In multiple medical textbooks (such as Robbins and Cotran) and popular health reference websites (such as Medscape, WebMD, UpToDate), I have seen race as a risk factor in disease and pathology, particularly among Black and Hispanic/Latinx communities. Whether it’s hypertension, kidney failure, interstitial lung disease, asthma, diabetes, and more…the medical community has cemented one’s race as a biological destiny and of inherent biological danger. This framing misses the point: Racism, not race, is a risk factor.
—Third-year medical student
The concept of race has no biological basis. Racism, not race, has been and continues to be a key determinant of health outcomes, especially in the United States. Research that falsely biologizes race dates back to colonialization and slavery, and contemporarily translates to poor clinical guidelines. And yet, medicine continues to uphold the idea of biological race—and, thus, racism—in diagnosis and treatment schema.
What does this look like in context? Clinicians will use a patient’s skin color and ethnicity as heuristics to determine their diagnosis and treatment plan. In fact, race serves as a shortcut for clinical thinking from the onset of training, as evidenced in the United States Medical Licensing Examination.
A study question tweeted by the American College of Obstetricians and Gynecologist (@ACOGAction) reads,
A 33-year-old married African American woman comes to your office and admits to thoughts of suicide for the last month. She was previously diagnosed with bipolar disorder, but has never attempted suicide before. Which of the following characteristics is associated with an elevated epidemiological risk for suicide? The listed options are A. Age < 35, B. Bipolar disorder, C. Lower socioeconomic status, D. Being married, and E. Black race.”68
Although the correct answer, according to the ACOG, is B. Bipolar disorder, question writers likely included “Black race” as an option because they thought test takers would rely on the pervasive, yet false, assumption that race is an epidemiological risk factor for various pathologies.
Another test prep resource offers the following on sickle cell anemia:
Sickle cell disease (SCD) is a multisystem disorder and the most common genetic disease in the United States, affecting 1 in 500 African Americans.69
Robbins and Cotran Pathologic Basis of Disease, one of the foremost pathology textbooks for medical students nationwide, offers this epidemiologic look at sickle cell disease:
About 8% to 10% of African Americans, or roughly 2 million individuals, are heterozygous for HbS….There are about 70,000 individuals with sickle cell disease in the United States. In certain populations in Africa the prevalence of heterozygosity is as high as 30%.70
Both sources pathologize—and racialize—African Americans as the only potential population for sickle cell anemia. This risks missing diagnoses in other populations or oversimplifying clinical reasoning for African Americans.
Yet another test prep blog offers this summation:
Board questions reflect an extremely judgmental worldview with heavy-handed generalizations about race, sex, and a wide variety of stereotypes. African American females in their 30-40s have sarcoidosis.71
Race is thus used as a tool to expedite not only test questions but also diagnostic processes. Frankly, this shortcut can be dangerous and inaccurate. For test questions, this enforces racial bias that may be present or introduces new ones.72 This translates directly to clinical care, where a patient’s race is seen as a risk factor for disease and requires that providers associate certain illnesses with certain races. As such, providers may never inquire into the root causes of illness for a person experiencing racism and inequality (such as structural and social determinants of health) or may miss more complicated and nuanced diagnoses. Furthermore, they may overlook diseases in patients of races and ethnicities that are not traditionally associated as “risk factors.” For example, sickle cell is thought of exclusively as a Black(-only) disease and thalassemia as a Mediterranean(-only) disease. Cystic fibrosis is underdiagnosed in populations of African ancestry because it is thought of as a white disease.73
In the following section, we provide examples of how health care and biomedical research conflate race with biology. We discuss the racist underpinnings of the diagnosis and treatment of heart, kidney, and lung disease. We also explore faulty science that reifies biological race within precision medicine. If medicine is to help alleviate racial health disparities, we need to eliminate these embedded heuristics and false assumptions while addressing social and structural determinants of health.
One day in clinic, my preceptor asked me to counsel a patient on cardiovascular disease risk and prevention, using the Atherosclerotic Cardiovascular Disease Risk Estimator provided by the American College of Cardiology. I spun the computer screen around and filled it out with him. Age, sex, then suddenly “race,” and the only options were “white,” “African American,” and “other.” I was confused. Even he was confused. “Why is this relevant?” he asked me. “And as a Spanish-speaking immigrant,” he went on, “what would I be?”
—First-year medical student
Black people disproportionately experience cardiovascular disease in the United States.74 Research on allostatic load and stress finds discrimination—resulting from internalized, interpersonal, institutional, and structural racism—to be an arbiter for poor cardiac health among Black people in the United States.75 Health disparities are consistent across multiple outcomes known to be markers for cardiovascular disease: hypertension, subclinical carotid disease, coronary artery calcification, coronary artery obstruction, elevated cholesterol, visceral abdominal fat deposits, and increased C-reactive protein.76
However, despite this research, clinical guidelines for diagnosis and treatment of cardiac disease do not take discrimination or structural factors into account. Instead, they attribute the cause of disproportionate outcomes to one’s race alone. For example, the following guideline is from the Eighth Joint National Committee, which sets national recommendations on treatment thresholds, goals, and medications in the management of hypertension in adults: “Initial antihypertensive treatment should include a thiazide diuretic, calcium channel blocker, ACE inhibitor, or ARB in the general nonblack population or a thiazide diuretic or calcium channel blocker in the general black population.”77 Furthermore, angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers are recommended as first-line agents only in Black people with comorbid chronic kidney disease.78
Here, Black or African American racial identity is treated as a proxy or a unique numeric variable for diagnostic equations and treatment indications. The use of Black racial identity as a proxy appears in claims ranging from increased “salt sensitivity” contributing to hypertension and the supposed need for specialized pharmaceutical treatments (e.g., BiDil). Use of racial identities as sole determinants of health outcomes frames Black people as having “inherently” poor cardiovascular health.
Framing racial disparities in cardiovascular disease as a product of the social category of race itself is harmful because it falsely attributes racial disparities to genetics and other underlying biological characteristics and it ignores the contributions of internal, interpersonal, institutional, and structural racism to these disparities.
