencies plummet. In sub-Saharan Africa, frequencies typically fall between 1 and 8 percent depending on the region. In a study from Ghana’s Volta region, about 7.5 percent of the population was Rh-negative.² In East Asian populations, including China, Japan, and Indonesia, the proportion of Rh-negative individuals drops below 1 percent.

The global outlier is a population in the Basque region and parts of Morocco, where Rh-negative frequency has been reported as high as 29 percent, the highest recorded prevalence anywhere.² Why the Basques carry such a high Rh-negative rate remains debated, but their genetic distinctiveness from surrounding European populations has long been noted across multiple genetic markers, not just blood type.

Why Frequencies Differ So Much

If blood type had no effect on survival, you might expect random drift over time to produce some variation between populations, but probably not the extreme patterns we see. The evidence increasingly points to infectious disease as a major sculptor of blood group frequencies. The ABO polymorphism is astonishingly old. Phylogenetic analyses of primate ABO genes show that the A and B alleles have been maintained by balancing selection for at least 20 million years, making this one of the longest-running examples of such selection in primates outside the immune system’s major histocompatibility complex.³ The B allele appears to have independently evolved from the ancestral A form at least three times across primate lineages, suggesting it keeps being “reinvented” because it offers a survival advantage in certain contexts.⁴

The leading hypothesis is that gut pathogens have driven this balancing act. Different blood group antigens are expressed on the surface of cells lining the gut and respiratory tract, and various pathogens exploit specific antigen structures as footholds for infection. When a pathogen sweeps through a population, individuals whose blood type happens to offer less binding opportunity may survive at higher rates. Over many generations, this creates fluctuating or frequency-dependent selection, where no single blood type wins permanently because the advantage shifts as pathogen landscapes change.⁵

The O allele itself tells an interesting story. The mutation that creates the “null” O allele, which produces no A or B antigen, has arisen independently at least three times in human evolution, producing distinct O allele lineages.⁶ The fact that different O mutations keep appearing and persisting suggests that carrying no surface antigen confers a survival advantage against certain pathogens, even if it comes with trade-offs against others.

Malaria and Cholera as Selective Forces

The best-studied example of a pathogen shaping blood type distribution is malaria. In Plasmodium falciparum malaria, the parasite causes infected red blood cells to clump together with uninfected ones, a process called rosetting that leads to the severe, often lethal complications of the disease. Type O red blood cells form smaller, weaker rosettes than type A, B, or AB cells, and research has confirmed that blood group O protects against severe falciparum malaria through this reduced rosetting mechanism.⁷ This likely explains, at least in part, why type O frequencies are high in malaria-endemic regions of sub-Saharan Africa and parts of Central and South America.

But the advantage of type O is not universal. People with blood group O are more susceptible to severe cholera. In areas where cholera is endemic, household contacts with blood group O who became infected with Vibrio cholerae were roughly twice as likely to develop severe illness compared with those of other blood types.⁸ This creates a genuine evolutionary tug-of-war in regions where both malaria and cholera are present, potentially explaining why type O, despite its malaria advantage, does not completely dominate in areas of South Asia where cholera has historically been a major killer.

The Near-Exclusive Type O of Indigenous Americans

Among the most striking patterns in blood group geography is the near-universal prevalence of type O among Indigenous peoples of the Americas. While all major ABO alleles appear in most populations worldwide, the majority of Native Americans are nearly exclusively type O.⁹ Some South American Indigenous groups test at close to 100 percent type O, a frequency unmatched anywhere else on the planet.

The explanation is debated. One possibility is a founder effect: the small groups that crossed into the Americas during the last Ice Age may simply have been disproportionately type O by chance, and that initial skew was amplified as the population expanded across two empty continents. Another hypothesis points to the catastrophic population declines following European contact, when epidemic diseases like smallpox killed the vast majority of Indigenous people. If blood type influenced survival during those epidemics, the resulting genetic bottleneck could have further concentrated type O.¹⁰ Ancient DNA studies are beginning to disentangle these possibilities, but the picture remains incomplete. The answer is probably some combination of founding population genetics, drift in small isolated groups, and selective pressure from pathogens encountered both before and after European contact.

