Fewer than 50 people in recorded history have been confirmed to have golden blood. The most commonly cited figure is about 43 reported cases worldwide since the blood type was first discovered in 1961. Of those, only about 12 are known to be active blood donors.
Why It’s Called Golden Blood
Golden blood has nothing to do with color. The nickname comes from its extraordinary value in transfusion medicine. Formally known as Rh-null, this blood type completely lacks all Rh antigens on the surface of red blood cells. Most people are familiar with the “positive” or “negative” label attached to their blood type (A+, O-, etc.), which refers to just one of these Rh antigens, called D. Rh-null blood is missing not only D but every single one of the more than 60 proteins in the Rh group.
That total absence makes Rh-null blood potentially compatible with anyone who has rare blood types within the Rh system. For patients with unusual Rh profiles who would react to standard transfusions, golden blood can be lifesaving. The catch is obvious: with roughly 12 active donors on the planet, the supply is almost nonexistent.
What Causes It
Golden blood is a genetic accident that requires a very specific set of mutations, inherited in an autosomal recessive pattern. That means both parents must carry the relevant gene variant, and even then, only one in four of their children would be expected to have Rh-null blood. Most confirmed cases trace back to families where the parents are blood relatives, which increases the odds of both carrying the same rare mutation.
There are two known genetic routes to the Rh-null phenotype. In the “amorph” type, mutations silence the genes that produce Rh proteins directly. These genes sit on chromosome 1, and both the RHD and RHCE genes must be knocked out. Since many people already naturally lack a working RHD gene (this is what makes someone “Rh-negative”), the amorph type typically arises when someone who is already D-negative also inherits mutations that disable the RHCE gene. Documented cases include families in Germany, Brazil, and other countries where researchers pinpointed specific deletions or splice-site errors in RHCE.
The second route, called the “regulator” type, involves mutations in a separate gene called RHAG that acts as a helper protein. When RHAG is broken, the Rh proteins can’t assemble on the cell surface even if the genes encoding them are intact. A 2024 case report from China described exactly this mechanism.
Health Effects of Having No Rh Antigens
Golden blood isn’t just rare. It comes with real health consequences. Rh proteins help maintain the structural integrity of red blood cells, so without them, the cells become misshapen and fragile. They break down faster than normal, leading to mild hemolytic anemia in most cases. The red blood cells may appear abnormally shaped under a microscope, with variations in size and a characteristic mouth-like indentation called stomatocytosis.
Because the red blood cells have shorter lifespans, the body works harder to replace them. This can cause an enlarged spleen and liver, mild jaundice, and elevated counts of immature red blood cells in the bloodstream. For most people with golden blood, the anemia stays mild enough that it doesn’t require treatment, but it’s a lifelong condition. Some cases identified during pregnancy have been associated with complications including restricted fetal growth.
The Transfusion Dilemma
People with Rh-null blood face a serious medical paradox. Their blood can help others with rare Rh types, but they themselves can only safely receive blood from another Rh-null person. If they’re transfused with standard blood carrying any Rh antigens, their immune system may produce antibodies against those proteins, triggering a dangerous transfusion reaction.
With fewer than a dozen active donors worldwide, this creates a precarious situation. Some Rh-null individuals bank their own blood in advance in case they ever need surgery or emergency care. International rare donor registries exist to coordinate across borders, but the logistics of locating, shipping, and using such an extraordinarily scarce resource are daunting. A single unit of frozen Rh-null blood might need to travel across continents to reach the patient who needs it.
Why So Few Cases Are Known
The first case was identified in 1961 in an Indigenous Australian woman. In the six decades since, only about 43 people have been documented. That number almost certainly undercounts the true prevalence. Rh-null blood is typically discovered by accident, during routine blood typing for a transfusion, pregnancy screening, or a medical workup for unexplained anemia. In regions without advanced blood bank testing, someone with golden blood might never be identified.
The genetics also work against detection. Because the trait is recessive, carriers show no signs of it. Two carriers could have children with perfectly normal blood types and never know they harbor the mutation. Only when two carriers happen to have a child together, and that child inherits both copies, does Rh-null blood appear. Given how rare each individual mutation is, the odds of two carriers meeting are vanishingly small outside of communities with higher rates of intermarriage among relatives.
As genetic testing becomes cheaper and blood banking technology spreads to more countries, more cases will likely surface. China, for instance, had fewer than five documented cases as of 2024, in a population of 1.4 billion. The true global number of living people with Rh-null blood is unknown, but it remains one of the rarest known human traits.