The COVID-19 pandemic laid bare the racial health disparities in the United States, with markedly increased mortality especially among Blacks and Native Americans. In this episode, Tony Breu and I will discuss the conception of race, racism, and the social determinants of health through three historic plagues in the United States — from yellow fever in New Orleans, to poliomyelitis, and finally the early days of HIV/AIDS — and what lessons we can draw for COVID-19. Along the way, we’ll discuss the unique social capital afforded by acclimation, immunity passports, the concept of the “original antigenic sin,” and constitutionalism and eugenics. This presentation was performed live at the annual meeting of the Massachusetts American College of Physicians, and is only lightly edited.
Slides are available here (Google slides)
- Monath TP, Yellow fever: an update. Lancet Infect Dis. 2001 Aug;1(1):11-20. doi: 10.1016/S1473-3099(01)00016-0.
- Kallas EG, D’Elia Zanella LGFAB, Moreira CHV, Buccheri R, Diniz GBF, Castiñeiras ACP, Costa PR, Dias JZC, Marmorato MP, Song ATW, Maestri A, Borges IC, Joelsons D, Cerqueira NB, Santiago E Souza NC, Morales Claro I, Sabino EC, Levi JE, Avelino-Silva VI, Ho YL. Predictors of mortality in patients with yellow fever: an observational cohort study. Lancet Infect Dis. 2019 Jul;19(7):750-758. doi: 10.1016/S1473-3099(19)30125-2. Epub 2019 May 16. Erratum in: Lancet Infect Dis. 2019 Nov;19(11):e370. PMID: 31104909.
- Blake LE, Garcia-Blanco MA. Human genetic variation and yellow fever mortality during 19th century U.S. epidemics. mBio. 2014 Jun 3;5(3):e01253-14. doi: 10.1128/mBio.01253-14. PMID: 24895309; PMCID: PMC4049105.
- Jelili Ojodu, MPH1, Mary M. Hulihan, MPH2, Shammara N. Pope, MPH2, Althea M. Grant, PhD2,, MMWR, Incidence of Sickle Cell Trait — United States, 2010.
- IthaMaps, Haemoglobin Epidemiology. https://www.ithanet.eu/db/ithamaps?country=GR
- Serjeant GR, The natural history of sickle cell disease. Cold Spring Harb Perspect Med. 2013 Oct; 3(10): a011783.
- Hamosh A, FitzSimmons SC, Macek M Jr, Knowles MR, Rosenstein BJ, Cutting GR. Comparison of the clinical manifestations of cystic fibrosis in black and white patients. J Pediatr. 1998 Feb;132(2):255-9. doi: 10.1016/s0022-3476(98)70441-x. PMID: 9506637.
- Gershman KD et al, Yellow Fever Vaccine & Malaria Prophylaxis Information, by Country. CDC.
- Kofler N and Baylis F, Ten reasons why immunity passports are a bad idea. Nature 21 May 2020.
- NASEM, National Academies Release Framework for Equitable Allocation of a COVID-19 Vaccine for Adoption by HHS, State, Tribal, Local, and Territorial Authorities.
- Schmidt H et al, Covid-19: how to prioritize worse-off populations in allocating safe and effective vaccines.BMJ 2020; 371 doi: https://doi.org/10.1136/bmj.m3795 (Published 05 October 2020).
- Siegal FP, Lopez C, Hammer GS, Brown AE, Kornfeld SJ, Gold J, Hassett J, Hirschman SZ, Cunningham-Rundles C, Adelsberg BR, et al. Severe acquired immunodeficiency in male homosexuals, manifested by chronic perianal ulcerative herpes simplex lesions. N Engl J Med. 1981 Dec 10;305(24):1439-44. doi: 10.1056/NEJM198112103052403. PMID: 6272110.
- Lushniak BD, Surgeon General’s Perspectives. Public Health Rep. 2014 Mar-Apr; 129(2): 112–114.
- Booske BC et al, “Different Perspectives For Assigning Weights to Determinants of Health,” University of Wisconsin Population Health Institute.
- Marc LG et al,HIV among Haitian-born persons in the United States, 1985–2007, AIDS. Author manuscript; available in PMC 2011 Aug 24.
- Rogers N, Race and the Politics of Polio: Warm Springs, Tuskegee, and the March of Dimes. Am J Public Health. 2007 May; 97(5): 784–795.