Hypertension—Salt Sensitivity Hypothesis
Many clinical researchers and medical providers today are aware of the Black health disparities in hypertension, oftentimes with many thinking that such disparities are a result of genetic or biological predisposition. However, few clinicians are aware that these assumptions are erroneous and originated in misguided assertions of the “African gene” hypothesis, in which Black people are more likely to have salt sensitivity as a by-product of the slave trade.79 This assertion is further misguided as critical theorists have pointed out that no current or contemporary West African populations suffer rampant hypertension. Despite this, the American Heart Association website declares: “Researchers have also found that there may be a gene that makes African Americans much more salt sensitive.”
On Medscape and WebMD, two popular publishers of medical information for the general public, cursory searches on the intersections of salt sensitivity and Black race argue that “high rates of high blood pressure in African Americans may be due to the genetic makeup of people of African descent. Researchers have uncovered some facts: In the United States, Blacks respond differently to high blood pressure drugs than do other groups of people.”80 Claims of biological racial differences in salt sensitivity have unclear origins. In a recent paper by Lujan and DiCarlo (2018), the authors note that “Wilson and Grim…published only a single peer-reviewed scientific paper on the Slavery Hypertension Hypothesis in 1991. As noted by Kaufman and Hall…the majority of the written work on the slavery hypertension hypothesis is limited to conference reports and nonreviewed abstracts and book chapters.”81
In 2005, media attention praising Harvard economist Ronald Fryer’s work on salt sensitivity began to influence clinical researchers of racial difference today. It was during this time when changes to clinical guidelines associating Black racial identity with salt sensitivity popularized in clinical medicine. In the seminal paper entitled “Racial Differences in Life Expectancy: The Impact of Salt, Slavery, and Selection,” Fryer et al. hypothesizes how specific factors in the slave trade experience could explain the hypertension disparities among Black people in the United States.82 They use a Darwinistic “bottleneck theory” of evolution, in other words claiming that the catastrophic population-wide effect of slavery led to the evolutionary selection of a trait that improved survival during the Atlantic Slave Trade. In making this claim, they cite data sources, such as precipitation data and historic images of “a slave trader licking a slave’s face to assess his fitness for the voyage across the Atlantic”:
As T. Buxton writes, “…nobody suffered more intensely from thirst than the poor little slaves, who were crying for water…Perspiration is one source of dehydration….”
In a setting of profuse water loss, the ability to retain salt and hence water substantially increased the chances of survival. Contemporary accounts indicate that at least some slave traders were aware of this, and selected slaves on the basis of the salt on their skin. Figure 2 captures a slave trader licking a slave’s face to assess his fitness for the voyage across the Atlantic. Most of the selection on the basis of salt sensitivity was likely unintentional, however. Salt depleting environments and diseases were ubiquitous throughout the slave trade, favoring individuals able to retain salt (33).83
Despite Fryer et al.’s false and limited arguments to support the slavery hypothesis, this work attracted popular media attention, such as forming the basis of the New York Times’ 2005 article, “To a Unified Theory of Black America.”84 In 2007, Dr. Oz appeared on the Oprah Winfrey Show and asked the audience, “Do you know why African Americans have high blood pressure?” to which Winfrey studiously replied, “African Americans who survived [the slave trade’s Middle Passage] were those who could hold more salt in their body,” with Dr. Oz’s enthusiastic agreement.85
With the widespread blind acceptance of the salt sensitivity hypothesis among clinicians, hypertension disparities faced by Black people are seen not as a consequence of stressful environments and situations caused by social and structural determinants but rather by false notions of biological differences in salt retention. As noted by critical race theory scholar Osagie Obasogie, perhaps the most important rebuttal to the hypothesized link of salt retention and racial difference is the fact that “no contemporary West African population suffers from rampant hypertension. Historical records suggest that Africans’ overall mortality during the Middle Passage was about 13 percent. For a bottleneck theory to hold up, the alleged ‘salt sensitive gene’ would have had to play a significant role for the roughly 87 percent that survived, implying that this gene was relatively common among enslaved West Africans.”86
False notions of salt sensitivity that are currently present in clinical medicine and practice will continue to inflict harm on Black communities, as such bad science deflects from attention to social, structural, and environmental stressors that are linked to susceptibility and exacerbation of hypertension.
The implications of the erroneous correlation of Black racial identity with hypertension have not only affected clinicians’ perception of disease and pathophysiology, but also treatment for Black people. In 2005, BiDil, a combination pill of two standard therapies—hydralazine and isosorbide dinitrate—for heart failure, became the first drug to receive approval from the US Food and Drug Administration (FDA) to treat a specific racial group—African Americans.87 However, the clinical development of BiDil was never intended for an explicitly racialized purpose—it was simply another drug to treat heart failure. In this section, we will reveal how the drug development of BiDil is an example of bad science and epidemiology. Moreover, we will explain how the development of BiDil predicated on the use of ideas of the biological inferiority of Black people in order to gain commercial and market success.
