Medical racism in the 21st century

An ad for BiDil, courtesy Ardor Pharmaceuticals. 

An ad for BiDil, courtesy Ardor Pharmaceuticals. 

Ten years ago this summer, the FDA approved BiDil, a drug treatment specifically indicated for African Americans. An antihypertensive and blood vessel dilator for patients with congestive heart failure (CHF), it was the first race-based prescription drug in American history. BiDil’s release generated enormous controversy. Some, including the NAACP and the Congressional Black Caucus, praised it as a step towards better addressing the often underserved and overlooked healthcare needs of Black patients. Others called it pseudoscientific medical racism that recalled the Tuskegee Syphilis Study.

BiDil was not originally intended to be race-specific. Its development began in the early 1980s, when the University of Minnesota collaborated with the Veterans Administration to develop a new treatment for heart failure. They found promising early results with a combination of hydralazine and isosorbide dinitrate and received a patent in 1989. A company called Medco licensed the patent and spent several years preparing an application to seek FDA approval. But the FDA rejected the application, saying that clinical trial data did not sufficiently prove that the treatment actually worked.

Dr. Jay Cohn, the cardiologist who organized and chaired the trials, reanalyzed the data and found that the drug seemed to work better in self-identified African Americans. He saw this as very good news, as it was widely known that the conventional drugs for treating hypertension in patients with CHF were less effective in Black patients.

With this new hypothesis, the patent was licensed to a different company, NitroMed, who then ran the African American Heart Failure Trial. The new drug seemed a miracle. In Black CHF patients, it reduced hospitalizations by 39% and mortality by 43%. The drug was so successful that the trial was ended early to avoid additional deaths among patients receiving a placebo. The FDA approved the drug, now called Bidil, in June 2005 and it was quickly added to standard treatment guidelines for CHF.

Done and dusted, right? A randomized, placebo-controlled, double-blind clinical trial showed that BiDil worked really well in Black patients, and the FDA agreed. A closer look at methodology of the landmark trial reveals two major concerns. First, the trial did not include any non-Black subjects, only a Black treatment group and a Black control group, from which it is not possible to conclude that BiDil works any better among self-identified African Americans than among other racial groups.

Still more troubling, the study relied on racial self-identification – which is problematic in a medical context, since race is socially constructed and does not a basis in biology. This is the larger issue for which BiDil serves as a poster-child: in the 21st century, old notions of racial essentialism continue to worm their way into mainstream science, including medical research and treatment.

This is the larger issue for which BiDil serves as a poster-child: In the 21st century, old notions of racial essentialism continue to worm their way into mainstream science.

BiDil is hardly the most recent example of this tendency. In 2013, Jason Richwine incited considerable media furor when it became known that his PhD dissertation from the Harvard Kennedy School suggested there was a genetic component to IQ differences between Hispanics and non-Hispanics. The backlash recalled that against The Bell Curve, a 1994 book making similar claims about race, heredity, and intelligence.

Claims like these make headlines, however, because they are not mainstream and a critical mass of the public find such claims repellant. To say that one race is less intelligent than another to say that races are both distinct and unequal, a clearly discriminatory notion. Most contemporary medical and scientific racism, however, is far more insidious, making only the claim that races are distinct and side-stepping the (judicially-established) implication that separateness is inherently unequal.

WebMD’s entry for “hypertension/high blood pressure,” for example, the condition that BiDil treats, includes the following: “High rates of high blood pressure in African Americans may be due to the genetic make-up of people of African descent…Blacks in the United States also seem to be more sensitive to salt, which increases the risk of developing high blood pressure.” Obviously, there is no malicious intent in this entry but it is problematic nonetheless. For one, it implies that race is an immutable and genetically discernible trait (i.e., I am white, therefore I could never have been anything except white, and if you had access to my genome you could tell beyond doubt that I was white). This is not true, as race is context dependent (consider that some people crossing state lines in the Jim Crow era would legally change race) and not identifiable by any specific biological or genetic markers (there is no “Asian” gene).

The idea that race is not rooted in genetics is often counter-intuitive when people first encounter it, which is understandable given the degree to which our rapidly expanding knowledge of the human genome sometimes appears to suggest that virtually every difference between individuals in rooted in our DNA. Geneticists speak of population groups, which often have a racial component (e.g., the Sami people of arctic Scandinavia are White), but in these instances race is a phenotypic trait that has little to do with any underlying biological traits – not unlike eye color. (But of course race is a powerful lived experience and often a source of individual and cultural identity, while eye color is rarely any of those things.)