- Curran JW and Jaffe HW, AIDS: the Early Years and CDC’s Response. MMWR.
- Olivarius Kathryn, Immunity, Capital, and Power in Antebellum New Orleans. The American Historical Review, Volume 124, Issue 2, April 2019, Pages 425–455,
Please note that transcript is based off a script used for editorial support, and does not 100% correlate to the content in the podcast.
This is Adam Rodman, and you’re listening to a live podcast of Bedside Rounds!
Tony: And I am Tony Breu, a proud internist and a long-time fan of Bedside Rounds. I am super excited to be back with Adam for another live podcast. Last year we talked about the French Disease at 500. Today, we’ll be discussing four more plagues, two of which are ancient, one which emerged a few decades ago, and the last having just emerged in the last year.
Adam: I think every internist here remembers March and early April, during the peak of the surge of COVID-19 in Massachusetts.[SLIDE] There was far more uncertainty about the disease than we have now. We were quickly discovering that this was far more than just a respiratory virus — we were seeing horrific cases of ARDS, cardiomyopathy, blood clots, even some bizarre neurological features. And there was just so much unknown about our capacity to hold against a deluge of disease — at BIDMC, where I work, we were converting floors to COVID ICUs weekly, pulling old ventilators out of storage. Very rapidly, I felt like a stranger in my own hospital. And in those early days, I remember a report [SLIDE] that was published that confirmed that we were all seeing — that COVID-19 was not striking evenly across our population, and that minorities — especially Black and members of Native American groups — were seeing drastically higher hospitalizations and mortality. And this, of course, came right around the same time as George Floyd’s murder and the subsequent protests.
Tony: But why are these populations seeing the brunt of COVID-19? Because the gaps are absolutely huge — from age 35-44 [SLIDE], Blacks die at a rate 10 times higher than whites. I think that most people here would agree that it’s not because there’s some fundamental difference between white and Black bodies — but rather that there are social differences that affect health outcomes: the stress of racism, history of housing discrimination, lack of equal access to healthcare, more exposure due to “frontline jobs”. All of these risk factors and more are now lumped into a broad category called the social determinants of health, which the CDC defines [SLIDE] are the conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.
Adam: This idea — that our social context is fundamentally linked to health — is usually thought of to be a rather new, late 20th-early 21st century innovation. But as you can surmise from the fact that we’re doing this presentation, this idea is actually as old as modern medicine itself. In the 21st century, in high-income countries, we usually think about racial and social disparities in chronic diseases — and because of the indolent nature of chronic diseases, they’re somehow more invisible. Plagues, however, lay these disparities out directly in front of us, for all to see. In this live podcast, we’re going to talk about two historical plagues in United States history, and how the scientific framing about race and social determinants of health has changed over time and brought us to this moment in 2020, with COVID-19 still raging. We are going to start in the bayous and swamps surrounding New Orleans in the 19th century, where “acclimation” to yellow fever became a new type of social capital, and scientific racism was at it height before traveling to the United States of the early- and mid-20th century, to talk about polio, where a constitutionalist view about race slowly gave way to a discussion about inequality.
Tony: And throughout, we’ll also show how these three plagues have been explained – at times incorrectly – using race and how this might relate back to COVID-19. And we will discuss American’s original sin and the idea of original antigenic sin.
Traditional Western Medicine [SLIDE]
Adam: Before discussing Yellow Fever, it would be helpful to provide some historical context. That the world around us — what we eat, where we live, who we know, where we’re born — fundamentally shapes our health and our disease was uncontroversial for over two thousand years. Tony loves to make fun of me whenever I talk about the four humors [SLIDE], but the traditional Western conception of disease was one of fundamental balance of constituent body fluids and “life energy” — pneuma — and our environment, as well as our fundamental constitution, were the main risk factors for developing disease. The relics of these ideas still pepper our language — to this day we talk about phlegmatic, melancholic, or choleric personalities, and we talk about a “sense of humor” — now meaning funny, but originally meaning well-balanced.
This is important because the four humors were also our initial way of understanding differences in human populations. This is usually glossed over in scientific history, but by the Enlightenment, humoral thinking was being used to set up the classification system now commonly known as scientific racism. [SLIDE] The most famous classification comes from Carl Linnaeus, the same guy who gave us classifications for species, as well as a classification system for diseases. [SLIDE]
We are in the early 18th century here, and you can see from the very beginnings of scientific racism that health — in this case, associations with the humors — is fundamentally linked to differences in health. Linnaeus’ racial classification wouldn’t last for long, nor would the humoral system that it was based on — this is an engraving from the middle of the 19th century, showing yet another system — but this idea that health and race were interwoven would perniciously persist.