In the 1980s, cardiologist Jay Cohn led two clinical trials—V-HeFT 1 and V-HeFT II—to study the drug. The investigators of these trials, however, “did not build the trials around race or ethnicity. They enrolled both Black and white patients and in the published reports of the trials’ successes, they did not break down the data by race. Rather, they presented BiDil as generally efficacious in the population at large, without regard to race and filed a patent.”88 However, despite these assertions, the FDA rejected BiDil’s approval due to statistical design flaws in these trials in 1997.89
The FDA rejection did not restrict use of data from the V-HeFT trials. In an attempt to reconsider how to best market the drug to the FDA and public, Cohn, along with his coinvestigators, returned to the V-HeFT data and recategorized the results by race. There was no scientific reason for this reanalysis, for Cohn and his coinvestigators only turned to race after the initial application to market failed for commercial purposes. In 1999, nearly fifteen years after the first V-HeFT 1 data was collected, the investigators claimed they had discovered a race-based differential response to BiDil treatment.90 Then, Cohn “filed for and was granted a patent identical to the first one, except that the use was now for African Americans suffering from heart failure, which had the financial and commercial benefit of extending his patent rights an additional thirteen years.”91
A company named NitroMed gained the license for BiDil from Cohn and conducted a new clinical trial, the African American Heart Failure Trial (A-HeFT), in order to test BiDil’s race-specific benefit. However, this new trial only included participants that self-identified as African American and did not include a comparison group. Therefore, the trial could not have demonstrated that BiDil works better in African Americans than in any other group. As a result, this specious “reanalysis” opened the door for an epidemiologically flawed race-based trial. Despite this fundamental design flaw, the A-HeFT trial produced data “demonstrating a 43 percent reduction in mortality, leading the FDA to approve a race-specific indication for use by Blacks with heart failure.”92 Neither Cohn nor any of his collaborators have been able to identify the biological markers responsible for Blacks’ receptiveness to BiDil. Cohn himself states that the drug is effective in non-Black patients as well. The same year that BiDil gained FDA approval, Cohn admitted to prescribing the generic drugs constituting BiDil to 25 percent of his white patients.93 He directly stated, “I actually think everybody should be using it.”94
Ever since its FDA approval, BiDil has been widely prescribed in a race-specific manner, based on the prevailing yet unfounded assumption that “self-identified race mirrored some underlying ‘real’ biological difference that shapes health disparities and drug reaction.”95 As medical students, we are implicitly taught the same assumption through uncritical textbooks and precepting clinicians. A widely used pharmacology textbook directly states, “A fixed combination of hydralazine and isosorbide dinitrate is available as isosorbide dinitrate/hydralazine (BiDil), and this is currently recommended for use in African Americans.”96
The race specificity of BiDil is unsubstantiated and commercially motivated, yet “it has come to reflect the legal, regulatory, and economic sanctioning of race as a biologically significant category of human difference that meaningfully affects human health” [Obasogie]. This framing falsely leads social categories of race to be perceived as the causes of disease and for structural causes of disease being ignored. Critical race legal scholar Dorothy Roberts powerfully summarizes,
While the racial gap in life expectancy widens, owing largely to the government’s failure to address structural inequities, the poor health of African Americans opens new markets for pharmaceutical companies. The claim that race-based biotechnologies will shrink the gap based on genetic difference is a powerful way to deflect concerns about their unjust social impact and the social inequality that actually drives poor minority health. We should be against an approach that promotes individual health through technological cures as a way of ignoring larger social inequities. This view sets up a false dichotomy between health and social justice: it treats health and justice as opposing values, weighs them against each other, and declares health the winner. It hides the social factors that determine health not only for individuals but for the entire nation. Letting health trump social justice does not really improve the welfare of most people; it supports the interests of big business and the most privileged members of society.
The promotion of race-based medicine misrepresents the relationship between genes, drugs, and health disparities. Of course, pharmaceuticals can help improve sick people’s health, and effective pharmaceuticals should be available to people who would benefit from them. But health inequities are not caused by genes and cannot be eliminated with drugs. Promoting race-based medicine with the myth that poor minority health is caused by genetic difference will only widen the gap, diverting us from the real solution. It makes no sense to put aside social justice concerns in order to improve minority health. A more just society would be a healthier one.97
Kidney Disease and Glomerular Filtration Rates
A faculty nephrologist at our school was talking to us at an event about the issue of using race so visibly in GFR rates. She noted that when alternative corrections were suggested, like having physicians estimate muscle mass instead, other physicians “freaked out” and asked her how they could possibly accurately measure a person’s muscle mass “just by looking.” She asked us, “Why are we so much more comfortable assigning someone a race, and differentiating their treatment based on that, than we are about estimating muscle mass?” I realized how blind I’d been to all the times my preceptor and other providers I worked with were assigning race to patients and adjusting their care accordingly.
—Second-year medical student
National and international studies show racialized disparities in chronic kidney disease (CKD) and end-stage renal disease (ESRD), the terminal stage of CKD.Unknown Object CKD has been named an important contributor to both national and global morbidity and mortality, with a vastly disproportionate burden falling on people of color. In America, as of 2013, although the rates of CKD were relatively comparable, Black people had four times the rate of progression to ESRD than non-Hispanic white people.99 The reasons behind this are complex, with structural factors at the forefront—lack of access to care, environmental toxins, chronic stress, and poverty—all highlighted by Nicholas et al.100
Biologically, kidney disease is intimately related to heart disease. Hypertension, or high blood pressure, is a leading cause of CKD, and Black people in the United States have a seventeenfold higher rate of hypertension as the etiology or cause of their ESRD than other populations.101102 An underdiagnoses of hypertension in Black people due to the previously mentioned clinical racism may thus also contribute to disparities in kidney disease, putting Black people at risk for long-term, severe kidney damage. But there are other, more direct issues.
Biological racism is embedded in a key tool used to measure kidney function—the glomerular filtration rate, or GFR. The GFR is a calculated measurement of a particular protein in the blood that the kidneys filter, which is then used to estimate kidney function because kidney function can’t be measured directly in a typical clinic. It provides clinicians with an approximation of how well the kidneys are performing their critical roles of filtering fluid in the body. The GFR is used to diagnose many kidney-related diseases, including CKD. It is thus especially important for classifying severity of CKD (up to and including ESRD) and for making decisions about diagnosis, prognosis, and treatment of kidney disease. Embedding biological race in this tool leads directly to a deadly underdiagnoses of severe kidney disease in Black people, contributing to the disparate epidemic of ESRD and CKD seen today.
The GFR is currently estimated through complex equations that take into account individual factors, including weight, age, sex, serum levels of creatinine (a waste product from muscle breakdown that is excreted in urine), and race. Based on these equations, the further someone’s GFR is below “normal,” the increased severity or stage of kidney disease. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) is the most commonly used equation and was developed in 2009 as an improvement to the 1999 Modification in Diet for Renal Disease (MDRD) study equation.
These two commonly used equations—CKD-EPI and MDRD—each contain a racial adjustment factor coefficient that is multiplied to the baseline GFR estimate for a Black person (1.16 for CKD-EPI; 1.21 for MDRD).103 This adjustment increases the GFR for a Black person for a given creatinine level in both equations, which means the adjusted GFR is closer to normal and thus creates a diagnosis of a lower disease severity. Compared to a white man of the same age, weight, and serum creatinine level, the estimated GFR of a Black man would be higher, suggesting that Black people have “better kidney function” than individuals of other races. Because of this, Black people must meet higher GFR thresholds of kidney function in order to be diagnosed with kidney disease compared to individuals of other racial groups.
