Race-Based Medicine in the Modern Era: Historical Practice, Current Evidence, and the Pharmacist’s Role

The human genome is 99.9% identical from person to person, with only 0.1% of genetic code accounting for the vast array of human phenotypes and disease states.¹ Despite race not being encoded within this 0.1% and the fact that most of human genetic variance occurs within populations rather than between racial groups, medicine has nevertheless treated race as a primary biological differentiator.² This reliance has embedded race into diagnostic algorithms, clinical calculators, prescribing guidance, and medical devices.³

The initial integration of race into clinical practice was predicated on population averages and historical assumptions that fail to isolate race from the confounding effects of social, economic, and political factors.³ Consequently, using race as a biological marker has been fundamentally challenged, leading to a pivotal shift in multiple areas of medicine.⁴ As modern guidelines move toward race-neutral frameworks and biologically specific alternatives, such as pharmacogenetics and individualized risk assessment, the traditional race-based shortcut is being dismantled.⁵ This article examines how race entered clinical medicine, which practices have been recently revised, and the implications of this evolving evidence base for the modern pharmacist.

Historical Origins of Race-Based Medicine

To understand how race became embedded in modern clinical practice, it is necessary to examine where these ideas started and how they evolved over time. In the US, race-based medicine began with slavery-era pseudoscience used to normalize the idea that Black people were biologically distinct to justify mistreatment.⁶ These beliefs were formalized by US medical schools throughout the 18th and 19th centuries. Physicians, philosophers, and scientists helped institutionalize stereotypes, including claims that Black individuals felt less pain, possessed thicker skin, and had distinct anatomic norms, which were treated as a biological fact rather than as social constructs.⁶

With this framework set, the idea of biological distinctness became quantified through medical technology. In the 1840s, physician Samuel Cartwright used the spirometer to argue that Black people had inherently lower lung capacity, helping establish a race correction in pulmonary testing and setting the stage for similar assumptions in other areas of medicine.⁷

By the 20th century, these assumptions were reinforced by eugenics and social Darwinist thinking, ultimately translating into clinical practice. This historical trajectory established White male physiology as the universal baseline and categorized any deviation from that standard as a racial difference.⁶

Race in Diagnostic Algorithms

One of the clearest examples of race-based medicine is the development of the estimated glomerular filtration rate (eGFR). The eGFR uses serum creatinine as a convenient surrogate for estimating kidney function indirectly.³ From the earliest equations, patients identified as Black were assigned a race coefficient that increased the eGFR compared with non-Black patients with the same clinical variables.³ The rationale for this was that Black patients were assumed to have greater muscle mass and, therefore, release more creatinine into their blood at baseline.

The primary issue with using race rather than individual body composition is that it may make kidney function appear more normal than it is. For the patients, this can delay a chronic kidney disease (CKD) diagnosis, referral to nephrology, and evaluation for a transplant in patients with advanced kidney disease. For the pharmacist, there is an added safety concern with overestimating renal clearance based on an inflated GFR. This increases the risk of administering dangerously high doses of medications with low therapeutic indexes or that require renal adjustments. Black patients already experience a disproportionately higher rate of kidney disease and mortality, so race-based eGFR equations may have exacerbated existing disparities by masking the severity of disease.³

Consequently, the clinical guidance has made some significant corrections. The Kidney Disease – Improving Global Outcomes (KDIGO) 2024 Clinical Practice Guidelines now explicitly state that “Race, which is not a biological variable but a social construct, should not be included as a covariate in an eGFR equation.”⁸ The guidelines advocate for the best-fitting validated equation within geographical regions rather than any universal formula. Furthermore, there is increasing promise in the creatinine-cystatin C equations in cases where more precision is needed for clinical decision-making, drug dosing, or when creatinine alone may be unreliable, such as in individuals with extremes of muscle mass.⁸

Medical Devices and Measurement Bias

Unfortunately, the issue of race has not only become ingrained in diagnostic algorithms but also in the devices used today. Pulse oximetry is just 1 example. Arterial blood gas testing remains the gold standard for confirming oxygenation levels in patients, but pulse oximetry is the universal tool used for rapid triage and for monitoring oxygen needs in real time. Clinicians and pharmacists have relied on these devices to guide oxygen therapy and assess respiratory stability, operating under the assumption that the technology was universally accurate.⁹

