In medical terms, race is classified as a social construct, not a biological one. The National Human Genome Research Institute states that the vast majority of genetic variation exists within racial groups, not between them. This distinction matters because medicine has historically treated race as if it were a reliable stand-in for biology, genetics, or ancestry, and that practice is now being actively reconsidered across nearly every medical specialty.
Why Race Is Not a Biological Category
Race as we use it in everyday life is a system of categories based on physical appearance, historical context, and social identity. It groups billions of people into a handful of broad labels. Genetic ancestry, by contrast, traces the specific geographic populations your DNA comes from and can be mapped using millions of genetic markers. These two things overlap loosely, but they are not the same.
A person who checks “Black” on a medical form might have ancestors from West Africa, East Africa, the Caribbean, or Europe in varying proportions. A person who checks “White” might carry genetic variants more commonly found in Middle Eastern or North African populations. The broad racial categories used in medicine are far less precise than actual ancestry data, and that imprecision can lead to misdiagnosis. Race is often self-reported or even assigned by hospital staff based on appearance, which introduces another layer of inaccuracy.
How Medicine Has Used Race (and Why That’s Changing)
For decades, race was built directly into clinical tools. Kidney function, for example, was estimated using an equation that included a coefficient for Black patients, producing a different result solely based on race. Lung function tests used race-specific reference ranges that set different thresholds for “normal” breathing capacity depending on a patient’s racial category. Cardiovascular risk calculators like the widely used ASCVD tool included race alongside blood pressure and cholesterol as if it were an equivalent biological variable.
These adjustments were based on observed statistical differences between racial groups, but they didn’t account for why those differences existed. In many cases, the underlying causes were environmental: chronic stress, air pollution, neighborhood poverty, limited access to healthy food, or disparities in healthcare itself. Baking race into a formula treated the downstream effects of inequality as though they were innate biological traits.
In 2020, the American Medical Association passed three landmark policies. They formally denounced racism as a public health threat, called for eliminating race as a proxy for genetics, ancestry, or biology in medical education, research, and clinical practice, and rejected what’s known as racial essentialism, the idea that racial categories reflect fundamental biological differences.
Kidney Function Tests: A Case Study
The clearest example of this shift involves estimated glomerular filtration rate, or eGFR, the standard measure of how well your kidneys filter waste. The old formula added a race coefficient for Black patients that made their kidney function appear better than it might actually be. This meant some Black patients were less likely to be diagnosed with kidney disease, less likely to be referred to specialists, and less likely to be placed on transplant waiting lists.
In 2021, the National Kidney Foundation and the American Society of Nephrology recommended immediate adoption of a new equation that removes the race coefficient entirely. Research published in the New England Journal of Medicine found that when Latino patients initially classified as having stage 3 chronic kidney disease were reclassified using ancestry-based data instead of race, about 10% were moved to the less severe stage 2, and their lab values matched the new classification more accurately.
Lung Function and Heart Risk Calculators
Pulmonary function testing has undergone a similar reckoning. The Global Lung Function Initiative developed race-neutral reference equations to replace the older race-specific ones. Under the previous system, a Black patient could have measurably reduced lung capacity but still be classified as “normal” because the reference range assumed lower lung function was a baseline biological trait rather than a potential sign of disease.
Cardiovascular risk calculators are also under scrutiny. The ASCVD tool, used by millions of clinicians to estimate heart attack and stroke risk, includes race as an input variable alongside cholesterol and blood pressure. Critics point out that the tool offers only limited racial categories, excludes large portions of the global population, and reinforces the false idea that race functions like a biological measurement. The American College of Cardiology and American Heart Association have been urged to formally remove race from the tool.
Sickle Cell Disease and the Geography Problem
Sickle cell disease is often described as a “Black disease” in medical education, but the genetics tell a different story. The sickle cell trait evolved as a defense against malaria. It’s most common in people whose ancestors come from regions where malaria was endemic: West Africa, parts of the Mediterranean, the Middle East, and India. A significant portion of Black Americans have ancestors from West Africa due to the transatlantic slave trade, which is why sickle cell rates are higher in Black Americans. But the link is to geography, not to skin color.
Framing sickle cell as a racial disease creates blind spots. Clinicians may not consider sickle cell in a patient of Middle Eastern or South Asian descent, even though the trait exists in those populations too. Roughly 300,000 children are born with sickle cell syndromes worldwide each year, with newborn prevalence ranging from 0.1 per 1,000 in non-endemic countries to 20 per 1,000 in parts of Africa. In European sickle cell cohorts, 73% of patients traced their ancestry to West Africa, but 10% were of European descent and 8% Caribbean. Using race as a shortcut misses this complexity.
Genetic Ancestry vs. Race in Drug Response
How your body processes medication depends heavily on enzymes in your liver, particularly a family of enzymes responsible for metabolizing roughly 70% to 80% of all drugs in clinical use. Genetic variants in these enzymes differ across populations, which means two people can take the same dose of a medication and have vastly different responses. One person might metabolize a drug so quickly it never reaches effective levels; another might metabolize it so slowly that a standard dose becomes toxic.
These enzyme variants do cluster by geographic ancestry, but they don’t map neatly onto racial categories. Research on one of the most studied drug-metabolizing enzymes found no significant geographic structuring of risk variants, meaning the dangerous variants weren’t confined to any single continental population. Other enzymes show clearer patterns across regions, but even then, the variation within any given continent is substantial. East Asian and South Asian populations, for example, show different drug reaction profiles for medications like certain anti-seizure drugs and blood thinners, but lumping all “Asian” populations together, as racial categories do, obscures these clinically important differences.
Compounding the problem, most pharmacogenomic research has been conducted in populations of European ancestry. This means genetic risk scores and dosing guidelines work best for people of European descent and become less accurate for everyone else. The result is a system that inadvertently prioritizes drug safety for one group while leaving others more exposed to adverse reactions.
What Race Actually Captures in Health Data
If race doesn’t reflect biology, why do health outcomes differ so starkly across racial groups? Because race is a powerful marker for exposure to structural disadvantage. The American Heart Association has identified structural racism as a fundamental driver of health disparities, operating through specific mechanisms: chronic discrimination triggers sustained activation of the body’s stress response, a phenomenon researchers call weathering. Over years, this chronic stress accelerates biological aging and increases the risk of heart disease, diabetes, and other conditions.
Many of the factors that determine health, including income, food availability, housing quality, and air pollution exposure, are closely tied to race in the United States because of decades of discriminatory policies in housing, employment, and education. These are real, measurable forces that produce real health consequences. But they are social and environmental in origin, not genetic.
The emerging consensus in medicine is that race should be understood as a risk marker, not a risk factor. It signals that a patient may face higher exposure to discrimination, environmental hazards, or barriers to care. It does not signal that their body is inherently different. This distinction shapes how a growing number of clinicians interpret the patterns they see in health data and how medical schools are beginning to train the next generation of doctors.