Hello, I’m Shelley Tremain and I’d like to welcome you to the sixty-second installment of Dialogues on Disability, the series of interviews that I’m conducting with disabled philosophers and post to BIOPOLITICAL PHILOSOPHY on the third Wednesday of each month. The series is designed to provide a public venue for discussion with disabled philosophers about a range of topics, including their philosophical work on disability; the place of philosophy of disability vis-à-vis the discipline and profession; their experiences of institutional discrimination and personal prejudice in philosophy, in particular, and in academia, more generally; resistance to ableism, racism, sexism, and other apparatuses of power; accessibility; and anti-oppressive pedagogy.
Today’s installment of Dialogues on Disability revisits the interview that I did with Quayshawn Spencer in May 2017. I acknowledge that the land on which I sit to conduct these interviews is the traditional territory of the Haudenosaunee and Anishnaabeg, covered by the Upper Canada Treaties and directly adjacent to Haldiman Treaty territory.
Quayshawn Spencer is currently Robert S. Blank Presidential Associate Professor in the Department of Philosophy at the University of Pennsylvania and specializes in philosophy of science, philosophy of biology, and philosophy of race. He enjoys powerlifting, running, and Southern cuisine, especially Kentucky Bourbon and Southern B.B.Q.,and, in particular, Memphis dry ribs.
[Description of photo below: Headshot of a smiling Quayshawn, a black man, who has short hair and is wearing rectangular glasses, a striped bow-tie, a button-down shirt, and a suit jacket.]

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Welcome to Dialogues on Disability, Quayshawn! You were born in Gardena, California, which is just west of Compton, and went to high school in Nashville, Tennessee, where you fell in love with science. Please fill in the details for us.
Thank you very much for the invitation to be interviewed, Shelley.
Well, it’s interesting when people ask, “Where are you from?” I was born in California, and, to this day, that’s the state where I’ve lived the longest. However, my childhood years were mostly spent in good ‘ole Tennessee. Living in Tennessee is really what made me who I am today. When my family moved to Tennessee, it was a culture shock to see how racially segregated life was there. Even as a third grader, I remember the lunch tables in the cafeteria were racially segregated and interracial friendships were taboo. In fact, that was a nice way to get labeled a “sell out” and become a target for harassment.
That’s actually how I first got interested in race issues. I grew up on a rather dangerous side of town known as “East Nashville.” East Nashville was also where low-income Nashvillians lived—surprise surprise—and I grew up below the poverty line or close to it for all of my childhood. I had a knack for academics, but, unfortunately, East Nashville public schools were not models of academic excellence. In fact, it was a safety hazard to get straight A’s in my school district! To be labeled a “nerd” was a surefire way to get harassed and beat up. Since my family could not afford to send me to private school, the only other option for “making it out” was to get into an academic magnet school. Eventually, I was lucky enough to get into the state’s highest ranked academic magnet high school: Martin Luther King Magnet. MLK (as we call it in Nashville) was a high school for health sciences and engineering, and it was there that I fell in love with science.
What convinced you to switch from your early goals of a career in science or medicine to a career in philosophy?
Like many in my high school graduating class, I came out of MLK with a plan of getting an M.D. I was a little different, though, because I also wanted to get a Ph.D. in biochemistry and pursue the career of a medical college professor. I fell in love with biochemistry due to a wonderful experience that I had at Meharry Medical College working in a biochemistry lab. Fortunately, life didn’t work out that way. I ended up double majoring in chemistry and philosophy at Cornell, which is where I went to college. I added philosophy as a major due to a really good feminist philosophy course I took with Jennifer Whiting. I particularly liked the black feminism literature we read, including, but not limited to, Angela Davis’s Women, Race, & Class.
Even after I added the philosophy major, I was still a scientist at heart. All of that changed when I took a graduate-level philosophy of science course with Richard Boyd. The course challenged whether science could give us objective knowledge about the world. In the course, we read The Bell Curve—an infamous attempt to explain racial gaps in average I.Q. scores with primarily genetic variation. We also read some really good philosophical critiques of that book. My favorite was Ned Block’s “How Heritability Misleads About Race.” I was really intrigued with how philosophers can make a difference to scientific practice. But I wasn’t hooked yet.