Tony: And one place where we see this is in the way observations about yellow fever were initially explained.
Yellow Fever [SLIDE]
Exactly. By the early 19th century, humoral medicine was falling by the wayside, at least among medical elites. [SLIDE] The dominant understanding of infectious disease in the early 19th century was miasma — that toxic vapors and odors caused epidemic disease. But how was it that these vapors affected people differently? This was an active debate through the 19th century, but the dominant view was different “diathesis” or constitution — the idea that there are fundamental differences between individuals that largely explain susceptibility to disease. We still use this terminology in internal medicine today, talking about a “bleeding diathesis.” One of the most striking examples of this can be seen in the reaction to yellow fever. [SLIDE]
Yellow fever was actually more commonly known as the Yellow Jack [SLIDE], named after the flag flown by diseased ships. The Yellow Jack, for those who might not know the maritime customs, is this yellow flag, flown since at least the time of the black death to signify that a ship in harbor is under quarantine. These days, it is still flown for the same purpose, as well as the variant Lima flag, seen here (and both seen in the Tin tin example)[SLIDE]. And yes, this is a picture of the Diamond Princess docked in Japan [SLIDE], and you can see the Yellow Jack flying. The other common, and very descriptive, name was the Black Vomit. [SLIDE] Yellow fever was endemic throughout the Americas in the 19th century. [SLIDE] The disease, which was then thought to be caused by noxious swampy smells and hot climate had devastated the capital of the United States, Philadelphia, in 1793, killing over 10% of the population and leading to a mass exodus of the population, including most of the doctors who left the poor in the city to die. And nowhere was this felt moreso than the port city of New Orleans. And as someone who went to med school there, I can tell you that the odors and heat have not dramatically changed.
In 1803, Napoleon sold Louisiana — and with it, the entirety of New France — to the United States. New Orleans officially entered the Union in 1812 as a dramatically different American city — with a multi-racial population made up of Creoles, French, including Haitians, enslaved persons, free Blacks — and soon to be full of immigrants from the United States, Ireland, Germany, and the rest of Europe. Starting in 1796, and then recurring every three years or so until the Civil War, the city was hit by wave after wave of the Yellow Jack. [SLIDE] The level of death from all diseases was massive — 8% of New Orleanians died each year, making it by far the deadliest city in the United States. But there were certain populations that were the most affected — American and European immigrants, and in those neighborhoods, the death rate was as high as 20% a year. German and Irish migrants, for example, died at a rate 20 times higher than Creoles.
Tony: It is still the case that up to half of patients who progress to severe yellow fever – also known as the period of intoxication – die of the disease. Just as we’ve seen with COVID, these patients die of multiorgan failure, including renal failure, myocardial and CNS involvement, and – of course – hepatic involvement with the jaundice that gave the plague its name.
Adam: There’s still, I think, an unanswered question. Was there actually a lower death rate between different racial and ethnic groups?
Tony: Probably not. One cohort study from Brazil [SLIDE] published in 2019 found that age and male sex were associated with higher mortality from yellow fever. Race was not, though there is a numerical difference, shown here. And although contemporary look [SLIDE] at data from the 1800s does support the observation that mortality rates are higher in Caucasian populations, this is far from certain. As you can imagine, using data generated from the 1800s is not without issue.
This second study concluded [SLIDE] that resistance to yellow fever may have conferred a selective advantage. The difference is not one of race, but rather one ancestry and geographic exposure. If your ancestry arose from areas where yellow fever was endemic [SLIDE], you may have a lower probability of death.
We have seen this with other infectious diseases, even to the point where mutations that would otherwise be selected against persist. The one we’re most familiar with is sickle-cell trait and the apparent protection against severe malaria. Importantly, sickle cell disease isn’t transferred with race. Shown here are the CDC reported incidence rates [SLIDE] for sickle cell trait. This is based on information provided by 13 states. Notice that although the rates are different, sickle cell trait is not race-restricted.
As a comparator, in Greece sickle cell trait affects ~2% of the population. The incidence for one Greek Island – Orchomenos – has been reported as high as 20-23% [SLIDE]. Sickle cell isn’t a disease of blacks but a disease of those whose ancestors were exposed to malaria.
