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I started this blog almost 5 years ago. Currently (excluding this one), there are 480 articles on this blog. Searching my blog name “notpoliticallycorrect.me” on Google Scholar leads to two citations—one on “IQ” and obesity and the other on inclusionism about race when it comes to medicine. These two cites pretty much perfectly show my views and their change in the past 5 years since the creation of this blog. I will discuss both papers that cited me in turn.
In the journal Social and Human Sciences. Domestic and Foreign Literature (a sociology journal), a 2016 article I published (back in my “HBD” days titled “Race, Obesity, Poverty, and IQ, writing:
income and education (which in the latter case presumably correlates with IQ levels). They have the highest prevalence of type 2 diabetes. In terms of ethnicity, overweight indicators are as follows: 67.3% for whites, 75.6% for African Americans and 77.9% for Latinos. Summing up all this, we obtain, in the words of the authors of the study, “politically incorrect conclusions”: African Americans and Hispanics are more at risk of living in poverty, have lower IQ, higher rates of obesity and a chance of developing diabetes; The main factor in these correlations is the IQ level (Race, obesity, poverty and IQ, 2016).
Almost four years later (after my views have undergone a significant change) I would draw different conclusions. Blacks are 51% more likely to be obese than whites (Lincoln, Abdou, and Lloyd, 2016) with the cause being a multitude of factors. Though it seems that black American men with more African ancestry may be protected against central adiposity (Klimentidis et al, 2016). Racial disparities in obesity are due to an interaction of a multitude of factors (Byrd, Toth, and Stanford, 2018). Interestingly, black kids with obesity don’t perceive themselves as obese (Lankarani and Assani, 2018), which, presumably, is due to higher rates of obesity in the black population. Black girls are more likely to have an earlier menarche than white giris (e.g., Freedman et al, 2000) and it is because black girls are more likely to be obese than white girls which is due to the effects of leptin being permissive for menarche, from the higher levels of body fat in black girls (Salsberry, Reagen, and Pajer, 2010).
We must look to social determinants of health to understand why certain non-white populations are more likely to be obese than others. Looking at “IQ” as causal for obesity—which I used to believe—obscures much more than it helps. We can look to epigenetic effects, for example, regarding biological explanations of obesity (Krueger and Reithner, 2016), for instance high BMI in black women being related to saliva-based DNA methylation, which is used as a marker for aging (Li et al, 2019). Even perceived racism (it does not have to be actual) can have physiologic effects on black women, heigtening cortisol levels, leading to a heigtened obesity risk (Mwendwa et al, 2016).
In any case, it’s cool that I got cited but uncool that it was something that I don’t believe anymore.
The second citation comes from Rossi (2020: 13) in the journal Social Science Information titled New avenues in epigenetic research about race: Online activism around reparations for slavery in the United States citing my article Race, Medicine, and Epigenetics: How the Social Becomes Biological:
Consequently, social scientists’ opinions about epigenetic research dealing with race and slavery have sometimes been scrutinized by blog authors. For example, the article untitled [sic] ‘Race, medicine, and epigenetics: How the social becomes biological’ published in 2019 on the blog Notpoliticallycorrect features a long discussion on whether race could be seen as a viable variable to discuss the epigenetics of trauma, especially relating to slavery in the US.14 After summarizing the views of legal scholar and sociologist Dorothy Roberts, who has argued repeatedly in her works against the use of the concept of race in biomedical sciences, the author sides with philosophers Michael Hardimon and Shannon Sullivan, who are both enthusiastic about the inclusion of race to discuss genetics and epigenetics:
Race and medicine is a tendentious topic. On one hand, you have people like sociologist Dorothy Roberts (2012) who argues against the use of race in a medical context, whereas philosopher of race Michael Hardimon thinks that we should not be exclusionists about race when it comes to medicine. If there are biological races, and there are salient genetic differences between them, then why should we disregard this when it comes to a medically relevant context? [. . .] So, we should not be exclusionists (like Roberts), we should be inclusionists (like Hardimon). [. . .] Furthermore, acknowledging the fact that the social dimensions of race can help us understand how racism manifests itself in biology (for a good intro to this see Sullivan’s (2015) book The Physiology of Racist and Sexist Oppression, for even if the ‘oppression’ is imagined, it can still have very real biological effects that could be passed onto the next generation – and it could particularly affect a developing fetus, too). It seems that there is a good argument that the effects of slavery could have been passed down through the generations manifesting itself in smaller bodies.
Relying also on Jasienska’s research, the author of this blog post therefore dismissed the idea that race should not be applied to the medical field, while using the words and legitimacy of humanities scholars such as Hardimon and Sullivan to back up their claims. These contributions show the way journalists and various blog authors write about epigenetics by mixing together scientific articles in various fields (the social sciences, philosophy, psychiatry, social work) in an effort to bring more legitimacy to the topic. This process highlights the ways in which lay circles produce new connections between various papers and texts dealing with epigenetics, no matter how different their fields of expertise may be.
This shows a very sharp contrast with my current views and my older views on race and obesity. Before, thinking that obesity was “determined” by IQ (e.g., Kanazawa, 2012; Kanazawa, 2014) was an error—people with low “IQs” are more likely to be in poverty and have less access to good foods, along with the abundance of fast food restaurants in areas with a higher concentration of blacks (James et al, 2014). Black women, for instance, have a lower RMR than white women (Gannon, DiPietro, and Poehlman, 2000)
These two articles of mine that were cited (on similar issues, no less) show the evolution of my views over the past four or so years in between the publication of the two articles on this blog. This is a good case study on how the one can view the aetiology of one thing completely different based on the types of views they previously held. The views of obesity and race I hold now are much more complex than the reductive “it’s genes/IQ” kind of guy that I used to be. A more holistic view of obesity disparities, factoring in access to food (food swamps/deserts), income, location etc is more informative than looking just to “IQ” or “genes for” obesity—because even if “genes for” obesity exist and even if “genes for” obesity are distributed unevenly across races, the predominant determinant of weight will be activity level/caloric consumption, which is based on SES and other factors—not “IQ” or “obesity genes.” The social does become biological, and it does have consequences for obesity disparities between and within races.
Charles Murray published his Human Diversity: The Biology of Gender, Race, and Class on 1/28/2020. I have an ongoing thread on Twitter discussing it.
Murray talks of an “orthodoxy” that denies the biology of gender, race, and class. This orthodoxy, Murray says, are social constructivists. Murray is here to set the record straight. I will discuss some of Murray’s other arguments in his book, but for now I will focus on the section on race.
Murray, it seems, has no philosophical grounding for his belief that the clusters identified in these genomic runs are races—and this is clear with his assumptions that groups that appear in these analyses are races. But this assumption is unfounded and Murray’s assumption that the clusters are races without any sound justification for his belief actually undermines his claim that races exist. That is one thing that really jumped out at me as I was reading this section of the book. Murray discusses what geneticists say, but he does not discuss what any philosophers of race say. And that is to his downfall.
Murray discusses the program STRUCTURE, in which geneticists input the number of clusters they want and, when DNA is analyzed (see also Hardimon, 2017: chapter 4). Rosenberg et al (2002) sampled 1056 individuals from 52 different populations using 377 microsatellites. They defined the populations by culture, geography, and language, not skin color or race. When K was set to 5, the clusters represented folk concepts of race, corresponding to the Americas, Europe, East Asia, Oceania, and Africa. (See Minimalist Races Exist and are Biologically Real.) Yes, the number of clusters that come out of STRUCTURE are predetermined by the researchers, but the clusters “are genetically structured … which is to say, meaningfully demarcated solely on the basis of genetic markers” (Hardimon, 2017: 88).
Races as clusters
Murray then discusses Li et al, who set K to 7 and North Africa and the Middle East were new clusters. Murray then provides a graph from Li et al:
So, Murray’s argument seems to be “(1) If clusters that correspond to concepts of race setting K to 5-7 appear in STRUCTURE and cluster analyses, then (2) race exists. (1). Therefore (2).” Murray is missing a few things here, namely conditions (see below) that would place the clusters into the racial categories. His assumption that the clusters are races—although (partly) true—is not bound by any sound reasoning, as can be seen by his partitioning Middle Easterners and North Africans as separate races. Rosenberg et al (2002) showed the Kalash in K=6, are they a race too?
No, they are not. Just because STRUCTURE identifies a population as genetically distinct, it does not entail that the population in question is a race because they do not fit the criteria for racehood. The fact that the clusters correspond to major areas means that the clusters represent continental-level minimalist races so races, therefore, exist (Hardimon, 2017: 85-86). But to be counted as a continental-level minimalist race, the group must fit the following conditions (Hardimon, 2017: 31):
(C1) … a group is distinguished from other groups of human beings by patterns of visible physical features
(C2) [the] members are linked by a common ancestry peculiar to members of that group, and
(C3) [they] originate from a distinctive geographic location
…what it is for a group to be a race is not defined in terms of what it is for an individual to be a member of a race. What it means to be an individual member of a minimalist race is defined in terms of what it is for a group to be a race.