It wasn’t until the last day of the course that I got hooked. In his closing statement, Boyd threw out a profound question to the class that I’ve been trying to answer ever since: “Are races even natural kinds?” The thought was that if races—as understood in The Bell Curve—were more like political affiliations than biological species, then it would be a category mistake for the authors of The Bell Curve to attribute non-accidental biological properties to them, such as possessing average differences in allele frequencies for genes related to intelligence—for a good philosophical discussion of category mistakes, check out this book. I thought that Boyd’s question was a great one; and that I should answer it. So, I changed my career goal to becoming a philosophy professor. Yeah, my parents were ecstatic about that!
[Description of image below: Quayshawn is standing behind a classroom media station. He is wearing rectangular-rimmed glasses, a dark suit jacket, a button-down shirt, and a tie with diagonal stripes. His right hand holds a microphone in front of his body; his left arm is outstretched, with his left hand on the media station; and his head is tilted slightly to the right. He appears poised to respond to an audience member’s question.]

What do you think are the most exciting avenues for philosophers to pursue in philosophy of race?
Good question! There are two main areas of research in the philosophy of race: the metaphysics of race and the moral and political philosophy of race. However, in recent years, race issues related to philosophy of language—for example, identifying the meaning of racial epithets—have risen as an important area of research as well. As for what’s exciting: it’s all exciting! But seriously, the most exciting philosophical topics, in my opinion, across specialties, are ones that tackle the socially and scientifically important issues of our time. And there’s lots of those to go around these days that scream out for help from philosophers of race.
For instance, after the Human Genome Diversity Panel was put together and used to divide people into different levels of genetic clusters in 2002, results came out that looked like races in certain folk racial discourses. In fact, I’ve talked to geneticists who literally didn’t know what to think about the metaphysical implications of their research. These initial genetic results and others like them led to an enormous amount of metaphysical research on whether it was possible to define “race” (in at least some contexts) in a biological way using these results. If biology isn’t your thing, but, say, social science is, then there is plenty of work to be done in the area of how social scientists should define and measure race-related cognitive biases, such as stereotype threat and implicit racial bias.
In case you haven’t heard, there is a replication crisis in social psychology, and stereotype threat research is at the center of this mess. As for implicit racial bias research, it’s recently taken a hit because the main tool used to measure implicit racial bias—the Implicit Association Test (I.A.T.)—has been shown to be neither precise nor accurate. Part of the solution, at least with respect to the I.A.T., will come from more carefully defining “implicit racial bias,” since the literature is a mess with respect to what that is. So, in my opinion, there’s lots of exciting research to be done on the race and psychology front.
Last, but not least, Trump’s presidency is going to generate lots of work for philosophers of race. I’ve already seen some excellent attempts to define “institutional racism” in more nuanced ways at philosophy conferences. Once Trump assigns another conservative judge to the U.S. Supreme Court, you can kiss race-based preferential affirmative action good-bye, unless philosophers come up with a way to defend it that translates into a viable legal defense. It’s on pretty shaky legal grounds now. So, there’s lots of work to be done in the area of race and justice as well.
You have researched the interaction between race and lactose intolerance. Please explain this research and your interest in it.
Yes, let’s get to it. I’m lactose intolerant and so are 65% of adults according to the NIH; yet, it’s considered an impairment by American medicine—a point to which I will return. I should say upfront that I’m torn about whether I’m a disabled person in virtue of being lactose intolerant. For one, I’m pretty sure that I wouldn’t qualify as legally disabled according to the Americans With Disabilities Act—although celiac disease and severe food allergies now qualify. Also, whether I would qualify as disabled varies with leading scholars on disability. For example, on Elizabeth Barnes’s view of disability, I wouldn’t qualify as disabled. But on your view, I would. If I’m not mistaken, to be disabled in your view is to occupy a low-power node in a network of power relations arising from common perceptions of one’s body and mind among people in the same society. Thus, people are disabled in virtue of being disempowered and disability is relative to a society and a time period in that society.
I like this view, and, if anything, I think it nicely explains why Americans view lactose intolerance as an impairment. I think they do only because of U.S. racial demographics and the food culture that results from it. But more on that later. First, I want to clarify what lactose intolerance is, what health impacts it has, its genetic causes, and its evolutionary origin. I want to do this because there is a tremendous amount of miseducation out there about lactose intolerance. For example, it’s not uncommon that I hear people say that all of us lactose-intolerant people can’t digest eggs or that we all can digest goat milk. Last, I’ll say a bit about my research on the link between lactose intolerance and race, as well as why I think it’s an interesting example for philosophers of disability to look at.