The same is seen with cystic fibrosis, a disease that likely protects against tuberculosis. In the United States, CF rates [SLIDE] again differ, but are not race-restricted.
Neither sickle cell disease nor cystic fibrosis is associated with a biological race but instead a biological disease: malaria for sickle cell and tuberculosis for CF.
Could the same be true for yellow fever? Although it is tempting to assume a similar selective pressure may have existed, as Mariola Espinosa [SLIDE] and others have argued, although elegant explanations are great, one still requires supporting evidence. For yellow fever, such evidence is lacking.
Adam: The people of 19th century New Orleans saw it another way — through a process called acclimation, or seasoning, or creolization — initially becoming, somehow, used to the noxious, toxic airs of New Orleans — and by the middle of the century was explicitly understood as having contracted and survived yellow fever. But acclimation was not simply immunity; it was tied up in a whole host of complex social structures. The historian Kathryn Olivarius, who wrote a fantastic paper on this topic, describes a [SLIDE] “socially acknowledged lifelong immunity that provided accessability to economic, political, and social power.” So you have a situation where immigrants don’t flee when the disease strikes — they try and contract it, even with a death rate as high as 50% — because surviving opened so many opportunities. Many jobs would not hire a young man unless he was acclimated; banks would refuse to lend to you knowing there was a high chance you might die in the next few months. Salaries were notably higher; and job prospects easier, especially since an epidemic year might kill half of the young men of an office. Being acclimated would secure a good marriage. By the middle of the 19th century, life insurers had caught wind, and would change their premium based on the medical verification of acclimation. There are even examples of widows using their acclimation to parlay a wealthy husband. Acclimation was so highly sought after that the Board of Health recommended in 1849 (in all capital letters) that THE VALUE OF ACCLIMATION IS WORTH THE RISK. [SLIDE]
Tony: Even today, some countries require proof of yellow fever immunity for entry. Here for example is the entry for Nigeria [SLIDE].
Adam: When I did my fellowship, there were still some countries such as South Africa that required proof of this as well, so I carried a yellow card in my passport So I think there are some fascinating parallels with COVID-19 here. The first is, I think, this idea of the Immunity Passport [SLIDE], which we heard a lot about in April and May of this year — as the Lancet described it “digital or physical documents that certify an individual has been infected and is purportedly immune to SARS-CoV-2. Individuals in possession of an immunity passport could be exempt from physical restrictions and could return to work, school, and daily life.” Some countries, Italy in particular, seriously considered this. And isn’t that a similar idea to acclimation? That catching a disease would give you some sort of social capital. Tony, what do you think about that parallel?
Tony: There are echoes of the “The value of acclimation is worth the risk” argument now heard in discussion of herd immunity with COVID-19. A couple months ago I had antibody testing for COVID. When I returned negative I was unhappy as it meant I was unlikely to have immunity and remained at risk.
But, as others have argued, the use of immunity passports is a bad idea. An editorial published on nature.com provided ten reasons [SLIDE]. Beyond the uncertainties related to lifelong immunity and possibility of reinfection, there are potential issues of access, discriminination, and marginalization. These issues are enormous.
Adam: Of course, acclimation referred explicitly to the white and Creole inhabitants of New Orleans — its social benefits did not accrue to the enslaved, or even free, Blacks that made a significant part of the population. While acclimated enslaved persons were sold for almost 25% more, at the same time it was argued that people of African descent were “naturally immune” to yellow fever. Physicians attempted to demonstrate that Blacks died at a far lower rate — for example, only three deaths were recorded in 1849 compared to 766 in whites. Surgeon and slaveowner Josiah Nott suggested that: “negro blood is an antidote against yellow fever, for the smallest admixture of it with the white will protect against this disease.” Of course, were this true, to me the logical solution would be to suggest increased mixing of the races, but that is not at all what the medical community suggests. Famous racist Samuel Cartwight, who you may know from developing the idea of drapetomania, or the illness that makes slaves want to run away, argued that the decreased toll on Blacks was Nature’s way to suggesting slavery was the natural order of things.
Tony, do you think that acclimation actually existed?
Tony: Let’s look back at Olivarius’ definition of acclimation [SLIDE]. If one were to define acclimation as lifelong immunity after Yellow Fever infection, then yes, it exists. But there is no racial or social underpinning for this. Whether the remainder of the definition existed… well you’ve already argued that it did.