However, in a 2020 study, Sjoding et al. compared pulse oximetry readings with arterial blood gas measurements and found that Black patients experienced occult hypoxemia at a rate nearly 3 times higher than White patients. Specifically, an arterial saturation of below 88% was found in 11.7% of Black patients versus 3.6% of White patients when pulse oximeter readings were 92% to 96%.⁹

The reason for this is within the device’s engineering. The pulse oximeter uses light wavelengths to estimate oxygen saturation by measuring how light is absorbed by hemoglobin. Because it was developed and validated primarily in homogeneous, lighter-skinned populations, the pulse oximeter fails to account for how higher levels of melanin absorb light.¹⁰ Unlike eGFR, where race was explicitly built into the calculation, pulse oximetry illustrates how bias can arise from the failure to validate medical technology across the wide array of human phenotypes, creating a dangerous bias. This creates a critical safety gap in which the hardware itself produces racially biased results, potentially leading to delayed interventions and under-treatment in patients with darker skin tones.

Race-Based Clinical Algorithms and Risk Calculators

Numerous clinical calculators are used for risk stratification in clinical practice. However, many include race as a variable in their equation. The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) pooled cohort equation (PCE), derived from 5 community-based cohorts, is the most prominent example of race-based cardiovascular risk prediction.¹¹ The calculator classifies race as Black or White along with cholesterol, blood pressure, diabetes, and smoking to project 10-year risk of developing atherosclerotic cardiovascular disease (ASCVD).¹² A clinical vignette example provided in Appendix 7 of the 2013 ACC/AHA guideline demonstrates how entering identical patient risk factor profiles yields a predicted 10-year ASCVD risk of 2.1% in a White female vs. 3.0% in a Black female, and 5.3% in a White male vs. 6.1% in a Black male.¹²

Another study sought out to quantify the magnitude of the risk difference that the PCE race variable alone produces when all other clinical inputs are held constant. The investigators created a comprehensive set of simulated patient profiles by combining all plausible combinations of the PCE input variables. The PCEs systematically assigned higher risk to Black individuals across the vast majority of identical risk profiles.¹³ The maximum risk differential was 22.8% for men and 26.8% for women, meaning that for certain risk factor combinations, a Black individual was assigned a 10-year risk more than 20 percentage points higher than a White individual with the exact same clinical profile.¹³ This implies that treatment and clinical recommendations could be based on race-related variations leading to a race-based approach. The researchers recommend that a cardiovascular risk calculator be developed that instead incorporates social determinants of health as opposed to race.¹³

In 2024, study findings published in the Journal of the American College of Cardiology and done by researchers at Mayo Clinic evaluated whether self-identified race independently contributed to coronary heart disease (CHD) risk after accounting for traditional clinical risk factors, polygenic risk scores, and a composite measure of social determinants of health (SDOH-CHD). Initially, individuals self-identifying as Black demonstrated higher odds of CHD, and the association remained after adjustment for conventional cardiovascular risk factors and genetic predisposition. However, after incorporating social determinants of health into the analysis, the association was no longer statistically significant.¹⁴ These findings suggest that racial differences observed in cardiovascular risk models may reflect the cumulative effects of social and structural inequities rather than biological variation. This study highlights that if social determinants are accounted for, racial disparities disappear.

The AHA PREVENT equations, published in 2023, represent a significant shift toward race-neutral cardiovascular risk prediction. Major differences in this equation, when compared to the PCEs, are the exclusion of race and the addition of a social deprivation index, which measures structural disadvantage versus race.¹⁵ Although race-neutral alternatives exist, the PCEs remain widely used in clinical practice. Delays in translating evidence into routine care may contribute to this continued reliance, as prior research has estimated an average lag of 17 years between the generation of evidence and widespread clinical implementation.¹⁶

Race-Based Medication Recommendations

One of the clearest historical examples of race-based prescribing in pharmacotherapy is hypertension treatment. Earlier hypertension guidelines explicitly separated initial drug therapy by race, recommending thiazide diuretics or calcium channel blockers as preferred first-line agents in Black adults with hypertension, as opposed to all other races standardly being prescribed angiotensin-converting enzyme inhibitors (ACE-I) as a first-line treatment option. The 2014 Joint National Committee-8 guideline recommended that Black adults with hypertension, including those with diabetes, begin treatment with a thiazide-type diuretic or calcium channel blocker.¹⁷ Similarly, the 2017 ACC/AHA hypertension guideline stated that Black adults with hypertension but without heart failure or CKD should receive initial therapy with a thiazide-type diuretic or calcium channel blocker.¹⁸

These recommendations were largely derived from population-level observations suggesting differences in average blood pressure response and renin physiology among groups of patients.¹⁹ However, race is not a biological mechanism, and it does not directly measure renin activity, endothelial dysfunction, sodium sensitivity, pharmacokinetic variability, or pharmacogenomic differences. As a result, race-based prescribing frameworks often functioned as approximations of underlying biology rather than precise assessments of individual physiology.