According to the NIH, lactose intolerance is the “impaired ability to digest lactose.” Lactose is a sugar that is almost exclusively found in foods that contain mammal milk since it’s a sugar found in almost all mammal milk. It’s hard to find naturally occurring lactose outside of mammal milk. Notice that I’m saying “almost” a lot. That’s because there are very few universal truths in biology. While it’s true that almost all foods that contain mammal milk have lactose and also true that almost all foods with lactose contain mammal milk, some foods with mammal milk contain no lactose and some foods with lactose contain no mammal milk. Good examples of the latter case are processed foods with lactose as an additive.
For instance, Utz Kettle Classics Old English Style Salt & Malt Vinegar potato chips have lactose as an ingredient, but no milk product as an ingredient—for example, whey, cheese, etc. As for the former case, it turns out that Pinniped milk contains zero lactose. Pinnipeds (officially, Pinnipedia) is the clade of species containing the walrus, the eared seals (e.g. California sea lions), and the earless seals (e.g. Northern elephant seals). While almost all mammals produce milk with lactose, Pinnipeds, for some reason, do not. So, for example, a glass of walrus milk would not trigger lactose intolerance symptoms, and, in fact, a highly lactose intolerant people, the Greenlandic Inuit, have been drinking walrus milk for centuries without any problems. While I could talk about these fascinating exceptions for days, I should get back to the point that lactose is almost exclusively found in foods containing mammal milk.
Lactose intolerance is usually accompanied by the symptoms of bloating, abdominal pain, flatulence, or diarrhea. However, some people experience nausea or vomiting, in addition to or in lieu of the typical symptoms. Only one of the typical symptoms of lactose intolerance—diarrhea—is a direct result of an “impaired” ability to digest lactose. All the other typical symptoms—bloating, abdominal pain, and flatulence—are only indirectly related to lactose intolerance. When lactose is not digested by your body, it’s digested by your intestinal bacteria instead. When these critters digest sugar, they respire hydrogen-containing gas, which results in bloating, abdominal pain, and flatulence. In fact, physicians usually diagnose lactose intolerance by detecting hydrogen gas in your breath.
I should also clarify that lactose intolerance is defined as an “impaired” ability to digest lactose, not an inability. So, lactose intolerance can, and does, come in degrees. Some lactose intolerant people only experience symptoms from eating lactose-dense foods, such as cow’s milk, while others, like me, will experience symptoms from eating foods with even trace amounts of lactose, for example, Lactaid milk or Camembert cheese.
The severity of lactose intolerance can vary widely. Some people find it to be a mere nuisance, while others find it to be a huge disturbance to daily life or a significant detriment to their health. For instance, I’ve found lactose intolerance to be a nontrivial disturbance to my daily life since I’m unable to digest any lactose whatsoever. Since lactase pills simply don’t work for me for meal-sized portions, I sometimes find myself unable to eat any food on a restaurant menu or at an academic event, such as a wine and cheese reception after a philosophy colloquium.
There is a pattern for which restaurants and events tend to be more accessible to lactose-intolerant people. Vegan-friendly restaurants or events are safe spaces for lactose intolerant people because, by definition, vegan food doesn’t contain mammal milk. On the other hand, restaurants or events that exclusively serve European or South Asian food tend to be less accessible to lactose-intolerant people. This is especially true for Northern European food—English, Irish, Swedish, and so on—and European American food. I will explain later why this pattern holds. It has to do with human genetics and human evolutionary history.
When I’m dining at a Chinese or Jamaican restaurant, I’m not at all worried about whether I can find something to eat. However, not too long ago, I went to an upscale European restaurant in downtown Philly and it was extremely difficult to order an entrée that did not have lactose in it. While they listed ingredients of each dish on their menu, they neglected to list all the ingredients, and mammal milk is a common hidden ingredient. What’s worse was that neither my server nor the manager knew what lactose intolerance was, so the accommodations they attempted to make were inadequate—for example, substituting goat cheese for cow cheese. Since lactose intolerance isn’t considered a legal disability in American society—at least, not yet!—I don’t know whether accommodating lactose intolerant people should be required by law; but it sure is a good business practice! Remember, most people on earth are lactose intolerant.
