The science of "race." A TNR Debate, Day 2

Editor's Note: This is the second part of a TNR debate about genetics and race. To read Merlin Chowkwanyun's original article, click here. To read Justin Shubow's response, click here.


Dear Justin,

I'm grateful for the serious engagement with the questions I raised, and I hope this debate continues long after our exchange. I cannot address many of the claims in the allotted space, but here are some.

You claim that I have two "chief problems" with the slavery hypothesis for hypertension. Actually, there's a third one you skirted, but it may be the most important: It's factually wrong, at least according to careful historical scholarship that I summarized and that I did not see you refute. Why is this so important? You claim that this new thinking on race, genes, and health reflects "truth." But using specific examples (beginning with the slavery hypothesis), I wanted to show that these claims in fact are often demonstrably false or much weaker than their proponents suggest. The evidentiary record is critical for evaluating the racial health claims more generally. It's not clear to me whether you buy the slavery hypothesis or not, nor do I see any direct reckoning with the other examples I pointed out.

You also suggest I am a reductive zero-sum thinker. In fact, my article is a brief against such thinking, which is far more common among those who link race, genes, and health. On the Oprah Winfrey episode I cite, it's notable that neither Winfrey nor Mehmet Oz, her expert guest, mentioned any explanations besides the one grounded in racial heredity. As for genetic explanations themselves, let me be clear: I do not deny that genes play roles in many health conditions. What I am concerned about is the overstatement of their role when the evidence isn't conclusive--and, more specifically, the sloppy labeling of certain health conditions (or their distributional patterns among the population) as "racial" and determined by biology. I grounded my critique in history to show that the racial categories have been porous. That will continue to be the case, despite those today who act as if we have hit taxonomic eureka on pinning down a supposed biological essence of race and then use it as a fixed empirical variable.


An example you use to make a case for the biology of race is very weak. You cite Census data that shows, in your words, that "Latinos, who have [like black Americans] suffered maltreatment, have a greater life expectancy than non-Latino whites." You imply there's something biologically special about "Latinos" (and this, again, is a very porous category) that may explain these numbers, especially since you "control" for environmental factors, so to speak, by noting that Latinos also suffer "maltreatment" but exhibit better numbers. There are many problems here. First, the category itself, like "Asian," encompasses such a huge swath of people--people from Mexico, Guatemala, El Salvador, and Colombia, to name just some (and that's not even thinking about the huge regional variations within these countries). As I argued in the piece, subsuming these disparate groups under a racial category and then banking on a health-outcomes explanation is hugely imprecise.

Second, I don't think you are interpreting the numbers in a sophisticated manner. The table you present only slices the mortality data in one way: by racial and ethnic Census categories. But if we were to dip into the much larger Census data set, we could slice the numbers in other directions--including country of origin, or generation, or Census tract, or income level (you and I can name more)--that would complicate generalizations about Latino health. You also make much of the higher life expectancy relative to non-Latino whites. But longer life expectancy does not mean a better health experience, as the gulf in various specific health conditions shows. A recent Centers for Disease Control and Prevention release summarizes numerous health inequalities between Latinos and whites--for example, much higher incidence rates of cervix and stomach cancer among Latinos.

And your analysis is very historically loose. It clumps together imprecisely the experiences of black and Latino Americans with racial subordination. While there is undeniable overlap in both experiences, your characterization ("likewise suffered maltreatment") is too broad. Black Americans, especially the poor, suffer more than any other group from racially segregated living in underdeveloped, under-resourced areas with high concentrations poverty, as sociologists Douglas Massey and Nancy Denton showed in American Apartheid. To put it simply, although Latinos and black Americans suffer from the same kinds of maltreatment, the overall degree is substantially different.

A fascinating micro-level example of how this can affect health outcomes comes from urban sociologist Eric Klinenberg in his stunning Heat Wave: A Social Autopsy of Disaster in Chicago, a study of the 1995 Chicago heat wave that left hundreds dead. In one of his most memorable chapters, Klinenberg focuses on two Chicago neighborhoods, North Lawndale (96 percent black) and Little Village (85 percent Latino). Why, in 1995, did North Lawndale see much more heat-related death (19 deaths: a rate of 40 per 100,000) than Little Village (3 deaths: a rate of less than 4 per 100,000)? Klinenberg rejects a racially essentialist explanation and instead grounds his explanation in the particular structural characteristics of each neighborhood. In contrast to North Lawndale, Little Village's economic development, stable community institutions, vibrant public spaces, and low crime rate gave it "an array of stores, banks, and other commercial centers in the area" that "provided seniors with safe, air-conditioned places where they could get relief from the heat." By contrast, a key reason for the higher rate of black Chicagoans' deaths was that "they are the only group in the city segregated and ghettoized in community areas with high levels of abandoned housing stock, empty lots, depleted commercial infrastructure, population decline, degraded sidewalks, parks, and streets, and impoverished institutions." Chronic underdevelopment and ghettoization of black neighborhoods in particular--best documented by historian Thomas J. Sugrue in his The Origins of the Urban Crisis: Race and Inequality in Postwar Detroit--are, to me, much more convincing and demonstrable root causes behind the black-Latino health differentials than Latino special genes that somehow keep Latinos alive longer.