The evolution of hypertension guidelines reflects a broader transition occurring throughout medicine. More recent approaches increasingly emphasize individualized treatment selection based on comorbid conditions, cardiovascular risk, CKD, and patient-specific clinical factors rather than race alone. This shift is also reflected in newer cardiovascular risk assessment models. The AHA PREVENT equations removed race as a predictive variable, citing the importance of directly measured health variables and social determinants rather than broad racial categories.²⁰

Importantly, this transition does not mean that earlier clinical observations were entirely incorrect. Rather, it reflects recognition that race is a heterogeneous and imprecise category and variation within racial groups often exceeds differences between them. Medication response is ultimately influenced by a complex interaction of genetics, environment, socioeconomic factors, diet, access to care, and comorbid disease states rather than race alone.²¹

In modern clinical practice, medication selection should therefore prioritize clinically meaningful variables, including CKD, heart failure, diabetes, renal function, overall cardiovascular risk, pharmacogenomic considerations, and patient-specific preferences. Pharmacists play an important role in ensuring that therapeutic decisions are guided by individualized risk assessment rather than race-based assumptions that may oversimplify patient care.

The movement away from race-based prescribing is also consistent with broader changes in medicine. The 2024 KDIGO CKD guidelines explicitly recommend avoiding the use of race in eGFR computation, reinforcing the health care system’s transition toward individualized and biologically grounded decision-making.²² Emerging approaches such as pharmacogenomics, biomarker-guided therapy, and precision medicine may provide more accurate methods of predicting therapeutic response than race-based clinical decision-making.

Ultimately, race-based medication recommendations historically represented attempts to simplify complex biology using population-level trends. Modern medicine is increasingly shifting toward directly measuring the factors that truly influence therapeutic response. For clinicians, this represents an important transition from pattern-based prescribing and dispensing to mechanism-based and patient-centered care.

Race-Specific Drug Approvals

The combination of isosorbide dinitrate and hydralazine (BiDil, Azurity) remains the most widely recognized example of a race-specific drug approval in the United States. The FDA labeling states that it is indicated for the treatment of heart failure as an adjunct to standard therapy in self-identified Black patients to improve survival, prolong time to hospitalization, and improve functional status.²³ The approval was based primarily on the African-American Heart Failure Trial (A-HeFT), which demonstrated significant reductions in mortality and hospitalizations among Black patients receiving fixed-dose isosorbide dinitrate and hydralazine in addition to standard heart failure therapy.²⁴

Although the A-HeFT trial demonstrated meaningful clinical benefit in the studied population, the findings also highlight a broader conceptual challenge within modern medicine. The trial established efficacy in the enrolled patient population, but it did not prove that race itself was the biological mechanism responsible for treatment response. Because the study enrolled only self-identified Black patients, the results are best interpreted as population-specific rather than evidence that race is an intrinsic biologic determinant of therapeutic efficacy.

This distinction is important because race does not directly measure nitric oxide bioavailability, endothelial dysfunction, pharmacogenomic variation, or other biologic mechanisms potentially influencing drug response. Race-specific approvals may therefore oversimplify the relationship between genetics, environment, and pharmacotherapy by treating race as a surrogate marker for biology.

Race-specific drug approvals also raise several additional concerns. First, they may unintentionally restrict therapy in patients outside the labeled population who could potentially benefit from treatment. Second, regulatory labeling frequently evolves more slowly than scientific understanding, creating a disconnect between modern evidence and historical approval language. Finally, race-specific labeling may reinforce misconceptions that racial categories represent fixed biological divisions rather than socially defined classifications with substantial internal genetic diversity.

Similar patterns have appeared in other therapeutic areas. For example, carbamazepine-associated Stevens-Johnson syndrome was initially associated broadly with Asian ancestry but was later linked more specifically to the HLA-B1502 allele.²⁵ Likewise, severe allopurinol hypersensitivity reactions have been associated with HLA-B5801, and variability in clopidogrel response has been linked to the CYP2C19 genotype. In each case, race initially functioned as a rough proxy for observed differences in treatment response or adverse event risk. As the underlying biologic mechanisms became clearer, clinical decision-making shifted toward genotype-guided approaches rather than race-based assumptions.