As for health ramifications, there are a few of these for lactose intolerant people. The main health ramification for lactose intolerant people, at least in the US, is developing a nutrient deficiency of calcium and vitamin D. This is because most US adults get calcium and vitamin D from cow milk and cow milk products. Calcium deficiency can lead to fatigue and muscle cramps, osteoporosis, rickets, or heart failure. Vitamin D deficiency can lead to muscle weakness, asthma, osteoporosis, rickets, or cancer.
As you might have guessed from looking at these lists, calcium deficiency is linked to vitamin D deficiency. We need vitamin D to absorb calcium, so anyone who is vitamin D deficient is almost certainly also calcium deficient. Usually, a change in diet or more sunlight exposure—since our skin cells can produce vitamin D from sunlight—can offset the health ramifications of lactose intolerance. For instance, calcium-fortified soy milk has a lot of calcium and mackerel has a lot of vitamin D. Nevertheless, dietary changes alone might be insufficient, especially for dark-skinned people who naturally produce much less vitamin D from sunlight than light-skinned people. For instance, I was vitamin D deficient for a long time until I started taking supplements. After doing so, I noticed positive changes in my fatigue, muscle cramps, and asthma attacks-I’m asthmatic. But what causes lactose intolerance and how did human diversity in lactose intolerance arise?
Lactose digestion is primarily a genetically controlled phenomenon. The digestion of lactose in humans is due to the enzyme lactase, whose production is controlled by a single gene: the LCT gene on chromosome 2. A person only needs one functional allele of the LCT gene to be able to digest lactose. However, the production of lactase in humans depends greatly on age. All of us, except people born without any functional LCT alleles (which is very rare), produce copious amounts of lactase from birth up until a little after our breastfeeding years. During this time in childhood, most people’s LCT gene naturally stops telling the body to produce lactase.
So far, what I’ve said concerns how most mammals regulate lactase production. However, in a minority of humans, a different gene, the MCM6 gene, also on chromosome 2, tells the LCT gene to continue telling the body to produce lactase after the time when the LCT gene would have normally stopped doing so, leading to a trait known as “lactase persistence.” People born without lactose intolerance, but who do not develop lactase persistence are said to have the “lactase nonpersistence” trait. Note that lactase nonpersistence is really a more accurate term to describe what I, and most other people, have, and as such, I’ll use it instead of lactose intolerance for the rest of the interview. It only takes one functional allele of the MCM6 gene to keep your body producing lactase throughout your life. I know that I don’t have the genotype that produces lactase persistence due to a recent 23andMe genetic test I took. I have G nucleotides from both parents at position 13910 in the MCM6 region, and when that happens, you’re almost certainly not going to develop the lactase persistence trait.
What’s equally fascinating is how our species acquired our diversity in lactase persistence. We now know from recent genetic studies that our diversity in lactase persistence did not arise accidentally. While the trait itself originated accidentally from mutation in one or more humans long ago, the spread of that trait was no accident. Rather, our lactase persistence alleles spread widely in human populations that relied heavily on mammal milk for survival due to natural selection. For example, the rise of dairy farming in Europe, South Asia, and the Middle East coincide nicely with the origin of various lactase persistence alleles in humans. Furthermore, the way that our diversity in lactase persistence arose had consequences for how the trait is distributed across human populations.
Population geneticists sometimes divide our species into five, comprehensive, so-called continental populations: Caucasians, East Asians, Native Americans, Sub-Saharan Africans, and Oceanians. While there are many ways to subdivide humans into biologically significant populations, the aforementioned way is useful to get a rough picture of how evolution has distributed genetically inherited traits across our species. It’s also common practice among medical geneticists to look at medically relevant, genetically inherited traits this way.
Using the continental population scheme, it’s easy to see that lactase nonpersistence is very common among all human continental populations except one: Caucasians. However, even among Caucasians, there is more lactase nonpersistence than lactase persistence. For example, according to the Global Lactase Persistence Association Database (GLAD)—which is the largest database for lactase persistence data on humans—lactase persistence has an average prevalence of 37% among Caucasian populations, but an average prevalence of 14%, 2%, and 0% among Sub-Saharan African, East Asian, and Oceanian populations, respectively. Furthermore, according to GLAD, among Northern European populations, the average prevalence of lactase persistence is a whopping 86%! Of course, there is variation within the continental populations. For example, according to GLAD, the lactase persistence prevalence among Ashkenazi Jews is just 16%, while it’s 85% among Maasai Kenyans. Lactase persistence is also low among Greeks (17-25%), Southern Italians (10-15%), and other Southern Europeans. This brings us to race.