The Duffy System and Vivax Malaria

ABO and Rh get most of the public attention, but the human blood group story extends well beyond them. One of the most dramatic examples of pathogen-driven selection involves the Duffy blood group system. The Duffy antigen on red blood cells serves as the entry receptor for Plasmodium vivax, one of the major malaria parasites. More than 95 percent of the population in West Africa carries the Duffy-negative phenotype, which makes their red blood cells resistant to P. vivax invasion.¹¹ This is why vivax malaria is essentially absent from West Africa despite being widespread across the rest of the tropical world. A single genetic mutation, expressed in both copies of the gene, eliminates the receptor the parasite needs.

Outside sub-Saharan Africa, the Duffy-negative phenotype is rare. In a study of North Macedonian blood donors, only about 0.2 percent were Duffy-negative.¹² The geographic pattern is so clean it reads almost like a map of historical vivax malaria pressure, offering one of the clearest cases in human genetics of a pathogen driving an entire blood group to near-fixation in an affected region.

Minor Blood Group Systems and Population Variation

Beyond ABO, Rh, and Duffy, there are more than 40 recognized blood group systems, and many of them show population-specific patterns that matter for transfusion compatibility. The Kell, Kidd, and MNS systems are the ones transfusion specialists encounter most often after ABO and Rh.

Kell antigen (K) frequency provides a good illustration of how these minor systems differ by ancestry. In a large Indian donor study, about 3.5 percent carried the K antigen, placing them between the typical frequencies reported for Caucasian donors (around 9 percent) and Black donors (around 2 percent).¹³ In North Macedonia, Kell frequency was about 7.5 percent, closer to the European average.¹²

The Kidd blood group system shows a different pattern. Kidd antigen frequencies in Indian donors were more similar to those of Caucasian and Chinese populations than to Black populations.¹³ In contrast, a study of Hispanic blood donors in South Texas found that while Kidd antigens were the only major group that did not differ significantly from published white and Black donor frequencies, most other minor blood group antigens in the Hispanic population showed significant differences from both groups.¹⁴ This is a practical problem, not just an academic one: patients who receive multiple transfusions over time can develop antibodies against minor antigens they lack, and if the donor pool does not match the patient population, compatible blood becomes harder to find.

Rare Phenotypes and Regional Surprises

Some blood group phenotypes are so uncommon that they require dedicated rare donor registries. A study from Uttarakhand, India, building such a registry identified small numbers of donors carrying antigens like Di(a), In(a), and C(w) that are unusual for the Indian subcontinent, as well as a single donor with the Bombay phenotype.¹⁵ The Bombay phenotype is a particularly fascinating case: individuals with it lack the H antigen that normally serves as the precursor for A and B antigens, so their blood tests as type O but is incompatible even with standard O blood. It occurs at extremely low frequencies globally but is somewhat more common in parts of India, particularly among certain communities in Maharashtra.

Even within Europe, unusual markers can reveal population history. The LW(b) blood group gene, uncommon almost everywhere, reaches about 6 percent frequency in Latvians and Lithuanians and declines in a regular gradient away from the Baltic region: roughly 4 percent in Estonians, 3 percent in Finns, 2 percent in nearby Russian populations, and near zero elsewhere in Europe.¹⁶ Researchers have proposed LW(b) as a “Baltic tribal marker” whose distribution traces prehistoric Baltic migrations and genetic influence on neighboring peoples. Blood groups, in this way, serve as fossils of human movement written in the genome.