It would be interesting to make some pathophysiologic comparisons [SLIDE]. Yellow Fever has just 1 serotype which results in lifelong immunity after infection. This is one reason why we have a successful vaccine for Yellow Fever. Compare this with another flavivirus: dengue. It’s worth noting that flaviviruses are named after the yellow fever virus (flavus means “yellow” in Latin). Dengue has 4 serotypes. Immunity to one serotype does not confer immunity to another serotype. In fact, and as many of you know, someone who experiences a mild infection with one serotype may experience hemorrhage fever if they are secondary infected with a different serotype.
This relates to the idea of “Original Antigenic Sin”. [SLIDE] Original antigenic sin has been best described in influenza. It is the idea that one’s immune system responds best to the original version of an infectious agent to which they are exposed. When they are exposed to a second, slightly different version, their immune system does not react in the optimal way. For influenza, this may mean an inadequate response to vaccination. Depending on the antigen against which antibodies are made in a first infection or immunization, subsequent immunization with a different antigen of influenza, may only boost the antibodies against the old antigen and may not recognize the new antigen.
In the case of dengue, when a second exposure is to a new serotype, this can result in an increased risk of hemorrhagic fever. This is an example of antibody dependent enhancement.
Returning once again to COVID-19, some have made arguments that are reminiscent of acclimation. Here, for example, is Rand Paul: arguing about “cross-reactivity” [SLIDE]. Well, it may be the exact opposite of what Senator Paul was suggesting. There have been a number of authors who have proposed the hypothesis [SLIDE] that prior exposure to the original SARS-CoV virus – the one that causes SARS – may predispose to a more severe response to SARS-CoV-2, just as can be seen with dengue. This, again, would be an example of the original antigenic sin.
Adam: Ultimately, yellow fever was defeated without having to contend with the racial and social inequities of the disease. By 1881, the Cuban physician Carlos Finlay had hypothesized that mosquitoes were the vector of the disease, soon after followed by sanitation and eradication campaigns even decades before Walter Reed provided the definitive proof. The last yellow fever outbreak in New Orleans (and the US) was in 1905.
Tony: And just as yellow fever disappeared, paralytic polio emerged.
That’s right Tony. Just as the end of yellow fever suggests, new scientific ideas had come into vogue both about the cause of disease, and about racial categorization. [SLIDE] Germ theory was fully developed, and along with it public health [SLIDE] — the idea that the government should take an active role in preventing disease, by increasing sanitation, draining swamps, providing free infectious disease hospitals to separate infectious individuals, and with aggressive quarantine and isolation measures in the settings of outbreaks. And consequently, mortality from infectious diseases started to drop over this period, 75 years before widespread use of antibiotics. [SLIDE] What we like to talk about less, though, is that the spread of public health was accompanied by ideas of eugenics — which disturbingly was explicitly linked to public health with the term “racial hygiene,” especially popular in Germany. If there were “constitutional” reasons that some groups of people were prone to disease — or in the minds of many eugenicists, “inferior,” did it not follow that the government should enact policies to encourage only the fit to have children? And make no mistake — eugenics was not a fringe movement but a part of mainstream scientific and medical life.
[SLIDE] The polio epidemics of the 20th century are a perfect example of this interplay between public health, social determinants of health, and eugenics. Polio had been a rare disease throughout most of human history until the early 20th century, when annual summer epidemics started to strike children in American cities. At its peak in the 1940s, polio paralyzed or killed over half a million people each year worldwide.
Tony, why did Polio suddenly flare up as things were improving?
Tony: As you noted, polio was not an emergent disease in the early 1900s. [SLIDE] It had likely been infecting humans for centuries. What we did see was more cases of paralytic polio.
Prior to the 20th century, most became infected with polio during infancy, a time when one continues to make use of passive immunity from breast milk. This meant that one could acquire active immunity while benefiting from passive immunity. The result was a relatively mild case of polio, specifically a lesser propensity for paralytic polio.
As sanitation conditions improved, polio was acquired at a later age. [SLIDE] This meant that those infected were less likely to have the benefit of passive immunity. The result was an increased propensity for severe polio, as shown in this study of the 1916 polio epidemic in NY City. Although this hypothesis has been challenged, it remains compelling.
