Have you heard this one? A sociologist, a lawyer, and a biologist walk into a bar, scoot their stools up to the counter, order drinks, and begin to chat. Suddenly, a booming voice (God, the bartender?) envelops them. “What is the meaning of race?” the voice asks.

While the question may seem straightforward on its face, it quickly spawns further questions, often vexing. Is race purely a political construct, or is it biologically encoded? Certainly there are aspects of human biology—skin color, hair color, the presence or absence of epicanthic folds, etc.—that are commonly associated with racial differences, but is race just the sum of these physical features, with all of the overlaps, exceptions, and ambiguities they involve? How do genes factor into the story? And what connection—if any—is there between biological markers of race and the social experiences of racial groups?

Each of the three drinking buddies has a lot to say to God or Sam Malone, and, by the way, their responses don’t end in laugh lines. The biologist, Richard Francis, engages other issues, though his concerns directly affect how we answer the loud voice. But the sociologist, Ann Morning, and the lawyer, Dorothy Roberts, are narrowly focused on the science of race and how medicine mediates racial experience. And with good reason: in the United States people of a darker hue (on average) die sooner than pink-skinned people. They are afflicted with higher rates of particular diseases, such as high blood pressure, strokes, and kidney failure. So the race you’re born with, or, rather, which race you are born into, might mean a healthier, longer life—or not.

These days large numbers of medical research dollars are devoted to finding genetic differences between races that might explain health disparities. But many students of biology and race, and at least some of our bar mates, think that is a bad idea. They are not against medical research per se but against bad research. Instead of looking for genes that cause race and attending health outcomes (the standard approach) they point to evidence strongly suggesting that everyday events alter our bodies, making them sicker or more resistant to disease—events that the political economy ensures are more or less common depending on which racial categories one is assigned to. Indeed, it may be that biology doesn’t create race but that racial marking creates new biological states via processes that all three of these thinkers discuss in new books.

In The Nature of Race: How Scientists Think and Teach about Human Difference, Morning gleans the meaning of race from interviews with university students and their professors and from close reading of high school textbooks. She presents detailed information with great care and enlivens the discussion with hilarious tongue-tied statements from students and professors as well as personal anecdotes. When she takes her two-week-old daughter for a doctor’s visit, the hospital admissions clerk won’t allow the baby to be seen without first having a racial designation. When Morning suggests “multiracial”—she usually identifies as black; her husband is Italian—the clerk replies, “That’s not an option” and settles instead for “race unknown,” as if that could offer significant clinical information.

Race is engrained in American medical practice. Sometimes beliefs about racial difference are even wired into medical diagnostic machines. For example, you can’t get a bone scan evaluated without designating a race, because the formulae programmed into bone densitometers use different standards for assessing bone thinning in white, Asian, Hispanic, and African American women. The evidence supporting different standards is rarely questioned and certainly unknown to the technicians who operate the machines. Often even the radiologists who evaluate the results don’t know much about the differing standards.

Or consider spirometers, which measure lung function. The normal functioning of black people’s lungs is typically presumed to be 10–15 percent below that of white people’s. As Lundy Braun, who studies the intersection of race and medical science and technology, has shown, the presumption stems from a poorly supported idea that blacks inherently have lesser lung capacities than whites. Yet spirometers are calibrated to account for this difference. Some machines actually have a “race” switch built into them, which technicians flip depending on what race they believe the patient to be. Pegging the lung function of blacks at a lower level means, among other things, that they have to be sicker than whites in order to qualify for worker’s compensation or other insurance for lung-related illness.

In The Nature of Race Morning uses the lenses of biology and medicine to isolate several conceptualizations of race. She finds that there is no consensus among either social or biological scientists and groups her respondents into three general categories: essentialists, anti-essentialists, and constructivists.

It may be that biology doesn’t create race but that racial marking creates new biological states.

Essentialists propose that there are biologically grounded human races that share some more or less immutable essence. In modern terms the essence is usually understood to be specific genes or groups of genes, or to result from evolutionary processes that have acted on genetically isolated populations.