Health Associations Beyond Infectious Disease

Blood type frequency variation has health consequences that go beyond the infectious diseases that likely shaped those frequencies in the first place. Type O individuals, while enjoying some protection against severe malaria and possibly lower cardiovascular risk, face a trade-off with the gut. Helicobacter pylori, the bacterium behind most peptic ulcers, binds more readily to the blood group O antigen expressed on the stomach lining. The bacterium attaches to the Lewis(b) antigen, and this binding is reduced when the antigen carries an additional sugar residue characteristic of blood group A or B.¹⁷ Consistent with this, studies have found that H. pylori colonizes the stomachs of type O individuals more densely and provokes stronger inflammatory responses, contributing to their higher rates of peptic ulceration.¹⁸

On the cardiovascular side, people with non-O blood types carry about 25–30 percent higher levels of von Willebrand factor, a clotting protein, in their blood compared with type O individuals.¹⁹ This translates into a measurably higher risk of venous blood clots for people with type A, B, or AB. The association is strong enough that non-O blood type is now recognized as a genetic risk factor for venous thromboembolism. In populations where type O frequency is low, a slightly larger share of the population carries this baseline clotting risk.

COVID-19 and Blood Type

Early in the pandemic, reports suggested that blood type O might protect against SARS-CoV-2 infection. A large Canadian population-based study found that type O individuals had a modestly lower risk of testing positive for SARS-CoV-2, with a roughly 12 percent relative reduction compared with non-O types. Being Rh-negative added further protection, and O-negative individuals showed the lowest infection risk of any group.²⁰ A separate study using a large New York City cohort reported small absolute risk differences between blood groups, with type A at decreased risk of intubation and death compared with type O, while type AB was at increased risk of both.²¹

However, these findings did not hold up uniformly across the pandemic. A study that tracked outcomes across multiple dominant variant waves found no significant differences in severe disease among the four blood types, with the proportion of severe outcomes nearly identical, ranging between about 8.6 and 8.9 percent across types.²² The honest read of the evidence is that any blood type effect on COVID-19 was small in absolute terms and may have been confounded by the correlation between blood type and ancestry. It is a useful reminder that association studies in the middle of a fast-moving pandemic can produce findings that fade as the evidence base matures.

Rh Incompatibility and Maternal-Fetal Medicine

The population frequency of Rh-negative blood has direct consequences for pregnancy. When an Rh-negative mother carries an Rh-positive fetus, her immune system can develop antibodies against the baby’s red blood cells, potentially causing hemolytic disease of the newborn in subsequent pregnancies. This is preventable with anti-D immunoglobulin injections, and in high-income countries with predominantly European-descent populations, prevention programs are well established.

Globally, however, the picture is grimmer. An estimated 13 million annual doses of anti-D immunoglobulin would be needed to fully prevent Rh sensitization through both prenatal and postpartum administration, but fewer than 4 million doses are currently given each year. More than 2.5 million additional annual doses are needed outside high-income countries just to cover postpartum prophylaxis alone.²³ In regions where Rh-negative frequency is low, the condition may be rarer but is also more likely to be missed. A study from a hospital in southern Ethiopia identified Rh-negative mothers making up a small fraction of deliveries, with cases of neonatal jaundice among their babies.²⁴ The paradox is that while Rh disease is a bigger issue in populations where Rh-negative frequency is higher, the preventive infrastructure is least available in lower-income countries where even a small number of affected pregnancies can result in preventable infant death.

Organ Transplantation and Blood Supply Equity

Blood type frequencies create a structural equity problem in organ transplantation. Organ allocation in most countries requires ABO compatibility, which means the probability of finding a match depends partly on how common your blood type is in the donor pool. In populations where one blood type is very common, those individuals have the largest pool of potential donors but also the most competition from fellow patients of the same type. Patients with rarer types in a given population may wait longer simply because fewer compatible organs become available. Challenges of ABO and minor antigen discordance in solid organ transplantation affect waitlist mortality unevenly across ethnic groups.²⁵

For blood transfusion, the issue is more concrete. Type O-negative blood is the universal donor for red blood cells, making it critical for emergencies when there is no time to determine a patient’s type. But in a community where very few people are O-negative, those few donors carry a disproportionate burden. In East Asian populations, where Rh-negative frequency is below 1 percent, maintaining an adequate O-negative supply requires either importing blood products, maintaining frozen rare-blood inventories, or recruiting from minority communities at higher rates. Conversely, in communities with many recent immigrants from diverse backgrounds, a blood bank designed around one population’s type distribution may not serve the full patient base. The mismatch between the ethnic composition of the donor pool and the patient population is a growing challenge in multicultural societies worldwide.