Murray (paraphrased): “Cluster analyses/STRUCTURE spit out these continental microsatellite divisions which correspond to commonsense notions of race.” What is Murray’s logic for assuming that clusters are races? It seems that there is no logic behind it—just “commonsense.” (See also Fish, below.) Due to not finding any arguments for accepting X number of clusters as the races Murray wants, I can only assume that Murray just chose which one agreed with his notions and use for his book. (If I am in error, then if there is an argument in the book then maybe someone can quote it.) What kind of justification is that?
Compared to Hardimon’s argument and definition. Homo sapiens is:
… a subdivision of Homo sapiens—a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographic ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population. (Hardimon, 2017: 99)
Step 1. Recognize that there are differences in patterns of visible physical features of human beings that correspond to their differences in geographic ancestry.
Step 2. Observe that these patterns are exhibited by groups (that is, real existing groups).
Step 3. Note that the groups that exhibit these patterns of visible physical features correspond to differences in geographical ancestry satisfy the conditions of the minimalist concept of race.
Step 4. Infer that minimalist race exists. (Hardimon, 2017: 69)
While Murray is right that the clusters that correspond to the folk races appear in K = 5, you can clearly see that Murray assumes that ALL clusters would then be races and this is where the philosophical emptiness of Murray’s account comes in. Murray has no criteria for his belief that the clusters are races, commonsense is not good enough.
Murray then lambasts the orthodoxy for claiming that race is a social construct.
Advocates of “race is a social construct” have raised a host of methodological and philosophical issues with the cluster analyses. None of the critical articles has published a cluster analysis that does not show the kind of results I’ve shown.
Murray does not, however, discuss a more critical article of Rosenberg et al (2002)—Mills (2017) – Are Clusters Races? A Discussion of the Rhetorical Appropriation of Rosenberg et al’s “Genetic Structure of Human Populations.” Mills (2017) discusses the views of Neven Sesardic (2010)—philosopher—and Nicholas Wade—science journalist and author of A Troublesome Inheritance (Wade, 2014). Both Wade and Seasardic are what Kaplan and Winther (2014) term “biological racial realists” whereas Rosenberg et al (2002), Spencer (2014), and Hardimon (2017) are bio-genomic/cluster realists. Mills (2017) discusses the “misappropriation” of the bio-genomic cluster concept due to the “structuring of figures [and] particular phrasings” found in Rosenberg et al (2002). Wade and Seasardic shifted from bio-genomic cluster realism to their own hereditarian stance (biological racial realism, Kaplan and Winther, 2014). While this is not a blow to the positions of Hardimon and Spencer, this is a blow to Murray et al’s conception of “race.”
Murray (2020: 144)—rightly—disavows the concept of folk races but wrongly accepting the claim that we dispense with the term “race”:
The orthodoxy is also right in wanting to discard the word race. It’s not just the politically correct who believe that. For example, I have found nothing in the genetics technical literature during the last few decades that uses race except within quotation marks. The reasons are legitimate, not political, and they are both historical and scientific.
Historically, it is incontestably true that the word race has been freighted with cultural baggage that has nothing to do with biological differences. The word carries with it the legacy of nineteenth-century scientific racism combined with Europe’s colonialism and America’s history of slavery and its aftermath.
The combination of historical and scientific reasons makes a compelling case that the word race has outlived its usefulness when discussing genetics. That’s why I adopt contemporary practice in the technical literature, which uses ancestral population or simply population instead of race or ethnicity …
[Murray also writes on pg 166]
The material here does not support the existence of the classically defined races.
(Nevermind the fact that Murray’s and Herrnstein’s The Bell Curve was highly responsible for bringing “scientific racism” into the 21st century—despite protestations to the contrary that his work isn’t “scientifically racist.”)
In any case, we do not need to dispense with the term race. We only need to deflate the term (Hardimon, 2017; see also Spencer, 2014). Rejecting claims from those termed biological racial realists by Kaplan and Winther (2014), both Hardimon (2017) and Spencer (2014; 2019) deflate the concept of race—that is, their concepts only discuss what we can see, not what we can’t. Their concepts are deflationist in that they take the physical differences from the racialist concept (and reject the psychological assumptions). Murray, in fact, is giving into this “orthodoxy” when he says that we should stop using the term “race.” It’s funny, Murray cites Lewontin (an eliminativist about race) but advocates eliminativism of the word but still keeping the underlying “guts” of the concept, if you will.
We should only take the concept of “race” out of our vocabulary if, and only if, our concept does not refer. So for us to take “race” out of our vocabulary it would have to not refer to any thing. But “race” does refer—to proper names for a set of human population groups and to social groups, too. So why should we get rid of the term? There is absolutely no reason to do so. But we should be eliminativist about the racialist concept of race—which needs to exist if Murray’s concept of race holds.
There is, contra Murray, material that corresponds to the “classically defined races.” This can be seen with Murra’s admission that he read the “genetics technical literature”. He didn’t say that he read any philosophy of race on the matter, and it clearly shows.
To quote Hardimon (2017: 97):
Deflationary realism provides a worked-out alternative to racialism—it is a theory that represents race as a genetically grounded, relatively superficial biological reality that is not normatively important in itself. Deflationary realism makes it possible to rethink race. It offers the promise of freeing ourselves, if only imperfectly, from the racialist background conception of race.
Spencer (2014) states that the population clusters found by Rosenberg et al’s (2002) K = 5 run are referents of racial terms used by the US Census. “Race terms” to Spencer (2014: 1025) are “a rigidly designating proper name for a biologically real entity …” Spencer’s (2019b) position is now “radically pluralist.” Spencer (2019a) states that the set of races in OMB race talk (Office of Management and Budget) is one of many forms “race” can take when talking about race in the US; the set of races in OMB race talk is the set of continental human populations; and the continental set of human populations is biologically real. So “race” should be understood as proper names—we should only care if our terms refer or not.
Murray’s philosophy of race is philosophically empty—Murray just uses “commensense” to claim that the clusters found are races, which is clear with his claim that ME/NA people constitute two more races. This is almost better than Rushton’s three-race model but not by much. In fact, Murray’s defense of race seems to be almost just like Jensen’s (1998: 425) definition, which Fish (2002: 6) critiqued:
This is an example of the kind of ethnocentric operational definition described earlier. A fair translation is, “As an American, I know that blacks and whites are races, so even though I can’t find any way of making sense of the biological facts, I’ll assign people to my cultural categories, do my statistical tests, and explain the differences in biological terms.” In essence, the process involves a kind of reasoning by converse. Instead of arguing, “If races exist there are genetic differences between them,” the argument is “Genetic differences between groups exist, therefore the groups are races.”
So, even two decades later, hereditarians are STILL just assuming that race exists WITHOUT arguments and definitions/theories of race. Rushton (1997) did not define “race”, and also just assumed the existence of his three races—Caucasians, Mongoloids, and Negroids; Levin (1997), too, just assumes their existence (Fish, 2002: 5). Lynn (2006: 11) also uses a similar argument to Jensen (1998: 425). Since the concept of race is so important to the hereditarian research paradigm, why have they not operationalized a definition and rely on just assuming that race exists without argument? Murray can now join the list of his colleagues who also assume the existence of race sans definition/theory.
Hardimon’s and Spencer’s concepts get around Fish’s (2002: 6) objection—but Murray’s doesn’t. Murray simply claims that the clusters are races without really thinking about it and providing justification for his claim. On the other hand, philosophers of race (Hardimon, 2017; Spencer, 2014; 2019a, b) have provided sound justification for the belief in race. Murray is not fair to the social constructivist position (great accounts can be found in Zack (2002), Hardimon (2017), Haslanger (2000)). Murray seems to be one of those “Social constructivists say race doesn’t exist!” people, but this is false: Social constructs are real and the social can does have potent biological effects. Social constructivists are realists about race (Spencer, 2012; Kaplan and Winther, 2014; Hardimon, 2017), contra Helmuth Nyborg.
Murray (2020: 17) asks “Why me? I am neither a geneticist nor a neuroscientist. What business do I have writing this book?” If you are reading this book for a fair—philosophical—treatment for race, look to actual philosophers of race and don’t look to Murray et al who do not, as shown, have a definition of race and just assume its existence. Spencer’s Blumenbachian Partitions/Hardimon’s minimalist races are how we should understand race in American society, not philosophically empty accounts.
Murray is right—race exists. Murray is also wrong—his kinds of races do not exist. Murray is right, but he doesn’t give an argument for his belief. His “orthodoxy” is also right about race—since we should accept pluralism about race then there are many different ways of looking at race, what it is, and its influence on society and how society influences it. I would rather be wrong and have an argument for my belief then be right and appeal to “commonsense” without an argument.
Nature vs nurture can be said to be a debate on what is ‘innate’ and what is ‘acquired’ in an organism. Debates about how nature and nurture tie into athletic ability and race both fall back onto the dichotomous notion. “Athleticism is innate and genetic!”, the hereditarian proclaims. “That blacks of West African ancestry are over-represented in the 100m dash is evidence of nature over nurture!” How simplistic these claims are.