These examples illustrate the broader movement toward precision medicine. Instead of asking which medication works best for a particular racial group, clinicians are increasingly focused on identifying which therapy is most appropriate for an individual patient’s biology, genetics, and clinical characteristics. Pharmacogenomics represents one of the clearest examples of this transition, allowing clinicians to directly evaluate drug metabolism and adverse effect risk rather than inferring risk from ancestry or race alone.

Pharmacists play a particularly important role in this evolving landscape. As medication experts, pharmacists are positioned to interpret pharmacogenomic data, evaluate the evidence underlying race-specific recommendations, educate clinicians and patients, and advocate for individualized approaches to therapy. This includes recognizing the limitations of race-based labeling while still appropriately interpreting evidence derived from population-specific clinical trials.

Rather than viewing BiDil strictly as a “race-based drug,” it may be more accurate to view it as a therapy proven effective within a specific studied population, while acknowledging that race itself may not represent the true biologic determinant of response. As medicine continues to evolve, race-based frameworks are increasingly being replaced by approaches centered on genetics, biomarkers, and individualized risk assessment. The goal moving forward is not to disregard historical evidence, but rather to reinterpret that evidence through a more precise and biologically informed lens.

Race vs Genetics: The Rise of Precision Medicine

Race has historically been used as an indicator for differences in drug metabolism, efficacy, and adverse reactions. However, it remains an imprecise marker for genetic variation. Although pharmacogenomic variants associated with medication response differ in prevalence across genetic ancestry groups, these variants do not align neatly with socially defined racial categories.²⁶ A comprehensive analysis of pharmacogenomic variation within the US All of Us cohort and the UK Biobank demonstrated that while pharmacogenomic profiles predicted self-identified race and ethnicity with relatively high accuracy, performance declined substantially among individuals identifying with more than 1 racial group, illustrating the limitations of race as a marker for genetics in increasingly admixed populations.²⁷

Genetic variation is estimated to account for approximately 15% to 30% of interindividual differences in medication response, highlighting the growing value of pharmacogenomics as a more precise alternative to race-based prescribing.²⁸ Several well-characterized drug–gene interactions further demonstrate this distinction. As previously mentioned, the HLA-B15:02 allele, found most among individuals of Southeast and East Asian ancestry, is strongly associated with carbamazepine-induced Stevens–Johnson syndrome and toxic epidermal necrolysis. As a result, the FDA recommends genotype-based screening prior to treatment rather than relying on racial or ethnic categorization alone. Similarly, CYP2C19 loss-of-function variants reduce activation of clopidogrel, and a 2024 meta-analysis demonstrated that genotype-guided antiplatelet therapy reduced major adverse cardiovascular events among patients undergoing percutaneous coronary intervention.²⁹ In each of these examples, the clinically significant factor is the presence of a specific genetic variant rather than the patient’s racial identity. Reliance on race-based assumptions risks both overestimating risks in some patients and overlooking clinically relevant variants in others.

As precision medicine advances, clinical decision-making is increasingly moving away from population-based assumptions and toward individualized genetic assessment. Rather than estimating risk based on racial identity, pharmacogenomics enables clinicians to identify clinically relevant genetic variants directly without overgeneralizing an entire racial group. A 2025 policy statement from AHA emphasized the expanding role of pharmacogenomic testing and noted that a single evaluation may help guide medication selection across a patient’s lifetime, while also acknowledging ongoing barriers such as limited clinician training and insufficient representation of diverse populations in genomic research.³⁰ Notably, some investigators argue that race should not be entirely discarded when genotyping is unavailable, as it may serve as a temporary bridge for pharmacogenomic risk stratification, particularly for Black and Hispanic patients who stand to gain the most from population-informed prescribing.³¹ However, this perspective largely supports the broader transition toward individualized care, as the clinical value of race-based approximations diminishes when direct genotyping is accessible.

Implications for Pharmacists

As medicine transitions away from race-based frameworks and toward individualized approaches to care, pharmacists play a critical role in translating evolving evidence into clinical practice. Pharmacists frequently serve at the intersection of medication selection, guideline interpretation, patient education, and interprofessional collaboration, positioning them uniquely to recognize where outdated race-based assumptions may still influence treatment decisions.