Image source: “Frequently Asked Questions about GFR Estimates,” National Kidney Foundation104
This racial adjustment factor has severe negative clinical implications. Those who identify as (or are identified by their providers as) Black may not be diagnosed early enough, may not receive intervention at a critical period, and are more likely to progress to higher stages of kidney disease and poor health outcomes.105 The racial adjustment means it takes worse kidney function to get diagnosed with CKD for Black people, and by the time they are diagnosed, they are often at ESRD (CKD is classified as stages 1–5, with ESRD being stage 5). Studies show a two- to fourfold higher incidence (counts of new cases) of ESRD among Black patients as compared with white patients.106 Yet the prevalence (new cases plus existing cases) of earlier stages of CKD in Black patients is similar or lower than that of white patients, meaning the GFR adjustments may be delaying diagnosis of earlier-stage CKD until Black patients have reached a significantly higher disease burden and are already at ESRD.
Other biological markers beyond GFR help the classification of CKD stages and ESRD, so we would expect those markers to match across CKD staging for different populations if the GFR measurement were accurate. However, white populations with stage 3 CKD display a strikingly lower prevalence of other risk factors for CKD, such as albuminuria and hypertension, compared to the Black populations.107 This evidence suggests that either white patients are being diagnosed with more severe disease than they actually have or that Black patients are being diagnosed with less severe disease than they actually have. Given the current race coefficients in measuring GFR, this evidence suggests that clinicians may systematically misclassify disease status among Black people to a falsely lower CKD stage (Peralta 2010). Despite having known risk factors for CKD, such as albuminuria and hypertension, young Black people may only be diagnosed once they reach advanced stages of disease.
This all adds up to a disproportionate disease burden. Black patients represent 30 percent of all ESRD patients in the United States, and just 13 percent of the total US population.108 The only cure for ESRD is a kidney transplant, yet Black patients are less likely to be identified as transplant candidates, more likely to be on waiting lists for longer, and less likely to receive a deceased or living kidney donation compared to white patients due to both institutional and structural factors.109 Not only is the current race-based system of determining GFR scientifically flawed, but it actively harms Black patients by systematically missing early diagnoses of CKD.
These dire health implications beg the question, Why do racial adjustment factors exist for GFR at all? The National Kidney Foundation states that race is included in CKD-EPI and MDRD equations because “African Americans have a higher GFR than Caucasians at the same level of serum creatinine.”110 However, this argument is somewhat circular and has many scientific limitations.
The MDRD and CKD-EPI equations appeared in 1999 and 2009, respectively, to improve upon an older equation (Cockcroft-Gault formula) developed in 1973 with a cohort of 249 men. The 1999 MDRD equation was then reformulated in 2005 (right at the time that the research in salt sensitivity was spiking), and the CKD-EPI was created shortly after that. Each equation represents an academic “doubling down” on race in the name of improving the accuracy of estimating kidney function.
First, the demographic profile of each study was crucial to the specific equation development, and often not representative of the United States (e.g., there are generally fewer people of color in the study as a percentage than the percentage of the US population—the MDRD study was 88 percent white). Therefore, extrapolations about the creatinine clearance for more diverse populations along any of the parameters used in the equation are bound to be of limited use.111 For example, age is a key factor in the equations, and the dataset for MDRD only included older people (average age 50.6) with CKD, which, therefore, may not apply to healthy populations, particularly younger populations. One study showed this was particularly true for young Black people, who may be significantly misclassified with lower or no CKD.112 And because the formulas were derived from American, mostly white populations, their utility may be limited for multiethnic populations especially in other geographies. A study of multiethnic Brazilian populations showed CKD-EPI has similar accuracy to MDRD regardless of race corrections when compared to the gold-standard direct measurement of GFR function, iohexol clearance.113
Second, creators of both the CKD-EPI and MDRD equations do not provide sound evidence for why race was included in the model for calculating GFR in the first place. The authors of the MDRD equation did not include an explanation in their methods for why they included race in their model. In their conclusions, they simply state, “on average, black persons have greater muscle mass than white persons.”114 The evidence base for this assumption is fundamentally flawed. The three studies the MDRD researchers cited to support their claim were fraught with questionable scientific methods regarding race, including “visual determination” of study participants’ race categorization and grossly racist “anthropometric measures” such as “densitometry” to generalize questions of overall muscle mass across races (Levey et al. 1999; Cohn et al. 1977; Harsha et al. 1978; Worrall et al. 1990).115 Harsha’s densitometry results are unlikely to hold up today, as he posited that Black children on the whole had much less body fat, while today children of color are far more likely to be obese. This points to the racist assumption that these characteristics were biological instead of structural or societally influenced. The creators of CKD-EPI, which was meant to improve upon MDRD, included race simply based on the fact that MDRD did.116
Furthermore, the race categories represented in the equations are arbitrary and do not reflect the heterogeneity of human populations. They reflect the social categories that society has designed, based on arbitrary visual and social standards. The MDRD study never explains how it classified participants by race nor how it defined race, while the CKD-EPI only notes their source data was the National Health and Nutrition Examination Survey, which tends to use self-identification within the given options. These options are typically drawn from the census options, which are both socially constructed and confusing by conflating race with ethnicity. As an example of the limitations of these arbitrary definitions of race, Zanocco’s study of a multiethnic Brazilian population showed that the race adjustment was not associated with better performance in evaluating GFR, demonstrating that it is not a necessary or useful tool in multiethnic populations.117 Further highlighting the arbitrariness of the racial categories used in calculating GFR, nephrologists have anecdotally admitted to misidentifying patients as African American based on their brown skin, meaning their understanding of the usefulness of the GFR equation is based on visual assumptions.118 This questions the scientific usefulness of such GFR estimations and highlights the racism inherent at every level of the interaction, from the structural construction of the flawed GFR equation to the interpersonal racism of misidentifying patients based only on skin color.
Third, the equations take into account several biological factors such as age and gender alongside (nonbiological) race, but do not include muscle mass. Muscle mass is crucial in the GFR calculation because creatinine, one of the main serum markers, is a by-product of muscle breakdown. Thus, those with higher muscle mass and those with poor kidney function would both have elevated serum creatinine levels, leading to lower estimated GFRs. The National Kidney Foundation guidelines themselves explain that the estimated GFR calculations are less accurate for patients who do not have an average muscle mass and standard diet, including athletes, people over seventy years old, the malnourished, the obese, vegetarians, or patients with changing kidney function.119 Although the biological mechanisms by which these factors affect muscle mass are well understood, only age is “adjusted” for in calculating GFR.