Steve Sailer, in his response to Birney et al on the existence of race, assumes that because those with ancestry to West Africa consistently have produced the most finalists (and winners) in the Olympics that race, therefore, must exist.
I pointed out on Twitter that it’s hard to reconcile the current dogma about race not being a biological reality with what we see in sports, such as each of the last 72 finalists in the Olympic 100-meter dash going all the way back to 1984 nine Olympics ago being at least half sub-Saharan in ancestry.
the abundant data suggesting that individuals of sub-Saharan ancestry enjoy genetic advantages.
For example, it’s considered fine to suggest that the reason that each new Dibaba is fast is due to their shared genetics. But to say that one major reason Ethiopians keep winning Olympic running medals (now up to 54, but none at any distance shorter than the 1,500-meter metric mile because Ethiopians lack sprinting ability) is due to their shared genetics is thought unthinkable.
Sailer’s argument seems to be “Group X is better than Group Y at event A. Therefore, X and Y are races”, which is similar to the hereditarian arguments on the existence of ‘race’—just assume they exist.
The outright reductionism to genes in Sailer’s view on athleticism and race is plainly obvious. That blacks are over-represented in certain sports (e.g., football and basketball) is taken to be evidence for this type of reductionism that Sailer and others appeal to (Gnida, 1995). Such appeals can be said to be implicitly saying “The reason why blacks succeed at sport is due to genes while whites succeed due to hard work, so blacks don’t need to work as hard as whites when it comes to sports.”
There are anatomic and physiological differences between groups deemed “black” and “white”, and these differences do influence sporting success. Even though this is true, this does not mean that race exists. Such reductionist claims—as I myself have espoused years ago—do not hold up. Yes, blacks have a higher proportion of type II muscle fibers (Caesar and Henry, 2015), but this does not alone explain success in certain athletic disciplines.
Current genetic testing cannot identify an athlete (Pitsiladis et al, 2013). I reviewed some of the literature on power genotypes and race and concluded that there are no genes yet identified that can be said to be a sufficient cause of success in power sports.
Just because group A has gene or gene networks G and they compete in competition C does not mean that gene or gene networks G contribute in full—or in part—to sporting success. The correlations could be coincidental and non-functional in regard to the sport in question. Athletes should be studied in isolation, meaning just studying a specific athlete in a specific discipline to ascertain how, what, and why works for the specific athlete along with taking anthropomorphic measures, seeing how bad they want “it”, and other environmental factors such as nutrition and training. Looking at the body as a system will take us away from privileging one part over another—while we also do understand that they do play a role but not the role that reductionists believe.
No evidence exists for DNA variants that are common to endurance athletes (Rankinen et al, 2016). But they do have one thing in common (which is an environmental effect on biology): those born at altitude have a permanently altered ventilatory response as adults while “Peruvians born at altitude have a nearly 10% larger forced vital capacity compared to genetically matched Peruvians born at sea level” (Brutasaert and Parra, 2009: 16). Certain environmental effects on biology are well-known, and those biological changes do help in certain athletic events (Epstein, 2014). Yan et al (2016) conclude that “conclude that the traditional argument of nature versus nurture is no longer relevant, as it has been clearly established that both are important factors in the road to becoming an elite athlete.”
Georgiades et al (2017) go the other way and what they argue is clear in the title of their paper “Why nature prevails over nurture in the making of the elite athlete.” They continue:
Despite this complexity, the overwhelming and accumulating evidence, amounted through experimental research spanning almost two centuries, tips the balance in favour of nature in the “nature” and “nurture” debate. In other words, truly elite-level athletes are built – but only from those born with innate ability.
They use twin studies as an example stating that since heritability is greater than 50% but lower than 100% means “that the environment is also important.” But this is a strange take, especially from seasoned sports scientists (like Pitsiladis). Attempting to partition traits into a ‘nature’ and ‘nurture’ component and then argue that the emergence of that trait is due more to genetics than environment is an erroneous use of heritability estimates. It is not possible—nor is it feasible—to separate traits into genetic and environmental components. The question does not even make sense.
“… the question of how to separate the native from the acquired in the responses of man does not seem likely to be answered because the question is unintelligible.” (Leonard Carmichael 1925, quoted in Genes, Determinism and God, Alexander, 2017)
Tucker and Collins (2012) write:
Rather, individual performance thresholds are determined by our genetic make-up, and training can be defined as the process by which genetic potential is realised. Although the specific details are currently unknown, the current scientific literature clearly indicates that both nurture and nature are involved in determining elite athletic performance. In conclusion, elite sporting performance is the result of the interaction between genetic and training factors, with the result that both talent identification and management systems to facilitate optimal training are crucial to sporting success.
Tucker and Collins (2012) define training as the realization of genetic potential, while DNA “control the ceiling” of what one may be able to accomplish. “… training maximises
the likelihood of obtaining a performance level with a genetically controlled ‘ceiling’, accounts for the observed dominance of certain populations in specific sporting disciplines” (Tucker and Collins, 2012: 6). “Training” would be the environment here and the “genetically controlled ‘ceiling'” would be genes here. The authors are arguing that while training is important, training is just realizing the ‘potential’ of what is ‘already in’ the genes—an erroneous way of looking at genes. Shenk (2010: 107) explains why:
As the search for athletic genes continues, therefore, the overwhelming evidence suggests that researchers will instead locate genes prone to certain types of interactions: gene variant A in combination with gene variant B, provoked into expression by X amount of training + Y altitude + Z will to win + a hundred other life variables (coaching, injuries, etc.), will produce some specific result R. What this means, of course, What this means, of course, is that we need to dispense rhetorically with thick firewall between biology (nature) and training (nurture). The reality of GxE assures that each person’s genes interacts with his climate, altitude, culture, meals, language, customs and spirituality—everything—to produce unique lifestyle trajectories. Genes play a critical role, but as dynamic instruments, not a fixed blueprint. A seven- or fourteen- or twenty-eight-year-old is not that way merely because of genetic instruction.
The model proposed by Tucker and Collins (2012) is pretty reductionist (see Ericsson, 2012 for a response), while the model proposed by Shenk (2010) is more holistic. The hypothetical model explaining Kenyan distance running success (Wilbur and Pitsiladis, 2012) is, too, a more realistic way of assessing sport dominance:
The formation of an elite athlete comes down to a combination of genes, training, and numerous other interacting factors. The attempt to boil the appearance of a certain trait to either ‘genes’ or ‘environment’ and partition them into percentages is an unsound procedure. That a certain group continuously wins a certain event does not constitute evidence that the group in question is a race, nor does it constitute evidence that ‘genes’ are the cause of the outcome between groups in that event. The holistic model of human athletic performance in which genes contribute to certain physiological processes along with training, and other biomechanical and psychological differences is the correct way to think about sport and race. Actually seeing an athlete in motion in his preferred sport is (and I believe always will be) superior to just genetic analyses. Genetic tests also have “no role to play in talent identification” (Webborn et al, 2015).
One emerging concept is that there are many potential genetic pathways to a given phenotype . This concept is consistent with ideas that biological redundancy underpins complex multiscale physiological responses and adaptations in humans . From an applied perspective, the ideas discussed in this review suggest that talent identification on the basis of DNA testing is likely to be of limited value, and that field testing, which is essentially a higher order ‘bioassay’, is likely to remain a key element of talent identification in both the near and foreseeable future . (Joyner, 2019; Genetic Approaches for Sports Performance: How Far Away Are We?)
Athleticism is irreducible to biology (Louis, 2004). Holistic (nature and nurture) will beat the reductionist (nature vs nurture) views; with how biological systems work, there is no reason to privilege one level over another (Noble, 2012), so there is no reason to privilege the gene over the environment, environment over the gene. The interaction of multiple factors explains sport success.
There are many superficial physical differences between the races. But differences in pain sensitivity would be one that is not really “superficial”, as you can’t really see it (you can see someone’s reaction to pain, but not see it). “Pain” is defined as physical discomfort caused by injury. There are some myths about pain differences between racial groups, that still persist today. And these myths have bad consequences.
For example, Hoffman et al (2016) state that “people assume a priori that blacks feel less pain than do whites.” Hoffman et al (2016) carried out two studies: (1) using a between-participants design, laymen were asked to assess the pain of white and black subjects and (2) again using a between-participants design, they asked students and medical doctors to assess pain between blacks and whites. In (2) they asked these 15 questions:
1. On average, Blacks age more slowly than Whites.
2. Black people’s nerve-endings are less sensitive than White
3. Black people’s blood coagulates more quickly–because of
that, Blacks have a lower rate of hemophilia than Whites.
4. Whites, on average, have larger brains than Blacks.
5. Whites are less susceptible to heart disease like hypertension than Blacks.
6. Blacks are less likely to contract spinal cord diseases like
7. Whites have a better sense of hearing compared with Blacks.
8. Black people’s skin has more collagen (i.e., it’s thicker) than
White people’s skin.