There are a number of similarities to COVID, Adam. For one, shutdowns [SLIDE] were part of the initial response to polio’s emergence in the early 1900s. [SLIDE]
Adam: And, just like in COVID-19, it became clear pretty quickly that there were patterns to the type of people that polio would strike. Initially it seemed to strike the urban poor, though as we learned more about the disease it became clear it affected all social classes, and maybe even the wealthy more. But there was one notable exception — Black children. Just as with yellow fever, there was a widespread perception that Black children rarely got the disease — and now vital registers were showing that as well; in the 1924 Detroit epidemic, only 5 of 300 cases were Black.
And one of the most prominent arguments was the Constitutionalist argument, essentially a eugenics argument. George Draper, the polio expert at the Rockefeller Hospital, and FDR’s personal doctor, argued that Black children didn’t catch polio because of their hereditary constitutions — the “primitive” races were more resistant to disease (other than syphilis) compared with the “complex and delicate” bodies of Europeans. And this was the framing that early epidemiological studies used as well. Epidemiologist Paul Harmon in 1936 published a racial analysis of polio, similar to the studies for COVID-19. He found that the Black morbidity rate was 241 per 100,000 compared to 383 for whites in New York City, while in his Southern samples, the incidence rate was 2-4 times higher in whites. Ultimately, he concludes that racial susceptibility is the best explanation.
Tony, I think there are two interesting distinctions here — does polio affect people differently based on race? Or socio-economic status? And why might that be?
Tony: As mentioned earlier, the difference in rates of severe polio in the early to mid-1900s likely results from differences in the age of polio acquisition. Those who otherwise benefited from the improved sanitation saw the negative consequence of more severe polio. This meant that marginalized populations who did not have these same socioeconomic benefits experienced the ironic benefit of less severe polio. But, again, this wasn’t based on race.
Adam: Right. And, interestingly, Harmon overlooked the best counter to that argument — poor Southern whites had incredibly low levels of polio. Likely because of poor sanitation and lack of electrification leading to widespread infant infection and adult immunity, and the South actually had no major polio outbreaks until the 1940s.
And these were not benign distinctions; constitutionalist arguments were explicitly used to deny care for Black children, and to keep Blacks out of polio treatment and rehabilitation centers.
But things began to change towards the middle of the 20th century. The changing politics of race and the Cold War, and the activism of Eleanor Roosevelt, led to the Tuskegee Institute becoming a national polio hospital. An influx of Black voices — physicians and nurses alike argued vociferously that there was no racial difference between whites and Blacks — instead there was unequal access to care, leading to less registration of black cases, and a greater likelihood that providers in Black communities might be unaware of polio. [SLIDE] The March of Dimes, again back by the Roosevelts, adopted an official policy that polio struck “all races” equally, and included Black and white children in their advertising, and when the Salk vaccine trials were run in the 1950s (on HeLa cells I might add), Black and white children were both included in the trials, and Black physicians were actively recruited in the administration of the vaccine.
I want to be explicitly clear here — we are only talking about medical conceptions of disease. The Tuskegee Institute is still in the Jim Crow South, and getting the vaccine didn’t change that. In May 1954, the same year as Brown v Board of Education, Black schoolchildren in Mobile gathered to receive their Salk polio vaccinations — on the lawns of the segregated school, because they wouldn’t be let inside under any circumstances. They weren’t even allowed inside to use the restroom.
Tony: It’s important to note that yellow fever and polio were not the only plagues to shake our country — arguably the most important of the second half of the 20th century was [SLIDE] HIV/AIDS.
Adam: And in classic Tony and me fashion we had to cut for time, and because I would never want to subject anyone to listening to us for this long. [SLIDE] By the early 1980s, we had started to recontextualize our understanding of disease into risk factors, and in the early days of GRID/AIDS, when it was still unclear how the disease was transmitted, this was the frame that physicians and policymakers used to talk about the disease. Was it from new party drugs? Drug use? Prostitution? Was it something about the sexual lifestyles of the patients themselves? And I should mention here, obviously homosexuality is clearly not a “lifestyle” but was considered such in the discourse of the 1980s. And some of the early names of this disease betray the focus on “risk factors” — the 4H disease, for homosexuals, heroin Users, hemophiliacs, and haitians), or even more bluntly, the Gay Plague. It literally took the Surgeon General C. Everett Koop mailing an 8-page explainer to every single household in the United States — 107 million of them, the largest mailing in US history at the time, to shift the conception “from the moral politics of homosexuality, sexual promiscuity, and intravenous drug use, practices through which AIDS was spread, to concern with the medical care, economic position, and civil rights of AIDS sufferers.”