Here is how one of Morning’s interlocutors, a biologist whom Morning classifies as an essentialist, chews over the definition of race:

Well, I think the textbook will say that there are three major races—Negroid, Caucasian, and Asian or Mongoloid . . . . So I guess in the old definition they’re like you would imagine they are: the edges are a little blurred, but the old classical definition of race is a lot clearer. And don’t we kind of look at people today [like that].

Referring to Morning, this scientist continues:

I said you’re part Caucasian and part black, so I’m taking two of the standard races, and I’m mixing them in some proportion, and that’s probably the best I could do in terms of race: three races . . . blurring at the edges.

But this blurring is a problem for anti-essentialists, who see the fuzziness of racial categories as a sign that they can’t be rigorously connected to particular genes. Anti-essentialists either emphasize the genetic unity of humans in a single race or highlight how difficult and arbitrary it is to draw biologically based racial boundary lines. Anti-essentialists agree that there is wide biological variation in human traits, but because groups of traits don’t link and vary together, this variation can’t be used to set up clear racial categories.

So anti-essentialists open the door to human agency in organizing racial groupings, but they don’t explain just how humans might construct and maintain racial groups. Enter the constructivists. Not only do they argue that race is a social category, but they also maintain that the science that produces claims of biological difference is itself shaped by social forces. One constructivist tells Morning the point

is not to . . . say it’s all cultural, it’s not biological, but rather to say that constructions of difference, be they characterized as cultural or biological . . . really operate in a sociopolitical framework that is about relations of inequality.

If the science and social science faculty at major universities sound confused or at odds on the question of race, where does this leave the students? In Morning’s study, they reflect some of the same divisions found among faculty but also worry that they not offend peers by appearing racist. Many express genuine concern about racial inequality. Here is how one student tries to combine views about difference and equality:

So the genes make them different, but, because they look different—we look different—the environment is going to play a role. People have darker skin; they might be less prone to skin cancer because they have that protective layering. But it doesn’t make them different people, so . . . I don’t think people act—if you just take the U.S. and different races here, and if they were born here, and they’re different races, I don’t think that makes them act differently, makes them any different.

Morning is surprised by the enduring strength of the biological view of race, given that many social scientists and some biologists still think that the biological concept of race disappeared after World War II, with the revelation of the horrific consequences of Nazi racial beliefs. She devotes considerable thought and analysis to the social and structural forces undergirding the idea that biology offers a good basis on which to construct our understanding of race. Morning believes that by moving from a view of race based on how we look (skin color, hair texture, etc.) to one based on genes, a biological explanation of human difference has been made suitable for the post-racial era in which we supposedly live. Essentialism has held its own against constructivism and anti-essentialism.

The persistence of biological understandings owes something to an unavoidable fact: race and health are inextricably intertwined. But this doesn’t mean biology produces race. It may be that race produces biology. A newer, but still embodied, view of human difference, one in which we conceptualize how social difference and deprivation change the body’s physiology, has yet to make inroads into public discussions of race. This is a concept that Roberts nails.

In Fatal Invention: How Science, Politics, and Big Business Re-Create Race in the Twenty-First Century, Roberts argues passionately and relentlessly—you can picture her making her case to a rapt jury—against the idea of race as a biological trait, which she calls, per her title, a fatal invention. Her evidence against biological causes (but not biological effects), and her insistence that believing in the biological basis of race is fatal to people of color, are compelling. Her case study of racial differences in breast cancer fatalities illustrates the point.

In Chicago in 1980, black and white women died of breast cancer at the same rate. Today, despite being slightly more likely to get breast cancer, white female Chicagoans are half as likely to die from it. Could the difference in death rates be due to genetic differences between black and white women? A wealth of evidence suggests otherwise.

In Chicago in 1980, black and white women died of breast cancer at the same rate. Today, the white women are half as likely to die from it.