9. Blacks, on average, have denser, stronger bones than Whites.
10. Blacks have a more sensitive sense of smell than Whites;
they can differentiate odors and detect faint smells better
11. Whites have more efficient respiratory systems than Blacks.
12. Black couples are significantly more fertile than White couples.
13. Whites are less likely to have a stroke than Blacks.
14. Blacks are better at detecting movement than Whites.
15. Blacks have stronger immune systems than Whites and are
less likely to contract colds.
(I’ll cover these questions in a future article.)
Here is the table showing the respondents’ answers to the questions:
So they established that whites with no medical training hold false beliefs about black-white differences that then carry over to pain management. They showed in study 2 that medical students’ and residents’ apparently false beliefs about racial differences in the questions they answered showed bias in the accuracy of the recommended pain treatments. Hoffman et al (2016) conclude that:
The present work sheds light on a heretofore unexplored source of racial bias in pain assessment and treatment recommendations within a relevant population (i.e., medical students and residents), in a context where racial disparities are well documented (i.e., pain management). It demonstrates that beliefs about biological differences between blacks and whites—beliefs dating back to slavery—are associated with the perception that black people feel less pain than do white people and with inadequate treatment recommendations for black patients’ pain.
(See also the Psychology Today article on the matter.)
Similarly, Hollingshead et al (2016) reported that subjects, regardless of race, rated the white person more sensitive to pain and more likely to report pain than the black person. Whites reported that they were less pain sensitive and less likely to report pain than their peers. Blacks reported that they were more sensitive to pain while reporting more pain than their peers.
Interestingly, Trawalter, Hoffman, and Waytz (2012) state that black NFL players are more likely to play in a subsequent game than whites when injured, and that, as found in many other studies, blacks are more likely to feel less pain than whites. However, what the literature really shows is the opposite: blacks are more likely to feel pain than whites.
Kim et al (2017) showed that blacks, “Hispanics” and Asians had lower pain tolerance, higher pain ratings and greater temporal sensation of pain. They also showed that blacks had lower pain tolerance and higher pain ratings but no differences in pain threshold.
Blacks report greater pain regarding AIDs, glaucoma, migraine, headache, jaw pain, postoperative pain, joint pain and many other types of pain compared to whites (Green et al, 2003; Klonoff, 2009). Riley III et al’s (2002) results indicate that blacks show a stronger link between pain and emotions than whites. Obana and Davis (2016) showed that Native Hawaiian/Pacific Islander male and females reported higher pain scores than whites when it came to joint pain (but they were not significant). Bolen et al (2010) showed that work limitation, severe joint pain, and arthritis-attributable activity were higher for non-“Hispanic” blacks, “Hispanics” and multiracial people compared to non-“Hispanic” whites. Even American Indians, Alaskan natives, and Aboriginal Canadians had a higher prevalence of pain and pain symptoms than Americans (Jimenez et al, 2011).
Chan et al (2011) surveyed older Singaporeans. They found that Malay people had lower pain sensitivity compared to Chinese people, and that Indians reported greater pain sensitivity when compared with Malay and Chinese people. Australian women rated menstrual pain higher and lasting 36 percent longer than Chinese women (Zhu et al, 2010).
When it comes to potential mechanisms, physiological mechanisms are hypothesized by Campbell and Edwards (2012) who write:
For example, in comparison to non-Hispanic whites, African–Americans have reduced nociceptive flexion reflex thresholds ; the nociceptive flexion reflex is an electrophysiological, spinally mediated reflex, which is not amenable to voluntary control or subject to issues of response bias that plague self-report of pain experiences. This finding suggests that the observed ethnic differences in pain are unlikely to be fully explainable by sociocultural influences and hints that neurobiological processes may contribute to such differences.
Mossey (2011) shows that “Racial/ethnic minorities consistently receive less adequate treatment for acute and chronic pain than non-Hispanic whites, even after controlling for age, gender, and pain intensity.” Martinez et al (2014) showed that when it comes to colorectal and lung cancer, mixed-race individuals and blacks are more likely to report higher pain severity than whites. (Also see Shavers, Bakos, and Sheppard, 2010.)
All of the literature points in the opposite direction of the myths about pain sensitivity in regard to race: blacks feel more pain than whites and are more likely to have a lower pain tolerance. So the myths people hold about differences in pain between racial groups (mostly blacks and whites) are false. Pain is a subjective experience. And there will be differences in pain thresholds between individuals and racial groups and the causes may be both sociocultural and physiological in nature. However, this bias (in the wrong direction) speaks to what I wrote about last night: physician bias when it comes to blacks and other minorities.
Barr (2014: 183-184) writes:
Based to a certain extent on the attention given to his earlier publication, Todd moved to a faculty position with the Emory University School of Medicine, in Atlanta, Georgia. There he was able to essentially repeat his earlier study, this time examining persons coming tothe emergency room of a large, inner-city community hospital in Atlanta that was affiliated with Emory (Todd et al, 2000). He evaluated the medical records of 217 individuals coming to the emergency room over a 40-month period for treatment of an isolated long-bone fracture. Given the racial makeup of Atlanta, these included 127 blacks and 90 whites. They found that
- 54 of the blacks (43 percent) received no medication for pain during their treatment
- 23 of the whites (26 percent) received no medication for pain during their treatment
As with the earlier study in Los Angeles involving whites and Hispanics, in this study, the blacks were nearly twice as likely to receive no pain medication while in the emergency room. With this study, the authors were keenly aware of the importance of documenting the extent to which the patients expressed painful symptoms. By thoroughly reviewing the medical records of these patients, they found that 54 percent of blacks and 59 percent of whites had a notation in their medical record that they had expressed painful symptoms. The nearly twofold difference in withholding pain medication in blacks and whites was because the doctor didn’t order the medication, not because the patient didn’t want the medication.
This, again, speaks to physician bias when it comes to race in a medical context. Race is a useful tool in medicine, but to hold biases in the complete opposite direction that they exist in is wrong. This study—and many others—speak to the type of bias that physicians have against minorities in a medical context. Understanding that the differences in pain are actually the opposite from what is commonly believed by both laypeople and medical doctors is important: if blacks feel more pain than whites regarding the same injuries and they are not getting the care needed, then this speaks to physician bias. What Barr showed was that blacks were treated at the emergency room based on their ethnicity. This is wrong. Race/ethnicity is a useful tool in medicine, but to outright use it as an assumption for numerous factors makes no sense and could cause more harm than good.
Using race in a medical context is a good thing. But using race in a medical context using essentialist, outdated views about race is wrong and can lead to many horrible outcomes. Of course, using race in this context can and does lead to certain things being discovered over others. For instance, if one’s race is assumed to be “driving” one’s illness (i.e., that one has a disease that that race/ethny is more likely to have), then race can and is a good marker to use—specifically geographic ancestry. However, when it comes to things like pain management, this obviously leads to false ideas about how different groups manage and feel pain.
Views about racial differences in pain affect both laypeople and medical doctors. These views can be and are harmful. The literature points to the case being the opposite of what is believed by people: blacks have lower pain tolerance and higher pain ratings than whites. These types of differences are also found between many other races and ethnic groups. The causes could be both sociocultural and physiological. A person’s response to pain depends on their unique physiology, life experiences, ethnicity and other factors. Understanding how and why physicians are biased toward how blacks feel pain is important, along with addressing the other biases that they have about other minorities when it comes to a medical context. Race and ethnicity are important tools for medicine, but these are some of the ways that the concepts can be used with nothing good coming out of it.
I’m currently reading Health Disparities in the United States: Social Class, Race, Ethnicity and Health by medical doctor and sociologist Donald Barr. In the book, he chronicles differences in health between races and ethnies, talks about the concepts of race used and cites well-known studies to people who read this blog, and he also shows that doctors are—either conscious or not—biased against minorities in certain medical contexts.
In Chapter 1 discusses the fact that, although Americans spend the most money on health care, Americans have a lower life expectancy and higher infant mortality rate than all other developed countries, showing the association in social inequality and health across all income levels and education. In Chapter 2, he asks the question “What is health?”, discussing many concepts of what “health” is. In Chapter 3, he defines “socioeconomic status” and shows the link between poor health and poor SES. In Chapter 4, he discusses the link between inequality and poor health, introducing the concept of “allostatic load”, which is the physiologic response to being in a spot of social disadvantage.
In Chapter 5, he looks at different race concepts, since it is a main premise of the book. In Chapter 6, he shows that minorities are more likely to be in a position of low SES. He asks, if minorities of the same SES as whites are consistently found to be of lower health than whites of the same SES, is it because those with poor health tend to be minorities, that they tend to have lower SES or both? In Chapter 7, he asks the same questions while focusing on children. In Chapter 8, he examines disparities in access to healthcare, showing that even when minorities have the same insurance and doctors that minorities still face worse health outcomes (he shows that they either do not receive appropriate healthcare or receive lower-quality care). In Chapter 9, he shows that physicians treat blacks and other minorities differently, albeit unconsciously. In Chapter 10, he discusses when—if ever—a physician would be justified in using racial/ethnic categories. And in Chapter 11, he states that not all of these disparities need to be eliminated.