However, the variable of race is adjusted for, not muscle mass, and often anecdotally referred to as a proxy for muscle mass without any explanation for why race would be related to muscle mass. A quick Google search will turn up hundreds of papers seeking to justify or explain differences in body habitus (e.g., muscle mass, body mass index, adiposity) with biological mechanisms that are then explicitly or implicitly tied to a biologized notion of race. These papers either ignore social and structural determinants of health (e.g., ignoring the effect that lived experience and environment may have on body composition) or have a blatantly racialized research agenda seeking to uphold a preconceived notion that racialized biological differences exist.120 Although differences in bodies do exist across different people, the differences are far more nuanced than the social category of race. These notions underscore the existing racist perceptions and stereotypes about Black physicality that links to the historical positioning of Black “fitness” for manual labor, and has continued today through stereotypes about Black athletes, among many others.121 The linkage of muscle mass to race has historical roots and is fundamentally rooted in racism.
If muscle mass is a key factor in calculating GFR, an estimation of muscle mass itself should be included in the equations. If it is not yet easy to measure in clinic, then we should create better tools to measure it. Race should not be crudely and harmfully used as a proxy for muscle mass.
As Dorothy Roberts explains in her TEDMED talk, “The Problem with Race-Based Medicine”:122
But what sense does it make for a doctor to automatically assume I have more muscle mass than [a] female bodybuilder? Wouldn’t it be far more accurate and evidence-based to determine the muscle mass of individual patients just by looking at them?…Race is a bad proxy. In many cases, race adds no relevant information at all. It’s just a distraction. Race also tends to overwhelm the clinical measures. It blinds doctors to patients’ symptoms, family illnesses, their history, their own illnesses they might have—all more evidence-based than the patient’s race. Race can’t substitute for these important clinical measures without sacrificing patient well-being.
Finally, the racial adjustment factor in GFR estimates can also be directly harmful to patients of color through psychological impacts. “Separating out one ethnic group from the general population on a laboratory slip” can lead to stigma and other interpersonal or internal forms of racism, as well as potentially delaying diagnoses.123 The psychological impact of false-positive tests is routinely discussed in the usefulness of screening tests for cancer, and although the GFR adjustment is a question of “false-negative,” every clinical field should be held to the same standard to “do no harm” through the psychological impact of how test results are displayed and discussed.124
As medical students, we are taught to follow the CKD diagnosis algorithms, which hide much of the reliance of race in GFR calculations, and we are implicitly taught to accept that Black patients simply have a higher disease burden. However, the reality of this is a direct repercussion of using race as an inappropriate heuristic, one that has dire health consequences for Black patients.
Lung Function, Spirometry, and Current Recommendations by the American Thoracic Society
Danielle M. is a patient at her local hospital coming in for a checkup with her doctor regarding difficulty breathing over the past few days. As her doctor is preparing for her visit, she looks at the information stated in the electronic medical record:
Reason for visit: Difficulty breathing for the past month
Race/Ethnicity: Black/African American
With these demographic “clues” from Danielle’s electronic medical record, the doctor arrives at the reasoning for possible differential diagnoses to discuss with Danielle: chronic obstructive pulmonary disease (COPD) and asthma. The physician plans to perform a spirometer test, a method of assessing lung function by measuring the volume of air the patient is able to expel from the lungs after maximal inspiration. Spirometry is the primary method that clinicians use to evaluate lung function. Spirometry reports include a set of values based on the patient’s volumes of inspiration and expiration, and these values are compared with a range of volumes considered to be normal.
For Danielle, the pulmonary lung function test results did not result in a clinical diagnosis, because her spirometry results were within normal limits. “Ethnic” correction factors were applied to calculate these normal limits, and Danielle’s lung function test results may have resulted in a clinical diagnosis without them.
Danielle’s doctor tells her that they’ll have to have a number of follow-up visits and additional lab testing in order to confirm her diagnosis. Danielle departs from the doctor’s appointment disappointed and nervous that her breathing continues to be labored and difficult and that it will take several more appointments to find out what is going on. She is unable to make appointments in the upcoming month due to family obligations and her hectic work schedule. Afterward, a medical student asks Danielle’s doctor if race correction factors could have impacted Danielle’s spirometry results. She replies, “Black people are always diagnosed and overmedicated. Thankfully these correction factors help with that.”
This anecdote is adapted from a true interaction one medical student had during a session with her preceptor. As medical students, we often hear statements like the one Danielle’s doctor made, where biological race is framed to us as a solution to health disparities. This framing makes it difficult to disentangle the insidious and harmful ways that the ingrained notion of biological race impacts patients like Danielle. However, challenging the notion of race as a biological trait should not be mistaken as advocacy for color-blind medicine. We want to be a part of medical practice that engages in antiracist medicine, not color-blind medicine. We advocate for medicine to acknowledge the role that flawed assumptions regarding biological race play in perpetuating racial health disparities.
This advocacy is vital because, as we show in the following example, race is dangerously built into algorithms that determine lung function, just as with kidney function. What could be considered “normal” function for Black people is repeatedly considered pathologic or unhealthy for white people. This discrepancy leads to late diagnoses and poorer treatment for Black people compared to their white counterparts.
Furthermore, the notions that racial and ethnic differences in lung capacity exist, and that these differences should be programmed into the diagnosis of lung disease, are fundamentally rooted in a history of racism. Next, we will elucidate this racist history, drawing largely from the critical work of Lundy Braun, including her book Breathing Race into the Machine.