First, the disparity is recent, so it is unlikely to be due to the slow evolution of genetic variations between populations. Second, the disparity is local. In New York City, where the disparity still favors white women, the difference is only 15 percent. Roberts interviews Dr. Steven Whitman, an epidemiologist at the aging Mt. Sinai Hospital—located in the overwhelmingly black community of North Lawndale on Chicago’s West Side—who seems to understand how such a huge divergence came about. As he explains, in the 1950s the residents of North Lawndale were white. But in that decade, 110,000 of the whites moved out and an equal number of blacks moved in. Then half the neighborhood burned down during the riots that followed Martin Luther King’s murder, and now only 40,000 residents remain. Their median income is about $28,000, whereas Chicago’s median is $46,700. Mount Sinai Hospital has suffered, so that comparing its bankroll and daily operating cash to that of Northwestern University’s Memorial Hospital is a bit like comparing an automobile assembly line worker’s income to Mitt Romney’s.

This disparity has consequences: the breast cancer death rate for Chicago’s black women has not changed since 1980. Women of color living in segregated neighborhoods have limited access to mammograms, sometimes having to travel on public transportation up to ten miles away, only to be told that their health insurance won’t cover the screening. Adding injury to insult, the quality of available mammograms is poor compared to what’s offered at the state-of-the-art facilities more commonly accessible to white women. Whitman cites a North Lawndale facility that catches only two cancers per thousand people screened, rather than the expected six. Getting advanced care is next to impossible for women living in black neighborhoods. In Whitman’s words, all “the fancy institutions . . . are in white neighborhoods.”

What ought to be done about the disparities in breast cancer deaths between blacks and whites in Chicago seems clear: build state-of-the-art hospitals in the black neighborhoods and treat women where they live. Or organize a transportation system that would bring women in need of high-quality screening and treatment to existing high-quality centers. But scientists instead seek funding for basic research focused on possible genetic explanations for race-based health disparities.

Roberts’s answer to the booming voice is clear:

Race is a political category that has staggering biological consequences because of the impact of social inequality on people’s health. Understanding race as a political category does not erase its impact on biology; instead, it redirects attention from genetic explanations to social ones.

With this framing, the question for biologists changes. It is no longer, how does biology create race, but how does racism become part of one’s cellular- and systems-level physiology? How does the social become biological?

Four interlaced frameworks structure answers to this question: embodiment, allostasis, dynamic systems, and epigenetics.

Nancy Krieger, the epidemiologist who developed the embodiment framework, defines it as the “many different ways that we literally incorporate the world outside of us” into the biological responses in our bodies. Krieger points to studies showing that people who experience racial discrimination have higher essential hypertension and, among women, are more likely to give birth to low-weight babies.

It is no mystery how this might happen. Until recently physiologists viewed the body as a self-stabilizing, or homeostatic, machine. The thought behind homeostasis was that when events cause a loss of physiological balance, the body rights itself, kind of like the shmoo dolls from my own childhood—you could keep punching them over, and they always popped back upright. Homeostasis works, conceptually, when there is an occasional stressor. But when stress never lets up, the body’s response (release of cortisol and accompanying increased heart rate and blood pressure) becomes constant, or allostatic. The body learns from past experience to respond to expected future events. Allostasis is a late twentieth–century physiological mechanism that has the potential to explain how the experiences of racism, poverty, and other social stressors become embodied as illnesses such as essential hypertension. Under constant stress, blood pressure remains elevated; immune systems stay alert. The body is always ready for the next battle.

Which brings us back to breast cancer. Not only rates, but breast cancer patterns differ between black and white women. When diagnosed, black women are more likely to be under the age of 35 and to die by the age of 50. Some have argued that their tumors spread more quickly because they differ physiologically from white women. Black women tend to lack key hormone receptors, which means that tumors respond poorly to familiar hormone-based treatments.

People who experience racial discrimination have higher essential hypertension and are more likely to give birth to low-weight babies.

Physician and cancer researcher Olufunmilayo Olopade noticed these differences and originally assumed that they were due to genetic, race-based differences between white women and women of African origin. Recently, however, she has begun to see things differently, looking to how women of color embody the daily stresses of racism and economic deprivation. The absence of hormone receptors could be a function of environmental factors, but, seeking other explanations, Olopade has teamed up with University of Chicago biopsychologist Martha McClintock to ask a new kind of question. In a study of mice that primarily modeled the growth rate for human breast cancer, they have shown that socially stressed mice express certain genes differently in their mammary tissue. Specifically, the stressed mice demonstrate an uptick in expression for suites of genes involved in lipid metabolism and a biochemical pathway that converts sugars into energy. Both pathways contribute to breast cancer growth. The stressed mice are genetically the same as unstressed controls, but it’s not what genes you have that count so much as which genes your cells express.