In Chapter 2, Barr (2014: 45) presents this table, showing rates of illness and selective rates of death between States in America. Obviously, the one to look at that is different than the others is Mississippi. Mississippi is 37.5% black.
Wow, I wonder why Mississippi has such a high rate of obesity, diabetes, and hypertension (high blood pressure). Must be all of those obesity, diabetes and hypertension genes (HBDer).
Obesity and diabetes
The first thing to look at is median income. It is substantially lower in Mississippi compared to California, Iowa, and New York. About 23 million people in America live one mile from a supermarket, while black Americans are about half as likely to have access to supermarkets while “Hispanics” are about a third likely to have access to them (New York Law School Racial Justice Project, 2012). So when it comes to those who have to travel more than a mile for fresh fruit and vegetables, they have poorer health (Stack, 2015). So combine lower median income, along with food deserts and one can start to see how minorities have poorer health due in part to their SES. In short, living in a food desert can affect public health.
Blacks are the most obese ethnic group in America, and this relationship is largely driven by black women. Now, it’s not weird that women have higher levels of body fat than men, since women it is needed for physiological functioning. Though, there is something weird here: Black American men with more African ancestry are less likely to be obese (Klimentidis et al, 2016). Since black women and black men in America are in the same economic bracket, there must be something in the West African male physiology that “protects” them against central adiposity, though variation in social, environmental and cultural factors may play a role as well. In any case, the more West African ancestry American blacks have, the less likely they are to be obese. Klimentidis et al’s (2016) study “suggests that there are specific genetic variants and physiological mechanism(s) that differ among West African and European populations.”
Obesity affects more ethnies in America than others: non-Hispanic blacks and “Hispanics” are more likely to be obese than non-“Hispanic” whites and Asians (Hales et al, 2017). This could be due to, in part, to the variation in supermarket access and access to good foods—the concept of food deserts. Look at any low-income area near you. You’ll see a majority of corner stores with cheap, garbage food. The lack of ability to buy good food (along with the education to know what to buy and when to buy it) can explain differences in obesity rates—obviously not all. Obesity is related with diabetes, and sinec the relationship is so strong, the term “diabesity” was coined.
Eating cheap, processed carbohydrates spikes insulin. Repeated insulin spikes over time leads to type II diabetes and, eventually, obesity too. One can be skinny and have diabetes (a phenomenon known as thin on the outside, fat on the inside “TOFI”). However, since both diseases are co-morbid, we need to look at them in similar contexts. The higher rates of obesity can help to explain the higher rates of diabetes and hypertension—since those who are obese have higher blood pressure (Aronow, 2017).
Minorities are more likely to develop type II diabetes (Tuchman, 2011), and the cause of this is access to high-quality foods. But racial differences in obeisty and SES do not fully explain the higher rates of type II diabetes in black Americans; being a black American is a strong, independent factor for developing type II diabetes and this is compounded by low SES (Brancati et al, 1996). Zizi et al (2016) showed that both long and short black sleepers have an increased risk of developing type II diabetes. There are racial differences in sleep, with blacks having higher durations of long and short sleep compared to whites (Adenekan et al, 2013).
Now let’s look at hypertension (blood pressure). Blood pressure is a physiological variable. Since it is a physiological variable, it can and does respond to social/environmental contexts. So blood pressure can be affected by social contexts, too. For example, Williams (1992) cites stress, socioecologic stress, social support, coping patterns, health behavior, sodium and more for reasons why blacks have higher BP than whites. Dressler (1991) shows that the struggle to maintain a middle-class lifestyle is related to higher levels of BP. Similarly, Keith and Herring (1991) show that skin color is a strong predictor of occupational status and that darker-skinned blacks in America are twice as likely to experience racial discrimination than lighter-skinned blacks. This, too, can help to account for higher levels of BP between the races. In any case, Williams (1992) shows, definitively, that the causes of black-white differences in BP lie in the social environment.
Similarly, Non, Gravlee, and Mulligan (2012) show that racial disparities in BP are explained by education, and not genetic ancestry. They show that the association between BP and education was much stronger for blacks than for whites. Their results also support “the minority poverty hypothesis because the worst blood pressures were predicted for people who faced the double burden of being less educated and identifying as African American.” People who face discrimination could, and do, have higher levels of BP due to the stress they feel due to the discrimination. (Note that I take no sides on whether the discrimination is real or imagined, because even if it were imagined, it still leads to real physiologic consequences.)
Do note that there is a just-so story to explain how and why blacks have higher levels of blood pressure than whites: The Slavery Hypertension Hypothesis (Lujan and Dicarlo, 2018). This has all of the hallmarks of a just-so story posited by evolutionary psychologists. The story goes like this: Black slaves who were on the way to America in the Middle Passage had genes that favored better salt retention. So it is noted that black Americans have higher rates of BP than whites, and then they work backward and attempt to posit the best story possible to explain the current-day observation. This is the usual method evolutionary psychologists use—the method of reverse engineering, the inference from function to cause. So (1) note that blacks have higher levels of BP than whites; (2) infer the function to cause (blacks with genes that favored salt retention were more likely to survive; so (3) this is why blacks have higher rates of BP than whites. Though the explanation fails, since education, and not genetic ancestry, explains the difference in BP between blacks and whites (Non, Gravlee, and Mulligan, 2012). One only needs to understand the intricacies of physiology and how our physiological systems respond to what occurs in the greater environment.
So, obesity can explain both the higher rates of diabetes and higher rates of blood pressure, with differences in the immediate social environment explaining the rest of the differences in blood pressure between blacks and whites. (Note that heart disease deaths are directly related to hypertension. Heart disease affects blacks more than whites.)
In Race, Medicine, and Epigenetics: How the Social Becomes Biological, I shortly discussed breast cancer in black women:
Black women are more likely to die from breast cancer, for example, and racism seems like it can explain a lot of it. They have less access to screening, treatment, care, they receive delays in diagnoses, along with lower-quality treatment than white women. But “implicit racial bias and institutional racism probably play an important role in the explanation of this difficult treatment” (Hardimon, 2017: 166). Furthermore, black women are more than twice as likely to acquire a type of breast cancer called “triple negative” breast cancer (Stark et al, 2010; Howlader et al, 2014; Kohler et al, 2015; DeSantis et al, 2019). Of course, this could be a relevant race-related genetic difference in disease.
Now note the infant mortality rate between the states: the infant mortality rate in Mississippi is 9.7%. Smith et al (2018) show that black women are at a higher rate of having their infant die at birth. Pre-term births are related to low birth weights, and they both are related to infant mortality. Matoba and Collins (2017) write:
In the United States, African-American infants have significantly worse infant mortality than white infants. Individual risk factors alone do not explain this persistent gap, just as they did not explain the disparity in preterm birth and low birth weight. Recent studies in social determinants provide insight into the contribution of community and environmental factors to the racial disparity. Select community-level factors are potential, but partial, determinants of the racial disparity. Interpersonal and institutionalized racism is an important, and increasingly recognized, stressor for African-American women with damaging consequences to maternal and child health.
The Guardian ran a recent story on infant mortality and race, positing racism as a cause of the disparity. In any case, the social environment can and does play a part in everything discussed here today since the social can and does become biological. Part of the reason why Mississippi has a way higher rate of years of potential life lost (10,214 compared to 5500-5900 for Iowa, New York, and California) is that rates of infant mortality are higher in Mississippi. So the median age of death is 75. If an infant dies at one year of age, then that is 74 years of life lost. Therefore it is not surprising that the State with the highest level of infant mortalities has a higher number of years of potential life lost. Further, one 2017 review found that segregation was associated with increased risk of preterm birth and low birth weight for blacks (Mehra, Boyd, and Ickovis, 2017)
Note how Mississippi has lower rates of asthma. This is explained by the fact that Mississippi is more rural than, say New York. Rates of asthma are associated with living in a metropolitan area (Frazier et al, 2012; Malik, Kumar, and Frieri, 2012). (Note that blacks and other races have higher rates of asthma than other races.)
The lower one’s position is on the social hierarchy the lower their probability of staying healthy and having a high life expectancy; when people have the same type of health insurance and are treated for the same disease in the same hospital by the same doctor, that minority groups get worse health care, either not receiving it or receiving lower standards of quality in care. What could account for such disparities? I asked PumpkinPerson the question, and he said:
1) EGI: Doctors put more effort into saving coethnics: she looks like my italian grandma. I’ll make sure she gets the best medicine.