How Blood Type Testing Has Changed What We Know

Much of what was historically “known” about blood type frequencies came from serological testing, in which lab reagents are applied to a blood sample to see which antigens are present. This works well for the major groups but can miss subtleties. Genomic typing, now increasingly used in blood banks, reads the DNA directly and can distinguish between alleles that look identical on a standard serological test. The O allele, for example, comes in several distinct lineages (O01, O02, O09) that arose from separate mutations but produce the same serological result.⁶ Knowing which O variant someone carries does not change their transfusion compatibility, but it enriches our understanding of population history and, in some rare cases, affects the interpretation of tricky typing results.

Genomic approaches have also revealed that some populations harbor blood group variants not captured by standard panels. The Indian study that built a rare donor registry found donors positive for antigens like Gp.Mur, a variant in the MNS system that is uncommon in South Asia but more frequent in parts of Southeast Asia.¹⁵ As genotyping platforms become cheaper, regional blood banks in lower-income countries are beginning to build local databases of rare phenotypes, filling a gap that has historically meant patients needing rare blood had to rely on international registries or go without.

1
PubMed Central. Genomic coordinates and continental distribution of 120 blood group variants reported by the 1000 Genomes Project
2
PubMed Central. Frequencies and ethnic distribution of ABO and RhD blood groups in the Volta region of Ghana, towards effective blood bank services
3
PubMed Central. The ABO blood group is a trans-species polymorphism in primates
4
Molecular Biology and Evolution. Evolution of primate ABO blood group genes and their homologous genes
5
PubMed Central. Ancestry runs deeper than blood: the evolutionary history of ABO points to cryptic variation of functional importance
6
PubMed. Evolutionary dynamics of the human ABO gene
7
PubMed Central. Blood group O protects against severe Plasmodium falciparum malaria through the mechanism of reduced rosetting
8
PubMed Central. Blood group, immunity, and risk of infection with Vibrio cholerae in an area of endemicity
9
PubMed. Blood group O alleles in Native Americans: implications in the peopling of the Americas
10
PubMed. An ancient DNA test of a founder effect in Native American ABO blood group frequencies
11
PubMed. Duffy blood group and malaria
12
PubMed. ANTIGEN FREQUENCY OF KELL, DUFFY, KIDD, MNS AND LUTHERAN BLOOD GROUP SYSTEM IN POPULATION OF NORTH MACEDONIA – TOWARDS RARE BLOOD GROUP REGISTRY
13
PubMed Central. Prevalence of Rh, Duffy, Kell, Kidd & MNSs blood group antigens in the Indian blood donor population
14
PubMed. Prevalence of Rh, Kell, Kidd, Duffy, and MNS antigens in the Hispanic donor population of South Texas
15
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16
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17
PubMed. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens
18
PubMed. Increased inflammatory responses of persons of blood group O to Helicobacter pylori
19
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20
PubMed Central. Association Between ABO and Rh Blood Groups and SARS-CoV-2 Infection or Severe COVID-19 Illness : A Population-Based Cohort Study
21
Nature Communications. Associations between blood type and COVID-19 infection, intubation, and death
22
PubMed Central. Association between ABO blood type and coronavirus disease 2019 severe outcomes across dominant variant strains
23
PLOS ONE. Hemolytic disease of the fetus and newborn due to Rh(D) incompatibility: A preventable disease that still produces significant morbidity and mortality in children
24
PubMed Central. Rhesus Negativity Prevalence and Neonatal Outcomes among Pregnant Women Delivered at Bule Hora University Teaching Hospital, West Guji Zone, South Ethiopia
25
PubMed Central. When Compatibility Creates Inequality: Blood Type O and the Korean Heart Transplant System