When you join the concepts of allostasis and embodiment, disease emerges as something that happens in bodies with histories. Each body forms a dynamic system not only with its current environment, but also with its particular history. Bodies are always in process, reflecting the past and incorporating the present. Dynamic systems theory explains stability in an organism or in a cell, but also offers a way to understand how, when a contributing process goes awry, a system destabilizes. If we think of breast cancer as a destabilized system, then it makes sense to ask what contributes to stability and how destabilization occurs.

Back at the bar, Roberts has supported her ideas with a dozen different examples from science, medicine, pharmacology, and genetic surveillance. But by now the biologist has gotten antsy. Freelance writer and neurobiologist Richard Francis, author of Epigenetics: The Ultimate Mystery of Inheritance, is excited to explain how new understandings of a long-known, but until recently poorly understood, phenomenon called epigenetics form part of the story. Although Francis does not specifically address the question of race, he realizes from listening to his drinking mates that what he has to say directly relates to answering the booming voice. Like Morning and Roberts, Francis recounts a bit about the history of genetics, focusing briefly on Morgan, Mendel, and the relationship between genes and phenotypes, as in that fruit fly with a gene for the phenotype of white eyes.

The Morgan-Mendel tradition gave rise to a reductionist approach to genes as causes of traits. Francis, however, emphasizes another tradition, one represented in the work of geneticists Sewall Wright and C. H. Waddington. Both focused on the complex pathways that intervene between genes and traits. Francis echoes these scientists, viewing genes as tools or cellular resources, responding to environmental input. Modern epigenetics is the study of gene modifications induced by local changes in the environment. An epigenetic event is not a mutation, because there is no change in the genetic code. Instead small molecular add-ons to DNA regions that control gene expression can silence a gene or boost its expression. Epigenetic changes aren’t permanent, but they can endure for long periods of time, even across generations.

Consider the fetuses that were gestating in their mothers’ wombs during the famine that swept the Netherlands at the end of World War II. Not surprisingly, the infants born from starving mothers were undersized and not so healthy. Less expected is that members of this same cohort, examined in adulthood, were twice as likely to be obese as those born before or after the famine. They also had an elevated risk for developing schizophrenia and other mental disorders. Epigenetic modification ranks first on the list of possible mechanisms that underpin these second-generation effects. Francis explains the science behind these conclusions with clarity and forthrightness. His path crosses with Roberts, Krieger, Olopade, and others in his argument that genes are responsive elements in the cell. Environmental impingements, especially at critical developmental moments such as pregnancy and childhood, have long-term biological consequences, in some cases yea unto the grandchildren’s generation.

So what is the meaning of race? Morning and Roberts argue convincingly that race is a socially produced set of categories that has profound and often terrible biological consequences. Without putting words into Francis’s mouth, since he doesn’t discuss race per se, he would, I think, agree that epigenetics provides a well-understood tool that ought to be used more frequently in studies of biological correlates of racial inequality in health. If our goal is not just to understand race, but to improve health, then we don’t need research to find genes that cause essential hypertension as much as we need to address the sources of chronic stress. And let’s get those mammography machines into the inner cities and out into rural America.

Understanding race as a producer of health outcomes, but not a result of genetic programming, doesn’t suggest that we abandon biomedical research as it relates to race, but it does suggest that looking for race-oriented genetic precursors of disease is a fruitless labor. We need a different kind of investigation. Already, the National Institutes of Health devote significant resources to studying the epigenome. But NIH’s illustration of epigenetics emphasizes an exploded segment of DNA, not air pollution or the lack of fresh, high-quality produce in blighted city neighborhoods. And funding for research into the allostatic mechanisms by which, say, blood pressure becomes chronically elevated, is hard to come by.

The question of what exactly race is may be with us for while. But if we are dedicated to delivering social services and doing the right kind of laboratory research, we can, right now, address the comparative ill health of people of color, the poor, and the medically underserved.