2) IQ: low IQ populations don’t understand the doctor’s advice and damage their health
3) r/K: some populations have faster life history so don’t live as long, even with good medical care
If (1), then the doctors need to be named, shamed, and have their medical licenses revoked. If (2), then they need better education (since IQ is just an index of middle-class knowledge). (3) is completely irrelevant, since it doesn’t make sense for humans and the concept is long-dead in ecology. In any case, PumpkinPerson danced around the true cause: differences in healthcare brought about by unconscious bias (of which (1) may be a cause). But positing (1) as a cause completely misses the point (and is the usual HBDer reductionism to genes causing most/if not all things). It’s the usual HBD/Rushtonian reductionism to genes. That’s all the HBD worldview reduces to: genes/IQ.
In any case, Reschovsky and O’Malley (2008: 229, 230)
Our results indicate that the minority makeup of physicians’ patient panels is associated with greater reports from physicians of difficulties providing high-quality care. At least some of this relationship appears to be explained by the lower resources flowing to high-minority practices.
The results of this study suggest that racial and ethnic disparities in primary health care are in part systemic in nature, and the lower resources flowing to physicians treating more minority patients are a contributing factor.
Thus, bias—whether conscious or unconscious—by physicians can explain how and why there are differences in health outcomes between people that have the same health insurance and doctor. Barr (2014: 168) states that “for black Americans, where a person lives sems to be associated with access to primary care, the quality of available hospital care, and the quality of available home care.” Barr shows that blacks receive a different level of care for a wide-range of diseases and illnesses compared to whites. For instance, Smedley et al (2003) write that “some evidence suggests that bias, prejudice, and stereotyping on the part of healthcare providers may contribute to differences in care.” Quite clearly, there is racial bias against minorities and it does seem to affect healthcare, whether or not it is intended or unintended (conscious or unconscious) (Williams and Rucker, 2000). Bird and Clinton (2001: 255) write:
Race and class-based structuring of the U.S. health delivery system has combined with other factors, including physicians’ attitudes—perhaps legacies conditioned by their participation in slavery and creation of the scientific myth of black biological and intellectual inferiority—to create a medical-social, health system cultural, and health delivery environment which contributes to the propagation of racial health disparities, and, ultimately, the health system’s race and class dilemma.
Blacks are more likely to take the advice of physicians, and to use the needed services, such as preventative care and are less likely to delay seeking care when the physician is of their own race (Saha et al, 2000; LaVeist, Nuru-Jeter, and Jones, 2008).
Blacks are more likely to perceive racism in healthcare and when they are able to choose their own doctors, they are more satisfied with their level of care (Chen et al, 2005). Chapman, Kaatz, and Carnes (2013) show that increasing awareness of implicit bias in healthcare can lower such disparities, stating that having more black doctors will alleviate such problems since they are less likely to be biased. Having a black doctor lead to more effective care for black men. Quite clearly, the race of the doctor matters for implicit biases and minority doctors lead to more effective healthcare for minorities, since they are less likely to be affected by racial biases. Minorities trust the healthcare system less than whites (Boulware et al, 2003). Black and white physicians even agree that race is a medically relevant data point, but do not agree on why (Bonham et al, 2009).
The table presented by Barr is telling. He purported to show that on certain indices of health, certain states fair worse than others. Rates of illness and rates of death between different states (with differing ethnic compositions) were compared. Using national data, he showed that Mississippi has the highest rates of death and illness (sans asthma). Social factors can and do account for the differences in hypertension between blacks and whites (and States); food deserts (lack of access to good food) can explain higher rates of obesity and diabetes and also higher rates of blood pressure between the races (and States with a higher percentage of certain racial/ethnic groups). Of course, physiological variables are affected by the social environment, so we have to look at differences in the social environment between groups to see how and why there are differences in any physiological variable we look at.
Doctors, whether consciously or not, treat minority patients differently and there is evidence that this leads to differences in health outcomes between ethnic groups in America. PP’s hypotheses don’t cut it (the only one that does it his “EGIs”, but that explanation fails; the cause is bias by the doctors but “EGIs” have nothing to do with the bias). In any case, there are social and cultural reasons why there are such health disparities between States and races/ethnies. Understanding the causes behind them can and will lead to closing the gap between them. The social can and does become biological, and this is the perfect way to show this. There are ways to lower the disparities in a medical context, and education seems to be one of them—for both patient and doctor.
Some states are healthier than others based on objective measures of health and mortality, and understanding the reasons why can and will decrease these differences.
Helmuth Nyborg published an article in Psych titled Race as Social Construct (Nyborg, 2019). In the article, he responds to a National Geographic article There’s No Scientific Basis for Race—It’s a Made-Up Label. In the article, Nyborg quotes, what apparently are quotations, from the article. Yet, for example when it comes to this:
‘There’s No Scientific Basis for Race’—‘It’s a Made-Up Label’… ‘Races do not exist because we are equals’, ‘the concept of race is not grounded in genetics’, etc.
The second quote “Races do not exist because we are equals” is not in the article. (Though this is probably a general call-out to so-called “social constructivists about race.”) Now, I won’t’ nit-pick about it, since he is apparently speaking to his critics who make these claims. In any case, Nyborg’s article is titled Race as Social Construct. Where are constructivists about race said to be anti-realists or eliminativists about race? If Nyborg is really speaking to constructivists about race, then he’s strawmanning their position. Because social constructivists about race are realists about race.
Take the new AAPA Statement on Race and Racism, where they write:
… race has become a social reality that structures societies and how we experience the world. In this regard, race is real, as is racism, and both have real biological consequences.
““race” as a social reality — as a way of structuring societies and experiencing the world — is very real.”
So, if constructivists about race claim that “Races do not exist”, then why are social constructivists about race literally saying “race is real” and “”race” as a social reality … is very real”? Weird… Almost as if Nyborg is strawmanning the constructivist position. Nyborg asks if “NG also think[s] of species as a social construct?“. See Elstein (2003) for a view that species are socially constructed. In any case, I don’t think that Nyborg is familiar with the philosophical literature on the status of species.
Here is Nyborg’s first syllogism:
Samuel Morton is a reprehensible model racist with a fixed defintion of race.
1. Samuel Morton is the father of scientific racism.
2. (We “know” that the father of scientific racism has THE correct understanding of race).
3. Morton thinks that races represent separate acts of creation.
4. Morton thinks that races are ranked in a divine hierarchy.
5. Morton did not think that races were closely related.
6. Morton thinks that races has distinct characters which:
(a) Are immutable or “fixed” across generations (i.e., no transmutation, aka evolution).
(b) Are homogenous of “fixed” (in these senses of fixation) across individuals within races.
Morton is wrong about 3-6, and thus represent the opposite of reality. We can then say, given 1-2 and 3-6, that races do not exist.
This is ridiculous. Where has anyone written anything like this, that since Morton was a “racist” that “races do not exist”? Did Gould make that claim in Mismeasure? I personally think that Morton’s analysis was flawed by his own biases, but I do not make the claim that “races do not exist” because of it.
In any case, when it comes to Gould’s critique of Morton’s skulls, contra Jensen (1982), Rushton (1997) , and Lewis et al (2011), Gould’s arguments about Morton were largely correct (Weisberg, 2014; Kaplan, Pigliucci, and Banta, 2015; Weisberg and Paul, 2016). Specifically, Weisberg (2014) writes that “Although Gould made some errors
and overstated his case in a number of places, he provided prima facia evidence, as yet unrefuted, that Morton did indeed mismeasure his skulls in ways that conformed to 19th century racial biases.”
Now when it comes to this one, we’re getting somewhere:
Race does not Relate to Geographic Location
1. There are no fixed traits with specific geographic locations …” because …
2. “… as often as isolation has created differences among populations, migration and mixing have blurred or erased them.
3. “… our pictures of past ‘racial structures’ are almost always wrong” and harmful.
This is a good argument. However, it fails, in my opinion. Yes, there is no sharp delineation in traits between what are purported to be racial groupings. However, for biological racial realism to be true, there do not need to be. Take my article You Don’t Need Genes to Delineate Race. By looking at average facial and morphological features that exist in any continent, we can say that, although there is no sharp gradation and there are clines in phenotypes, that does not mean that there is no what we can say “average look” for the group. (Nyborg discusses “IQ” there, but I won’t get into it.)
Now take this one:
Races do not exist: We are Equals and Africans
1. “… all humans are closely related.”
2. In a very real sense, all people alive today are Africans.”
3. Genetic diversity in Africa is much larger than outside this continent.”
4. Because they [migrants] were just a small subset of Africa’s population, the migrants took with them only a fraction of its genetic diversity.”
5. Admittedly, “… the longer two groups are separated, the more distinctive tweaks [mutations] they will acquire”, BUT …
6. “The concept of race has no genetic or scientific basis.” (NG here refers to a Craig Venter statement at a White House meeting, June 2000; see later).
7. “Science tells us there is no genetic or scientific basis for race. Races do not exist because we are [all] equals.”