Interest in modern spirometers first took hold as a means of assessing the fitness of police forces and military personnel and life insurance applicants in England during the outbreak of tuberculosis in the nineteenth century.125 John Hutchinson, an English surgeon, was credited with inventing the spirometer in the 1840s and also coining the measurement “vital capacity,” after his assertion that such measurement was critical in assessing premature mortality.126
The application of Hutchinson’s spirometer quickly spread, including Samuel Cartwright’s use of spirometry on slavery plantations. Cartwright was a Southern physician and plantation owner who was the first person to use the spirometer as a tool for comparison of lung function between Black people and white people.127 In particular, he asserted that “the expansibility of the lungs is considered less in the Black than the white race of similar size, age and habit.”128 Benjamin Apthorp Gould published the first study in 1869 that would reinforce notions of biological inferiority of Black people with data on racial comparisons of lung function with large sample sizes and anthropometric measurements of Union soldiers. These assertions, alongside subsequent studies that found that slaves had poorer nutrition status and higher rates of pneumonia, typhoid fever, and respiratory illnesses, contributed to racist assertions that African American slaves had physical pathologies and thus needed to be kept under the institution of slavery.129
Political leadership who profited from the institutions of slavery, including Thomas Jefferson, reinforced the influence of notions of biological inferiority of Blacks and non-Caucasian populations. Despite taking part in asserting that “all men are created equal,” Thomas Jefferson, in his Notes on the State of Virginia, featured racial differences in lung function between white colonialists and slaves, asserting that there were marked distinctions between such groups and “a difference of structure in the pulmonary apparatus.”130
This brief history of key figures involved in the history of the spirometer illustrates how notions of biological racial difference in lung capacity and fitness related to the foundations of public health and slavery. In particular, the motivation for the creation of the spirometer by Hutchinson and its subsequent use by Cartwright and Gould to obtain scientific data claiming racial difference in lung function between slaves and colonialists was used to first assess and calculate the fitness disparities of diseased individuals in society and subsequently to achieve the subjugation of slaves and control of non-Caucasian populations. By obtaining “scientific” anthropometric information that attempted to objectively assert the biological inferiority of Black people, slavery was further justified through medical and public health institutions and methods.
Perhaps the most striking element of this history is how its roots continue to be embedded in how physicians conduct differential diagnoses and patient assessments every day due to recommended guidelines. Medicine continues to uphold racist notions of biological inferiority in lung function.
For example, the web page on UpToDate regarding spirometry states the following:
Healthy African-Americans have spirometric values that are approximately 12 percent lower than Americans of Caucasian descent of the same age, sex, and height. This difference is, in part, due to a difference in the ratio of trunk size to standing height, i.e., African-Americans have longer legs for a given height. Genetics and nutritional factors may also play a role in differences by race/ethnicity.131
UpToDate is considered an “evidence-based clinical resource” that clinicians use every single day after patient appointments for information about medications, diseases, clinical guidelines, and more. This statement by a frequently used, highly regarded medical resource is problematic for many reasons. First of all, we know that when studies use the category “African Americans,” race is typically self-identified or guessed by the clinician. To think that a statement as simplistic as “African Americans have longer legs for a given height” could possibly apply to all people who would fall into that category is absurd. Secondly, it is unclear how trunk size to standing height ratio can be emphasized as so critical in explaining spirometric values.
UpToDate cites two articles to support their claim. The first article cites another article that cites another article, and all the articles in this chain repeat the same statement without further explanation. For example, the first citation by UpToDate states, “African-Americans on average having a smaller trunk:leg ratio than do Caucasians,” and does not offer any evidence for why this observation should be singularly focused on over environmental and structural factors as a basis for correction factors in spirometry.132 The second citation by UpToDate regarding trunk to height ratio says, “Differences due to ethnicity are not well defined.”133 If the differences are so poorly defined, it is shocking how a resource so frequently used as UpToDate can so uncritically repeat that conclusion. Additionally, despite this lack of evidence, if trunk to standing height ratio really is the key factor in determining spirometric values, then race is a poor proxy for this ratio.
In practice, these assumptions about differences in lung function are built into spirometers as “race correction” factors that lead to different diagnoses for patients of different races. Anne Fausto-Sterling describes, “Technicians present spirometry results ‘corrected’ for race, so that for an African American to receive a diagnosis of impaired lung function—for example, a worker seeking disability compensation for lung damage from asbestos—he or she has to be dramatically sicker relative to a white American before receiving an equivalent disease diagnosis.”134 Here, Fausto-Sterling is referencing a case in 1999 in which Owens Corning, a company that sickened thousands of workers through its asbestos-containing products, requested that African American workers filing lawsuits against the company show that they have worse scores on lung function tests than white workers as a result of asbestos exposure in order to qualify for a trial against the company.135 Owens Corning cited “medical evidence” that Black people have different lung capacities than white people.
Currently, the American Thoracic Society (ATS) specifically recommends that the Global Lung Function Initiative (GLI) 2012 multiethnic spirometry reference values be used in North America and elsewhere for the ethnic groups represented.136 The ATS establishes standards of care relating to respiratory disorders through the publication of statements, workshop reports, and clinical guidelines that health providers and trainees across the country are expected to be up to date on. There are several issues with guidelines based off of the ATS recommendations. First, the popularly used GLI reference values are extracted from datasets of overwhelmingly Caucasian populations. In addition, GLI reference values confound false notions of biological race with environmental exposures and stressors, as the following quotation from the GLI authors demonstrates:
The well documented ethnic and racial differences in pulmonary function arise from differences in body build (such as chest size or the ratio of sitting to standing height), socio-economic status (which determines bodily development in early life and leads to secular trends in body size and pulmonary function), growing up at altitude, and possibly other environmental factors. In the present study race and ethnicity were self-reported, which may not be accurate enough for clinical purposes. Indeed, in the absence of genetic typing, predicted values in self-reported African Americans may be biased by up to 200 mL.”137
These current ATS and GLI guidelines demonstrate the blatant confusion and oversimplification of using categories of race as a means of adjusting for spirometry values. Race is not the same as ethnicity, which is not the same as body build, which is not the same as socioeconomic status, which is not the same as the environment. It cannot be used as a proxy for these structural and environmental factors, which have repeatedly been proven to directly impact lung function on their own.
Lundy Braun further elaborates on this unnecessary emphasis on racial correction factors despite greater evidence supporting how environmental factors, not race itself, mediates lung disease:
There have been scientific studies showing that people who live around high pollution areas have lower lung capacity. High pollution areas also map onto minority status. Why we have chosen both in the US and internationally to focus on race to the exclusion of social class, I can only speculate. One piece of the story is that the accumulation of scientific research around a particular idea can make it hard to dislodge. With the spirometer, having the correction factor actually built into the machine makes racial assumptions invisible.”138
The consequences of the oversimplification of structural and environmental factors into racial correction factors are that these guidelines are transferred from institutional memory into everyday physician practice that affect patients, contributing to poor treatment and diagnosis assessment for people of color and subsequent racial health disparities. Despite these concerns, the ATS fails to address any responsibility in contributing to racial health disparities by encouraging the practice of applying haphazard guidelines such as those of the current spirometry reference values according to race and ethnicity. By failing to see or challenge their inappropriate use of race and the unintended consequences of the recommendations, the ATS and the clinicians who follow such recommendations continue to perpetuate the unjust, racist framework upon which the spirometer was founded.