I found your characterization of race as a "cluster concept" provocative and intellectually honest, since you admit its imprecision (which seems inconsistent with what you write elsewhere). But you say this imprecision does not preclude the application of them "accurately to things in the world." The problem is--as I tried to show with Sally Satel--arbitrarily bounded cluster concepts don't really work as proxies for the likelihood of illness. Satel's own number--40 percent--isn't even a majority. Sickle-cell trait, in fact, only occurs with higher concentration among populations descended from certain areas of Africa (Western and Central). Yet those who advocate a race-based medicine make sweeping generalizations for the entire black population and the supposed frequency of this trait within it. It is a confusion of geographically concentrated health conditions with race. You make the same mistake in your citation of Pinker, again mapping race onto salient geographical genetic variations. But who decides the boundaries? This ambiguity is what Jonathan Marks is criticizing when he discusses Cavalli-Sforza's "genetic map" and its coloration of four regions that suggests real distinct races. I think you misread the page, and I invite readers to judge--especially in tandem with Marks's main homepage of Human Genome materials. (I also note that you try to turn Marks on me, but you don't engage Richard Lewontin, whom I also cited, and his classic claim that, to use Marks's own summary of it, "the overwhelming bulk of detectable genetic variation in the human species is between individuals in the same population.")

On the comeback of race, I was disappointed that you did not engage substantively with the two explanations I offered--financial interest and often well-intentioned techno-utopianism in the precision of new scientific metrics. Instead, you dismiss them abruptly by calling them "[not] very helpful" with little elaboration. By itself, the financial explanation is too simple, and I suggest as much by devoting only one paragraph to it and writing that "it's not just self-interest fueling the boom in genomics." But it cannot be discounted, either. BiDil, which I discuss, was originally not developed as a racial drug. Only after the failure of a clinical trial for its antecedent did its proponents, as Pamela Sankar and Jonathan Kahn detail in a 2005 Health Affairs article, successfully repackage it as having racially particular effects. Medical sociologist Steven Epstein, in his just released Inclusion: The Politics of Difference in Medical Research, also notes that BiDil's classification as a racial drug has also allowed it a patent extension of an extra 13 years. He quotes further a New England Journal of Medicine writer who characterizes BiDil as conceived "in large measure by regulatory and market incentives."

You declare boldly that "the simplest explanation for the revival of race is that it reflects the truth." I pointed out that people a century ago also invoked the language of truth to claim objective measured basis for whatever number of natural races they felt existed. You admit these prior incarnations were "quack science" but seem to suggest that, this time, the proponents of racial biology have finally gotten it right. For you, we have reached an end of history--the teleological jackpot when it comes to locating the real races and their biological bases. Why this time as opposed to the waves of previous claims? You refer to "leading scientific arguments" about race's biological validity with a certainty that they are right about race while their counterparts in 1923 (who were just as certain) were not.

Finally, I agree, though for different reasons than you, that race "is still an important variable in research." To quote historian David Hollinger, I believe that "racism is real, but races are not," which poses a challenge for data collection. How can one track racism without re-perpetuating racial categories that helped cause it in the first place? How do we reject race as an intellectually viable concept while at the same time identifying very real inequality in health? Not collecting data by race would be a boon to segments of the political right who would love to deny that racial inequality in health persists today. What do we do? In his article (which I quoted), Adolph Reed identifies a promising start in the work of Judith Kaplan and Trude Bennett who, in a 2003 Journal of the American Medical Association article, proposed that researchers more clearly reflect and articulate why they use race in research. Two of their propositions include:

1. When race/ethnicity is used as a study variable, the reason for its use should be specified. ...

5. In the interpretation of racial/ethnic differences, all conceptually relevant factors should be considered, including racism and discrimination, SES, social class, personal or family wealth, environmental exposures, insurance status, age, diet and nutrition, health beliefs and practices, educational level, language spoken, tribal affiliation, country of birth, parents' country of birth, length of time in the country of residence, and place of residence.

Thanks again for this letter, which made me think hard about many of my own views. I think readers will profit from both sides. In the end, though, I find your case does not persuade me to support one of history's most questionable faith-based initiatives: the ideology of race.

Best,
Merlin

By Merlin Chowkwanyun