1-5 are true; though 6-7 are false. In any case, the existence of race is not a scientific matter. The questions “What is race?”, “Is race real?”, and “If race is real, how many races are there?” are philosophical, not scientific, matters. Nyborg brings up “Lewontin’s fallacy”, but take what Hardimon (2017: 22-23) writes about the matter:
It is worth noting that the force of the argument against the existence of racialist races from Lewontin’s data analysis is unaffected by the critique A.W.F. Edwards made in his 2003 paper “Human Genetic Diversity: Lewontin’s Fallacy.” The fallacy Edwards imputes to Lewontin consists in inferring that racial classification has no taxonomic signifigance from the finding that the between-race component of human genetic diversity is very small. The inference is fallacious because the fact that the between-race component of human genetic diversity is small does not entail that racial classification has no taxonomic signifigance. Lewontin’s locus-by-locus analysis (which does not consider the possibility of a correlation between individual loci) does not preclude the possibility that individual loci might be correlated in such a way that people could be grouped into traditional racial categories. The underlying though is that racial classification would have “taxonomic signifigance” were it possible to group people into traditonal racial categories by making use of correlations between individual loci. However, Lewontin’s argument that there are no racialist races because the component of within-race genetic variation is larger than the component of between-race genetic variation is untouched by Edwards’ objection. That conclusion rests solely on Lewontin’s statistical analysis of human variation (the validity of which Edwards grants) and does not pressupose the absence of correlational structure in the genetic data. In short, Lewontin’s data do not preclude the possibility that raciual classification might have taxonomic signifigance but they do preclude the possibility that racialist races exist.
Nyborg is, obviously, pushing the concept of racialist races, though Hardimon has shown that they do not exist. Nyborg says that “Educability and IQ are arguable [sic] physiological (Spearman, 1927)“. Nope.
Nyborg then presents his next syllogism:
Admixture and Displacement Have Erased All Race Differences
1. Race implies unadmixed groups between which there are fixed—“fix”, in the sense of fixation index—traits.
2. (From Reich (2018) race implies “primeval” groups…separated tens of thousands of years ago”.
3. Genetics shows that mixture and displacement have happened again and again”… and … as a result “Differences have been blurred or erased”.
4. Thus, “there are no fixed traits associated with specific geographic locations…”
5. And “our pictures of past ‘racial structures’ are almost always wrong” and harmful.
Since human descent groups are mixed and do not exhibit fixed trait differences and since there are no 10-thousand-year-old primeval groups, there are no races.
This one is strong, and if an eliminativist/anti-realist about race were to use this argument (remember, Nyborg doesn’t understand that social constructivists are realists about race), then it would be strong. But that human populations are mixed and do not exhibit trait differences does not mean that race does not exist, that does not follow. That is a carry-over from the racialist concept of race, which is false.
Nyborg then presents his fifth syllogism:
Race is only Skin Color Deep
1. “When people speak about race, usually they seem to be referring to skin color and, at the same time, to something more than skin color.”
2. “This is the legacy of people such as Morton, who developed the “science” of race to suit his own prejudices and got the actual science totally wrong.”
3. “Science today tells us that the visible differences between people a re accidents of history. They reflect how our ancestors dealt with sun exposure, and not much else.”
4. There is no homogenous African race.
Since race is only based on skin color, it is made up by racists.
I have heard an argument similar to this, and it fails. Race isn’t ONLY BASED ON skin color, but it is a marker of race, along with ancestry and location. Of course, morphology and other phenotypic traits ground the scientific concept of “race” (minimalist/populationist race). Race, of course, does not mean only skin color, there are many other ways to delineate races, with skin color being but one tell.
Nyborg then writes:
Ducrest, Keller, and Rouling, 2008)  thus observed that darker color is associated with greater aggressiveness in 10 mammal species, three kinds of birds, and more Lizard forms entirely evaded them. They condemned the color analogue with respect to humans, and reacted forcefully when Rushton and Templer (2009)  drew data from no less than 113 countries and found that “… murder, rape, and serious assault were associated with darker skin color, lower IQ, higher birth rate, higher infant mortality, higher HIV/AIDS rate, lower life expectancy, and lower income”
Yea, Ducrest, Keller, and Rouling (2008) is one study that Rushton loved, as it, supposedly, gave a basis for darker color being associated with aggressiveness in a slew of different animals. I rebutted Rushton and Templer, in any case. Their study was ridiculous and they did not even heed what Ducrest, Keller, and Rouling (2008: 507) stated “… that human populations are therefore not expected to consistently exhibit the associations between melanin-based coloration and the physiological and behavioural traits reported in our study.” Must be hard for Rushton and Templer to read.
In sum, Nyborg is wrong that racial constructivists claim that “Races do not exist”, for if they did not exist, then what would constructivists be fighting for? Nyborg seems to be talking to anti-realists/eliminativists about race. Nyborg pushes a racialist concept about race, which was refuted by Hardimon (2017: Chapter 1). Races exist in a minimal sense (Hardimon, 2017) and U.S. sense (Spencer, 2014), but not in the racialist “HBD” sense. In this case, biological racial realism (Spencer, 2011) is true, but if we are going by Kaplan and Winther’s (2014) definitions, Rushton, Jensen, Lynn, and Nyborg would be the biological racial realists, whereas myself, Hardimon and Spencer would be biogenomic/cluster race realists. It seems that Nyborg needs to brush up on the philosophical literature, because what he claims that social constructivists about race believe are not true; he just strawmanned their position. In any case, I’ve shown that constructivists about race do not believe that race is not real. They may not believe that race is real in a biological manner, but they do in a social one, and that is enough for them to be race realists and believe that race exists.
(Also note how Kaplan and Winther (2014) note that “Social racial realism defends the existence of distinct human groups in our ordinary discourse and social interactions. Such groups are often identified and stabilized by “surface” factors such as skin color or facial features.” So, again, those who push a socialrace-type concept do not deny that race exists, on the contrary, they are realists about race. Nyborg got it wrong, and some of his critiques are good against those who deny the reality of race, but his racial ontology is false.
I recently bought Dorothy Roberts’ Fatal Invention: How Science, Politics and Big Business Re-create Race in the Twenty-First Century (2011) (it was $1.99 in the nook store, couldn’t pass it up), which, how the title of the book explains, discusses how race is recreated today using methods of the past as well as methods of the future. One of her main claims is that race is a political entity. Now, while I don’t disagree here (there are of course social aspects to what we call “races”), she completely rides against biological racial realism (eg Spencer, 2014; Hardimon, 2017). Her concept, though, is similar to Hardimon’s (2017) socialrace concept, and it is already a part of Spencer’s Blumenbachian partitions (since race is both biologically and socially constructed in the American view of race). While I do not believe that you need genes to delineate race, Roberts also goes on the attack on Rosenberg et al (2002), who both Hardimon and Spencer cite to buttress their arguments on the reality of biological races.
Race is not a biological category that is politcally charged. It is a political category that has been disguised as a biological one. (Roberts, 2011: 14)
Note how this is extremely similar to Hardimon’s socialrace concept. In Hardimon’s concept, socialraces have a biological correlate: minimalist races. Hardimon’s concept says, for example, that “Hispanics/Latinos” are socialraces but they are a group that do not have a corresponding minimalist race—because “Hispanics/Latinos” are a mixture of different races. Race IS a biological category that has been politically charged: Groups look different; groups that look different share geographic ancestry; groups that look different that share geographic ancestry are derived from the same geographic location; therefore race is a biological category and is therefore politically charged (one reason) since people do not like the out-group—people that look different from themselves.
This distinction is important because many people misinterpret the phrase “race is socially constructed” to mean that the biological category of race has a social meaning, so that each society interprets differently what is means to belong to a biological race. According to this view, first we are born into a race, and then our society determines the consequences of this natural inheritance. There is, then, no contradiction between seeing race as both biological and socially constructed. (Roberts, 2011: 14)
There, actually, IS NO CONTRADICTION between seeing race as socially and biologically constructed. Racial categories pick out real kinds in nature—which is what “biological racial realism” means. Since our racial categories pick out real kinds in nature, then, when it comes to society and social construction, whatever is believed about certain races in that society will be socially constructed. You can’t, for example, call a Nigerian Caucasian (see more on this below) because it does not make any sense.
Roberts then goes on (p. 14-15) about how “human beings do not fit the zoological definition of race” since a “biological race is a population of organisms that can be distinguished from other populations in the same species based on differences in inherited traits.” And so, since no human groups have this high degree of genetic differentiation, there are no human races, but only one human race.
Though Hardimon (2017: 99) articulates the best definition of race I have come across:
A race is a subdivision of Homo sapiens—a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographic ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population.
So we know that (1) populations exhibit distinctive features; (2) these populations that exhibit these distinctive features correspond to that population’s geographic ancestry, (3) these populations that exhibit these distinctive features which correspond to geographic ancestry belong to a biological line of descent which was initiated by reproductive isolated and geographically separated founding populations; so (4) race exists.