Thus, when one scrutinizes so-called racial genetic differences, one tends to find that race has been layered over a population group difference in a reductive and misleading way. For example, sickle cell disease is sometimes thought of as “Black” illness, but really, it’s just a genetic mutation of hemoglobin that is favorable in malarial areas (as it conferred some resistance) but unfavorable elsewhere. Having sickle cell disease means that you had ancestors that lived in places where malaria was endemic. This includes many Black Americans but also many people of Mediterranean descent. And there are many Black Americans whose ancestors did not live in malarial areas. The more we study genetics, indeed, the better able we are to reject any kind of biological racial reductionism.

But this seems lost in contemporary medical discussions. In addition to its suggestion that race is based in biology, the WebMD entry also incorrectly generalizes a probabilistic statement: “Blacks are more likely to be sensitive to salt” becomes “Blacks… seem to be more sensitive to salt.” This is a small and innocuous semantic difference but one that would logically lead to two different clinical mindsets: one suggests an opportunity to personalize and customize care while the other suggests an opportunity to depersonalize care based on appearance. It is good that a doctor be aware that a black patient has a higher likelihood of salt sensitivity but important that that doctor not assume that patients will have salt sensitivity because they are black.

BiDil has been hailed as a step towards personalized medicine for African Americans but its effect is likely the opposite, with the use of race as a crude and misleading proxy.

In this sense, BiDil has been hailed as a step towards personalized medicine for African Americans but its effect is likely the opposite, with the use of race as a crude and misleading proxy for genetic variation making treatment decisions for Black patients with CHF more impersonal and, potentially, less effective. It is good that BiDil exists as an effective treatment for heart failure patients. It is doubly good that BiDil exists given that it provides a strong alternative in patients who are not receptive to other antihypertensive drugs. But it is bad that BiDil was approved in a methodically dubious race-specific manner that conflates phenotypic racial difference with genetic difference.

Let’s set aside what happens to individuals in their doctors’ offices. Jonathan Kahn, a prominent critic of BiDil’s race-specific designation, believes that race-specific medicines are counterproductive in the fight to narrow racial gaps in health outcomes, as they help “locate the responsibility for individual health disparities through biology or ‘personal choice’ rather than society” and structural racial injustice. Race is a powerful predictor of health. But the primary reason for this is racial disparity in healthcare access and quality. Black Americans are far more likely than Whites to live in poverty, which is strongly associated with worse health. Blacks tend to have less and worse health insurance in addition to fewer and worse options for healthcare facilities compared to Whites. Blacks often have higher incidences of chronic conditions like obesity and diabetes (which derive in large part from the diet and lifestyle constraints of chronic poverty) which increase the likelihood of numerous health problems.

There is also a racial disparity in “allostatic load,” the cumulative wear and tear on the body that occurs when individuals are subjected to chronic or repeated stress. When you are stressed, there are negative physiological consequences. If our bodies are constantly managing acute stress, it hurts us in the long run. Being poor and being Black are both believed to significantly raise the rate at which one’s allostatic load increases, offering a compelling explanation for why many diseases (including heart problems) often have earlier onset in Blacks than Whites. In short, Blacks on the whole have worse health than Whites primarily for reasons beyond individual control, and once they need healthcare their options are often more restricted.

Drugs like BiDil obscure these facts. And ten years later, BiDil is still recommended in clinical treatment guidelines “for patients self-described as African American” despite a dearth of evidence that it works any better in blacks than it does in anyone else. Notably, it is only recommended for these patients when they are already receiving the conventional drugs, ACE inhibitors, ARBs, and beta-blockers. Further, it is also recommended for patients of all races who cannot be given the conventional drugs.

BiDil has not created a new and racially segregated medication regimen for black CHF patients: everyone is first given ACE inhibitors, ARBs, and beta-blockers if possible, with BiDil used as a substitute or compliment. The market has not exploded with new, race-specific drugs in the last ten years. But BiDil is still clinically indicated for a socially constructed, non-biological trait. As long as that is the case, BiDil will continue to set a dangerous precedent. Not only may it compromise personal care, but suggesting that biological differences are the primary cause of racial health disparities is a backdoor way of suggesting that structural injustice is not the primary cause. When genetics are to blame for racial health disparities, society is not.