Furthermore, the continued presence of the racist history of establishing race-based differences in lung function within the modern-day practice of pulmonology signals how the medical community has refused to address this hidden history of racism and subjugation of Black and brown bodies. There is a profound need for this history to be interrogated, discussed in dialogue within the medical community, and incorporated into medical practice. This conversation has the potential to shift focus away from misguided notions of biological difference. Medicine must acknowledge how racism and social inequalities have had a harmful impact on health outcomes in order to address racial health disparities related to lung function.
Genetics Research, Precision Medicine, Race, and Ancestry
I was a graduate student instructor for a neuroanatomy lab in which the final task for the undergraduate students was to come up with and answer a research question using the Allen Brain Atlas. One student told me he wanted to “pick a gene associated with a disease and map it to different human races.” This wasn’t even in the scope of the project assignment—we had specifically told students that we expected them to utilize the mouse brain connectivity and gene expression atlases, not the human atlas.
But this incident highlighted to me how early in our education and upbringing “race” is ingrained in us as a biological certainty, because he assumed there would be a difference in genes and brains by race. We’re taught race as a biological cause of disease and health disparities, rather than racism. It emphasized to me how vital it is that we not only understand the health consequences of racism for our individual practices as future doctors, but also that we are able to distill, disseminate, and communicate that truth as future (and current) health educators. We must eradicate the conflation of race with biology from clinical education, research, and practice. And we must also correct this false conflation of race and biology that has spread from health institutions to education and society at large.
—Second-year medical student
Research in genetics, ancestry, and precision medicine has grown exponentially due to the Human Genome Project and advances of CRISPR technology. Precision medicine is the use of advanced computing tools to integrate data from a diverse range of health and research settings. The Human Genome Project catalogued and identified the more than three billion genes in the human genome to create a baseline “reference map” of the human genome. CRISPR refers to both the gene-editing tool (an enzyme called Cas9) and its targets (clustered regularly interspaced short palindromic repeats, pronounced “crisper”). This tool has the promise to target and edit specific portions of genes (identified by the Human Genome Project) within an organism at a level of precision unseen before, which has led to many exciting developments in biological research, biotechnology, and possible treatment for certain diseases. However, advancements in these fields have concerned many scholars, ethicists, and activists, as this research and its technologies have the potential to reinforce and expand upon flawed biological notions of race.
By seeking to identify genes that could be “cured” via CRISPR, such research runs the risk of repeating eugenicist history and simplifying the complicated role that social and structural inequalities play in perpetuating racial health disparities to a gene or set of genes.
Understanding links between genetics and disease is a major component of modern health care. However, linking race with genetics is a fundamental intellectual flaw with consequences for patient diagnosis, care, and treatment. Within medicine’s history of oppression and racism, using “race” in the field of genetics and precision medicine is inherently political with complex sociopolitical origins. Without a critical analysis of this history and the categories used to define “ancestry markers,” such research in genetics and precision medicine hold the possibility and danger of reifying biological racial difference again in a newer, shinier package.
Current research in genetics, ancestry, and precision medicine falls into this trap of continuing to biologize race by several flawed methods that are simply bad science. These include, but are not limited to, (1) using predetermined racial categories to group ancestral markers (i.e., confirmation bias of racial categories) and (2) ascribing health disparities to genetic differences rather than accounting for the complex role of social, environmental, and structural factors on epigenetics and the body.
First, using predetermined racial categories to match to group ancestral markers elides the history of the creation of race as a social construct. Furthermore, the research seeking to match genetic markers to these groups shows that ancestral markers exist, but they are not consistent across the social groups of race. Early and ongoing work in genetics has shown consistently higher in-group variability than across-group variability, thus showing no genetic loci to differentiate between racial categories.139 Thus the use of “race” in genetics and precision medicine usually relies on scientists creating arbitrary categories for groups of ancestry markers that incorrectly substantiate racial categories rather than challenge the social construct of race.
One example shows the difficulty of applying precision medicine within the existing racist history of medicine. In July 2010, the New England Journal of Medicine published “Genetic Ancestry in Lung-Function Predictions” by Rajesh Kumar et al. In this article, the authors sought to improve upon the racial classifications used in lung function tests. Existing methods utilize patients’ self-identified race (or physician-identified race) to define the normal lung function range for spirometry, so the researchers sought to identify alternative, genetically derived “normal” values. The aim was to use genetics to provide a more “objective” set of normal values. The authors argued that the self-identified racial categories were problematic because individuals are racially admixed, and limited racial categories are “crude descriptors of individual genetic ancestry.”140 That is, racial mixing is so frequent, and individuals have such complex racial backgrounds, that the self-identified racial categories establish inaccurate baselines for the lung function measurement.
Unfortunately, the research by Kumar et al. ultimately still seeks to confirm what genetic markers might show as “truer” racial categories. This work uses genetics to make a biological argument about social constructs. Although this is a step forward from crude racist assumptions discussed in the spirometry section, their research still fell into the trap of trying to match “ancestry informative markers” (single-nucleotide polymorphisms posited to represent statistically significant genetic differences among those of different ancestries) to socially constructed racial identities (individual self-identified race).
Rather than using genetics to identify markers that may predispose anyone to lower lung function, their study sought to solidify which markers could best predict lowered function for African Americans only. Without addressing the complex factors that mark lived experience (e.g., racism, structural, and societal factors) nor the racist history of the spirometer, this research begins with the assumption of difference for African Americans (again, using the social construct as the starting point for their supposedly more objective scientific approach). Therefore, the study only confirms racial biases by using genetics to try to prove some sort of inferiority in lung function (specifically in “forced expiratory volume”) in African Americans.