In a recent paper, I’ve argued that one widely used meaning of race in ordinary American English—namely, the one used by the U.S. Office of Management and Budget (OMB)—is the set of human continental populations. In OMB race talk, there are five races: American Indian, Asian, Black, Pacific Islander, and White; I’ve argued that, given a wide variety of evidence, the best candidates for OMB race term meanings are the human continental populations, and the best candidate for the meaning of race in OMB race talk is just the set of these populations. In other words, in my view, what it means to be Black (in OMB race talk) is just to be a member of the Sub-Saharan African population. If I’m right about all of this, it follows that, in at least one way we talk about race in the U.S., lactase nonpersistence is distributed unevenly across races and for nontrivial genetic and evolutionary reasons. I find that fact fascinating as a race scholar and a philosopher of science, but here’s why a philosopher of disability might be interested in all of this.
If OMB racial demographics are just right in a society, then, in that society, lactase nonpersistence will look like an “impaired ability” (as the NIH labels it), when it’s really just the norm (in a statistical sense) for how people digest food. For example, according to one study, 75% of European Americans possess lactase persistence alleles, while for Mexican Americans, African Americans, and American Indian Americans, less than 30%, 20%, and 5%, respectively, possess lactase persistence alleles. Couple these data with the known demographics of our country, and you will get the fascinating fact that most Americans are both European Americans and have lactase persistence alleles. Since the European-American majority imposes its cultural preference for drinking and eating dairy products onto the non-European American minority in the U.S. (e.g. in supermarkets, restaurants, cafeterias, etc.), it’s no surprise that Americans view lactase nonpersistence as an “impaired ability.”
What may be even more fascinating to a philosopher of disability is how European Americans’ domination of American food has transformed lactase nonpersistence into a “health condition,” as the NIH calls it, in the U.S. For instance, my struggle with vitamin D deficiency is not unusual among African Americans. Rather, it’s a well-known health consideration for African Americans due to our routine avoidance of dairy products. Moreover, if European Americans continue to add lactose to more and more foods and these additions are not offset with non-lactose food accommodations, I would not be surprised to see lactase nonpersistence transform into a legal disability in this country. However, I personally don’t see that happening. Unless the xenophobes in this country get their way, the U.S. is going to continue to get more and more racially diverse (in an OMB sense), which will pressure businesses to develop more and more lactose-free food options.
Quayshawn, do you worry that this work reinstitutes the idea that races are biologically fundamental, that is, exist in some metaphysical sense?
Well, let me unpack that question. You’re asking whether I’m worried that my research might reinstitute the idea that races are biologically real and fundamental human divisions. On the first front, I hope that I convince some people that there are ways that we use the term race and race terms in this country to pick out biologically real groups. Getting philosophers and other scholars to realize this has been a huge part of my research so far. In particular, I hope that I’ve convinced some scholars that OMB races are biological groups and biologically real. With that said, there are two things that I hope people don’t take away from my work.
First, I hope people don’t think that I think that every way we use the term race and race terms in ordinary language, or even American English, is biological. I’m not in that camp. In fact, I don’t even think there is a dominant way that we use the term race and race terms in American English, which is a revised position of mine since my 2014 paper. In American English, as far as I can tell, the position that best fits the empirical data is pluralism.
In other words, I don’t believe that the term race is anything like, say, tiger in American English. If you randomly grab a few hundred American English speakers, take them to China or India, and ask them to point out the tigers, there will be near unanimity on what they point out. You can also ask them what are the superficial properties that almost all tigers share, and you’ll get largely overlapping answers. However, there’s plenty of empirical work that’s been done that shows that American English speakers don’t share that sort of agreement about what “the races” are or what “the features” are that makes something a race. Readers and listeners of this interview can go here and here, for example. Of course, there are non-pluralist ways of dealing with these experimental results.
Sally Haslanger has argued, for instance, that we should ignore “the ordinary person’s ideas about race” because “the very social processes that create the divisions of privilege and advantage also obscure their workings.” However, I’m not convinced that experimental data about what ordinary people think about race is entirely worthless. Ordinary people should be reliable indicators of their own racial memberships. So, if racial self-reporting data are all over the place—which they are—then pluralism is a live option. Some other philosophers of race who have embraced racial pluralism, or something close to it, are Lionel McPherson and Michael Hardimon. Also, note that a pluralist about what race is in a linguistic community is compatible with being a biological realist about what race is in particular discourses in that linguistic community.