One of the most immediate implications involves interpretation and implementation of clinical guidelines. Several historical treatment recommendations incorporated race into prescribing decisions, particularly in areas such as hypertension and cardiovascular risk prediction. However, newer models increasingly prioritize patient-specific factors, including comorbid conditions, renal function, cardiovascular risk, and pharmacogenomic variability, rather than race alone. Pharmacists must therefore remain aware of evolving guidance and ensure that medication decisions reflect current evidence rather than outdated prescribing patterns.

Medication selection represents another important area of pharmacist involvement. Rather than relying on race as a surrogate for therapeutic response, pharmacists should focus on clinically relevant variables such as kidney function, drug-drug interactions, pharmacodynamic considerations, adverse effect profiles, adherence barriers, and patient preferences. This individualized approach helps avoid oversimplification of patient care while improving both medication safety and efficacy.

Changes in kidney disease management further illustrate the pharmacist’s evolving role. Historically, race-adjusted eGFR equations influenced CKD staging, nephrology referrals, and medication dosing decisions.³² The removal of race from eGFR calculations may alter dosing thresholds for renally cleared medications, requiring pharmacists to reassess therapeutic regimens and monitor for changes in efficacy or toxicity during implementation of race-neutral equations.

Pharmacogenomics also represents a major area of opportunity for pharmacists. The increasing availability of genetic testing allows clinicians to directly evaluate biologic factors influencing medication metabolism and adverse event risk rather than relying on race-based assumptions. Pharmacists are well positioned to interpret pharmacogenomic results, recommend appropriate testing, and integrate genotype-guided therapy into clinical decision-making. This shift reflects the broader movement toward precision medicine and individualized pharmacotherapy.

Education remains another central responsibility for pharmacists. Pharmacists frequently educate clinicians, students, trainees, and patients regarding evidence-based pharmacotherapy and evolving clinical guidance. In the context of race-based medicine, pharmacists can help clarify the distinction between race as a social construct and genetics as a biologic determinant, while also promoting more nuanced and individualized approaches to treatment decisions.

Ultimately, the movement away from race-based medicine does not eliminate the need for clinical judgment; rather, it requires a more precise application of that judgment. Pharmacists must critically evaluate the evidence underlying historical prescribing practices, recognize the limitations of race-based frameworks, and advocate for patient-centered approaches grounded in biology, clinical context, and individualized risk assessment. As health care continues to evolve, pharmacists will remain essential in helping translate precision medicine into everyday clinical practice.

The Current Moment: Medicine in Transition

Modern medicine is undergoing a broad transition away from race-based clinical decision-making. Across multiple specialties, professional organizations have increasingly adopted race-neutral frameworks in favor of approaches grounded in directly measured biologic and clinical variables. In nephrology, the National Kidney Foundation and American Society of Nephrology recommended in 2021 that US laboratories adopt the race-free CKD-EPI equation, a position reinforced by the 2024 KDIGO guidelines, which explicitly discourage inclusion of race in eGFR estimation.^8,33 Similarly, pulmonary medicine has shifted toward race-neutral spirometry reference equations, with the American Thoracic Society and European Respiratory Society recommending replacement of race-adjusted models with the Global Lung Function Initiative equations, a position further reinforced in the 2026 GOLD guidelines for chronic obstructive pulmonary disease.^34,35 In cardiovascular medicine, the AHA PREVENT equations intentionally excluded race from cardiovascular risk prediction and have increasingly replaced the race-based pooled cohort equations in contemporary guideline recommendations.¹⁵

Despite this progress, elements of race-based medicine remain embedded within clinical practice. The pooled cohort equations continue to be incorporated into many electronic health record systems and prescribing workflows despite the emergence of race-neutral alternatives.¹¹ BiDil also remains the only FDA-approved race-specific medication, reflecting the continued influence of historical population-based frameworks on contemporary therapeutics.³⁶ More broadly, recent analyses suggest that race and ethnicity continue to appear in numerous clinical risk calculators, prescribing recommendations, and device performance considerations across medicine.³⁷

Taken together, these developments reflect a broader shift toward individualized, biologically informed care. Increasing emphasis is being placed on genotype, biomarkers, comorbid disease states, social determinants of health, and environmental exposures rather than broad racial categories alone. However, implementation of these changes remains inconsistent, and the well-documented delay between emerging evidence and routine clinical adoption suggests that race-based frameworks may continue to influence patient care for years to come.¹⁶ The challenge moving forward is not solely the removal of race from clinical algorithms, but the development and equitable implementation of more precise alternatives that improve care without unintentionally reinforcing existing disparities.

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