Other scientists have similarly sought to more precisely measure differences in lung function between racial and ethnic groups, though definitions and conclusions regarding the influence of racial categories has varied widely.141 Some researchers accept without question the outdated, yet popularized, notions that African Americans have lower lung function than European Americans.142 One study, examining the utility of multiethnic adjustment for spirometry, posits that adjustment works for some, but not all, racial groups.143 This study concluded that ancestry markers would be helpful to better explain observed lung function differences.
Kumar et al.’s research is different because it fits within a larger body of genetics work that seeks to better understand racial disparities in health.144 This is in contrast with other genetics research that excludes nonwhite participants as a means of “controlling” for race.145 Yet even research with a progressive, disparities-oriented health research goal can fall into these “traps” of genetics research.
Kumar et al., for example, seek to provide tools for more efficient and effective care for severe asthma and COPD, which they note African Americans have higher rates of both. Kumar et al. thus represents the good intentions of seeking to improve upon issues of inclusion and to better explain the disparate health outcomes seen across racial lines. But without a critical analysis of what racial categories mean, researchers with good intentions will continue to put forth bad science that uses ancestry markers to (purposefully or not) confirm racialized differences in biology or use genetics to explain away racial health disparities caused by social and structural determinants of health. For example, Parker et al. (2014) pick up on the ancestry-based claims of Kumar et al. to claim that a particular genetic marker can predict lower COPD lung function metrics for African Americans only, again reinforcing a biological “brokenness” in African Americans rather than addressing the role society and other factors may play.146 This is unlikely to be helpful in addressing health disparities as Kumar et al. intended, instead explaining away the disparities with genetic differences. Addressing health disparities through genetics and precision medicine is therefore very much a slippery slope, which is why we feel this critical analysis of racism and race is crucial to improving the science.
We offer instead two “red flags” for researchers and readers to consider as the field of genetics continues to move forward. We furthermore encourage all researchers and readers to dive more deeply into the field of bioethics, which has been grappling with the implications of this flawed science, to better understand the recommendations for change.
First, categories used to cluster ancestral markers are established by the scientists themselves, rather than by the clustering of the data, and rely on slippery definitions that are, at best, “mired in confusion.”147 Kumar et al., for example, chose to stratify their data to specifically estimate only “the percent African and European ancestry, assuming two ancestral populations.”148 This means that the major assumption on which ancestry markers are based is one of confirmation bias (assuming only African and European ancestry in this case), such that scientists’ quests to look for patterns (oftentimes with racial categories as their foundation) will be found. Scholars of race, technology, and health justice have produced significant work for decades, pushing back against the reification of racial categories. Yudell et al. write that “historical racial categories that are treated as natural and infused with notions of superiority and inferiority have no place in biology.” They write furthermore that “using race as a political or social category to study racism and its biological effects, although fraught with challenges, remains necessary” (emphasis added) to “understand how structural inequities and discrimination produce health disparities in socioculturally defined groups.”149 Other scholars, such as Duana Fulwiley, Dorothy Roberts, and Troy Duster, have argued similarly against the use of a priori categorization in genetic research.150
Second, focus on ancestral markers fails to acknowledge the role structural and societal factors play (as Yudell et al. acknowledge) and what role epigenetics thus plays in the development of structural health disparities. As expanded upon in the following section, epigenetics is the modification of gene expression, such that environmental influences can affect to what degree genetic susceptibilities and predispositions are “active” and “inactive.” Given the breadth of public health and medical literature showing how social, structural, and environmental factors affect the expression of genes, research into the genetic foundations of health outcomes must also examine epigenetic influences that factor into differences between phenotype and genotype. Any focus exclusively on genotype with no exploration of how and why certain genes are expressed and influenced by environmental and structural factors is wholly insufficient and should be questioned. The current research landscape of “ancestral identity markers” (single-nucleotide polymorphisms, also called AIMs) runs the risk of ignoring and overlooking this process, attributing focus on racial health disparities to genetic factors rather than social, environmental, and structural influences. The goal is not to practice color-blind medicine, but rather antiracist medicine that addresses all levels of racism.
Why does this matter to us as medical students? We are being taught that the newest, “best” science has the power to individualize our cures, to explain more and more of the mysteries of the human body, and yet it is still steeped in the history and context of racism in medicine. We are often caught unawares by the way educators and clinicians claim genetics as evidence of racialized differences, and this worries us for the future of our practice.
The perpetuation of biological racism in genetics research has important implications for the practice of medicine and health care. Health care is increasingly “evidence-based.” Clinicians rely on researchers to understand physiologic processes, direct innovation, and guide assessments of risk for each patient. Genetics research is, at its most functional, intended to improve health care and is characterized as an “objective” science. However, if such research fails to acknowledge its own biases based on ahistorical and racist foundations, race will continue to be biologized and discussed under the false guise and synonym of “ancestry markers,” and structural issues will continue to be hidden under those same guises.
Furthermore, the issues in genetics research create a dire future for precision medicine, the promising “evidence-based” health care of the future. Precision medicine aims to allow us to tailor treatments and diagnoses to each individual based on their unique genetic footprint. If we continue on this path of misappropriating genetic patterns to biological race, precision medicine will not only fall far short of its goal of treating individuals better, but instead will perpetuate the false notion of biologized race. This hides the social construct of race behind the same false guise of ancestry markers and could harm patients more than individualize and improve their treatment. It allows for and contributes to explicit racial profiling and stereotyping of patients and stands to exacerbate existing disparities in treatment and access to care.
Despite good intentions, such research fails to be innovative at addressing racial health disparities and instead simply “reinvents” conversations about race using the proxy of ancestry and genetics to solidify the social construct of race as falsely “objective science.”
Semantics matter in genetics research and the practice of medicine. The difference between ancestry and falsely biologized race is critical, and it’s our duty as advocates for the health of our patients, as well as creators, disseminators, and users of science, to be careful as the field of precision medicine booms. This will be the field we work in, but we are not trained to engage with it critically. Therefore, we seek to amplify the critical and difficult conversations already existing in the field of genetics in order to ensure clinicians and providers have the tools to practice critically engaged precision medicine.151
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- 102. The American Heart Association describes the mechanism as “over time, uncontrolled high blood pressure can cause arteries around the kidneys to narrow, weaken or harden. These damaged arteries are not able to deliver enough blood to the kidney tissue.”
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