Second, I don’t believe at all that there’s anything “fundamental” about dividing people into human continental populations. Like I said earlier, it’s one out of many ways of dividing people into biologically significant groups. So, I’m a deflationist about the biological racial realism that I do endorse. However, there could still be medically and other socially important biological differences among human continental populations, such as non-accidental lactase nonpersistence distributions. Of course, these are going to be contingent outcomes of human evolution, not fundamental features of belonging to a continental population. Belonging to a human continental population is just a genealogical fact.
Nevertheless, I do worry that politically right-winged people—for example, Charles Murray—might try to misuse my research for their own purposes. I’m also worried about the educational research that shows learning about human genetic differences in racial terms—for instance, lactase persistence alleles—increases racist attitudes among the learners. I worry about these two problems a lot, and I haven’t made up my mind about what to do about them. My initial thought about the second problem, though, is to work extra hard to improve the general public’s understanding of evolutionary biology and genetics. In fact, a colleague of mine, Michael Weisberg, has started The Penn Laboratory for Understanding Science—a.k.a. The PLUS Project—to achieve exactly this goal.
Would you like to recommend some books and articles to our readers and listeners?
Oh yes! Some philosophy of race books that tackle the links, or apparent links, between medical conditions and racial groups are Joshua Glasgow’s A Theory of Race (especially chapter 5) and Sally Haslanger’s Resisting Reality (especially chapters 8 and 10). Also, I would highly recommend Fatal Invention by Dorothy Roberts. She’s a sociologist, not a philosopher, but her book is a staple in the race and medicine literature. There are also some very good interdisciplinary volumes out there that address the links between race and medicine, such as Revisiting Race in a Genomic Age, by Lee, Koenig, and Richardson. I’m editing a forthcoming volume on race and medicine that has some fantastic contributors. It’s entitled The Race Debates from Metaphysics to Medicine and it should be out next year with Oxford University Press (OUP). I’m also tackling this topic in [What is Race? Four Philosophical Views], a book that I’m co-authoring with Sally Haslanger, Joshua Glasgow, and Chike Jeffers. That book should also be out next year with OUP.
As for articles on the topic of race and medicine, there’s too many to list here, so a better strategy would be to follow the publications of particular scholars on the topic. Among philosophers, I’ve learned a lot about the topic from reading the work of Robin Andreasen, Lisa Gannett, Jonathan Kaplan, Koffi Maglo, Michael Root, Shannon Sullivan, and Sean Valles. Among human geneticists, I’ve learned a lot from Esteban Burchard, Elad Ziv, Hua Tang, Neil Risch, Sarah Tishkoff, Noah Rosenberg, Marcus Feldman, Rick Kittles, and Richard Lewontin. Among sociologists, in addition to Dorothy Roberts, I’ve learned a lot from Ann Morning and Duana Fullwiley. I know that I’m leaving out a lot of good books and brilliant scholars to follow on this topic, but this is a good start. Thanks!
Quayshawn, thanks so much for your incredibly interesting remarks throughout this interview. I learned a tremendous amount from them and I’m sure that our readers and listeners did too. I look forward to the publication of your forthcoming books.
Readers/listeners are invited to use the Comments section below to respond to Quayshawn Spencer’s remarks, ask questions, and so on. Comments will be moderated. As always, although signed comments are encouraged and preferred, anonymous comments may be permitted.
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Please join me here again on Wednesday, June 17th at 8 a.m. E.S.T., for the sixty-third installment of the Dialogues on Disability series and, indeed, on every third Wednesday of the months ahead. I have a fabulous line-up of interviews planned. If you would like to nominate someone to be interviewed (self-nominations are welcomed), please feel free to write me at s.tremain@yahoo.ca. I prioritize diversity with respect to disability, class, race, gender, institutional status, nationality, culture, age, and sexuality in my selection of interviewees and my scheduling of interviews.
[…] May 2020: Dialogues on Disability: Shelley Tremain Interviews Quayshawn Spencer Redux […]
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[…] Spencer even worries that those—like Charles Murray who don’t even have a coherent concept of race—may try to use his research for their own purposes: […]
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