Which then, of course, brings us back to COVID-19. What, if any, lessons can we draw about race and the disease from looking at America’s past plagues?
You can certainly see how we’ve evolved in talking about race and disease. In the nineteenth century, ideas about scientific racism and inherent health differences between races — often used to justify slavery — were firmly entrenched. By the 20th century, though, discourse had shifted to talk about different risk factors for disease, and how these affected groups differently — poverty, housing, education. And now in the 21st century, with COVID-19, discourse has shifted again to talk about how structural racism and bias leads to systemic health inequities.
But, of course, at the end of the day, we can’t exactly pat ourselves on the back for that, since, like I mentioned at the beginning of the show, you can’t explain spin away the fact that a 40 year-old Black man with COVID-19 is 10 times more likely to die of the disease than a white man. And I think one of the most pertinent and timely issues here, just as in polio, is the deployment of a vaccine.[SLIDE]
The CDC and NIH through the US National Academies of Science, Engineering, and Medicine or NASEM, have been thinking about how to equitably distribute a vaccine ever since the 2009 Swine Flu outbreak. Their framework has traditionally drawn a distinction between prioritizing high risk occupations, especially first responders, and then high risk by health comorbidities, as you can see here. But based on what we know, you can easily see how the distribution would still be inequitable between these groups. Since May, the WHO has urged that “unjust disparities” be reduced in any distribution of a vaccine, and just last month NASEM updated [SLIDE] this approach to meet three equal aims — maximum benefit for all people, equal concern for all, and mitigation of health inequities. The new protocol, as you can see, is a bit different than the pandemic influenza protocol, first because COVID-19 is a different disease. And in each phase, each population group has equal priority. But within population groups, NASEM states, “vaccine access should be prioritized for geographic areas identified as vulnerable through the Social Vulnerability Index [SVI] or another more specific index.” A BMJ paper on this subject gives an example:
Tony: The authors write [SLIDE] “owing to their age, two 70 year-old women will both be at increased risk of dying from covid-19. But a well-off white suburban woman still faces a lower risk than a worse-off inner-city Black woman. Likewise, while neurosurgeons and nurses are health workers, the former are at far less risk than the latter, at work and at home. Accounting for such differences can considerably improve fairness.”
Adam: Tony, you spend a lot of your time in the world of clinical ethics. What are your interpretations of this?
Tony: Many models for vaccine allocation use the principle of treating people equally. The classic example of this is a lottery, as was seen in the movie Contagion.[SLIDE] There, birthdates were selected at random and vaccines were allocated to all those with that birthday. This is what was done with the draft during the Vietnam War. But, although this may treat people equally, it fails to incorporate important considerations – like social determinants of health – and therefore perpetuates inequities.
Adam: That’s helpful, Tony. So, it’s time for some conclusions. [SLIDE]. What are your takeaways from today’s discussion?
Tony: My major takeaway is that although we may see different rates of infection, morbidity, and mortality in different populations, it is not race which causes these differences. Prior explanations used these observations to support racist belief systems. And some remain susceptible to drawing similar conclusions. Hopefully some of what we’ve discussed has shown that there are alternate explanations.
In some cases it is ancestral factors like infectious disease exposure. This is true for sickle cell disease and cystic fibrosis, two diseases that are not race-restricted but which experienced selection based on relative protection against malaria and tuberculosis. A similar story has been argued for yellow fever, but not only is there uncertainty about the historically described racial differences, an evolutionary explanation is far from proven.
I don’t think we can explain COVID based on geographic exposures and ancestral inheritance, though I must say some intriguing data was published in Nature last week.
In other cases, observed racial differences are better explained by the social determinants of health. For polio, these social determinants may have afforded a paradoxical protection. For most conditions, and COVID is one of them, the social determinants of health lead to worse outcomes.
Adam: I think that’s a good insight, and part of a larger and long overdue conversation we’re having in general about “race essentialism” in medicine and biological sciences in general. But I still struggle with the takeaway from working on the episode. I think it’s undeniable that the medical conception of race, the social determinants of health, and plague has dramatically progressed over the past two centuries, even if there is still the persistence of old ideas. But have we gotten better at actually doing anything to combat these inequities? Or better care for our patients? On that, I’m less certain — but the fact that all of us here, at the Massachusetts ACP, and nationwide, and having this conversation gives me hope. Thank you so much for listening! Any questions?