We know race is a political grouping because it has its political roots in slavery and colonialism, it has served its political function over the four hundred years since its inceptio, and its boundary lines—how many there are and who belongs to each one—have shifted over time and across nations to suit those political purposes. Who qualifiies as white, black, and Indian has been the matter of countless rule changes and judicial decisions. These racial reclassifications did not occur in response to scientific advances in human biology, but in response to sociopolitical imperatives. They reveal that was is being defined, orgainzed, and interpreted is a political relationship and not an innate classification. (Roberts, 2011: 15)
We can take this two ways here: (1) point out that Roberts is conflating minimalist/populationist races with socialraces (which is exactly what she is describing to the tee). Yes, since race is partly social, then, based on the social attitudes of people which do change over time. Then, in that society, certain groups who were barred from being in another group may be allowed “into” the group. This does not mean that race is not biological. “Oh the Irish were considered “not white” at one point in time, therefore race doesn’t exist since groups can exit group A and become group B based on sociopolitical inclinations.” This, of course, goes over the distinctive phenotypic differences between groups with peculiar geographic ancestry. THAT is what defines race; what Roberts is discussing is important, since race is partly political, but it is not the whole story.
In addition to the grotesque lynchings that terrorized blacks throughout the South, an especially brutal form of reenslavement was the false imprisonment of thousands of black men who were then leased to white farmers, entrepreneurs, and corporations as a source of cheap labor.
It is in this accute distinction that between the political status of whites and blacks, this way of governing the power relationship between them, that we find the origins of race. Colonial landowners inherited slavery as an ancient practive, but they invented race as a modern system of power. They employed Aristotle’s concept of natural slaves and natural rulers to define permanent features of black and white people. Race separated human beings into two fundamentally distinct groups: those who were indelibly born to be lifelong servants and those who were born to be their masters. Race radically transformed not only what it meant to be enslaved, but what it meant to be free. (Roberts, 2011: 23)
Let’s accept Roberts’ argument here that the political status of whites and blacks was a way to govern the power relationship between them: so what? That group A subjugated group B and attempted to justify it with X, Y, and Z doesn’t mean that group A and group B are not biological races—it just means that group A subjugated group B and, in the future, there were social repercussions (which is also a part of the phenomenon of race as a partly social construct).
Roberts then discusses the Census (p. 31-35) and how ever-changing racial definitions undermine the claim that biological racial realism is true. In Spencer’s argument, the US meaning of “race” is just a referent, “specifically the referent of US racial discourse” (Spencer, 2014: 1027). This is because, in America, race-talk is tied to the census. We Americans are familiar with the racial groupings on the census since they are not only in use on the census but numerous other institutions. Spencer (2014) then discusses how we can use “phonetic cues alone (e.g., African American Vernacular English), surnames alone (e.g., “Chen”), first names alone (e.g., “Lakisha”), and visual cues alone (e.g., a person’s face)” (Spencer, 2014: 1027) to know someone’s race. Therefore, according to Spencer, the discourse used in the census is the discourse used nation-wide.
But the census does not set what “race” means on these forms: the OMB (Office of Management Budgeting) does. The OMB refers to race as a “set” of populations, and so this leads Spencer to believe that the “sets” of populations that the OMB is referring to are whites, blacks, Asians, Pacific Islanders, and American Indians. So race is a particular, not a kind as Hardimon argues.
Roberts then argues against the “new racial science”, most forcefully, against Rosenberg et al (2002). She brings up the usual discourse “…the number of genetic clusters is dictated by the computer user, not the computer program” (Roberts, 2011: 74). Roberts says that the clusters are “arbitrary.” Roberts says that Rosenberg et al’s (2002) study failed to verify 18th-century racial typology, but it did confirm what we have known since Lewontin’s (1972) analysis: that there is more genetic variation within races than between them. About 93-95 percent of human genetic variation was found to be within race whereas 5-7 percent of human genetic variation was found to be between groups.
Roberts says that the clusters are “arbitrary.” This is a common critique, but it is irrelevant. The five populations found by Structure are genetically structured—they are meaningfully demarcated on the basis of genetic markers (Hardimon, 2017: 88). Roberts also discusses the K = 6 run, which identified the Kalash people.
The fact that structure represents a population as genetically distinct does not entail that the population is a race. Nor is the idea that populations corresponding to the five major geographic areas are minimalist races undercut by the fact that structure picks out the Kalash as a genetically distinct group. Like the K=5 graph, the K=6 graph shows that modulo our assumption, continental-level races are genetically structured” (Hardimon, 2017: 88).
The five clusters identified by Rosenberg et al (2002) represent continental-level minimalist races so the five populations which correspond to the major geographic locations throughout the world are continental-level minimalist races. So it is, in fact, possible to place individuals into different their continental-level minimalist race without knowing anything about the race or ancestry of the individuals from which the microsatellites were drawn. Rosenberg et al (2002) studied the populations based on language, culture, and geography, not skin color or race.
It is true that Rosenberg et al (2002) found 4.3 percent of the overall human genetic variation to be between races—but this does not ride against claims from biological racial realists. The genetic variation is enough to say that we have partitions at K = 5.
“People are born with ancestry that comes from their parents but are assigned a race” is how Camara Jones, a research director at the Centers for Disease Control (CDC) explains it. (Roberts, 2011: 77)
People are assigned races based on the ethnicity/ancestry of the parents. A Nigerian would not be assigned to the Asian race, since the Nigerian has none of the features which make “Asians” Asian.
This is very simple: if both parents belong to race R, then the child will be race R as well. If parent 1 belongs to R1 and so does parent 2, then the child will belong to R1 as well (since the parents have distinct physical features which correspond with geographic ancestry and their ancestors derived from a distinct geographic location. So, since people are born with ancestry that comes from their parents, then they are assigned their PARENT’S race; they are not assigned A race, as if one can assign any individual to any race. But what if one parent belongs to R1 and the other belongs to R2? Hardimon’s minimalist concept is vague here; it only shows that races exist, it does not say which populations are races. If an individual’s parents belong to R1 and R2, then that individual is mixed race. The existence of mixed race people, of course, does not rail against the existence of biological races.
In sum, Roberts does make some good points (in what I have read of the book so far), but she gets it wrong on race. Hardimon and Spencer have both defended the methodology/concepts used by Rosenberg et al (2002) and in doing so, they successfully argued for the existence of biological races—though their two viewpoints differ. That race is, in part, socially (politically) constructed is irrelevant. What Roberts does not understand is that these socially constructed groups (“white”, “black”) still, very much so, capture biological differences between them. That they are socialraces does not mean that they DO NOT have different physical features which correspond to geographic ancestry. The socialrace concept (which Roberts espouses in her book) is separate from Hardimon’s other scientific race concepts. But it is already inherent in Spencer’s, since his Blumenbachian partitions are social constructs of a biological reality. You don’t need genes to delineate races and minimalist races exist and are biologically real.
(I will cover other things from her book as I get to them. I will discuss race and medicine at length.)
At least three arguments establish the existence and reality of biological race:
Argument (1) from Michael Hardimon’s (2017) book “Rethinking Race: The Case for Deflationary Realism” (The Argument for the Existence of Minimalist Races, see Chapters 2, 3, and 4):
The conditions of minimalist racehood are as follows:
(C1) … a group, is distinguished from other groups of human beings by patterns of visible physical features
(C2) [the] members are linked be a common ancestry peculiar to members of that group, and
(C3) [they] originate from a distinctive geographic location (Hardimon, 2017: 31).
This is the argument to prove the existence of minimalist races:
P1) There are differences in patterns of visible physical features which correspond to geographic ancestry
P2) These patterns are exhibited between real groups, existing groups (i.e., individuals who share common ancestry)
P3) These real, existing groups that exhibit these physical patterns by geographic ancestry satisfy the conditions of minimalist race
C) Therefore race exists and is a biological reality
Argument (2) from Michael Hardimon’s (2017) book “Rethinking Race: The Case for Deflationary Realism” (The Argument for the Existence of Populationist Races, see Chapters 5 and 6):
P1) The five populations demarcated by Rosenberg et al (2002) are populationist races; K = 5 demarcates populationist races.
P2) Populationist race=minimalist race.
P3) If populationist race=minimalist race, then everything from showing that minimalist races are a biological reality carries over to populationist races.
P4) Populationist races capture differences in genetic variation between continents and this genetic variation is responsible for the distinctive patterns of visible physical features which correspond to geographic ancestry who belong to biological lines of descent which were initiated by geographically isolated founding populations.
C) Therefore, since populationist races=minmalist races, and visible physical features which correspond to geographic ancestry are genetically transmitted by populations who belong to biological lines of descent, initiated by reproductively isolated founding populations, then populationist races exist and are biologically real.
Argument (3) from Quayshawn Spencer’s (2014) paper “A Radical Solution to the Race Problem” (The argument for the Existence of Blumenbachian Populations):
P1) The term “race” in America refers to biologically real entities; when speaking of race in America, Americans defer to the US Census Bureau who defers to the Office of Management and Budget (OMB).
P2) The OMB refers to race as “sets of” categories, while considering “races” to have 5 members, which correspond to the five major geographic regions.
P3) Rosenberg et al show that, at K = 5, meaningful, though small (~4.3 percent) genetic variation exists between continental-populations
C) Since Americans defer to the US Census Bureau who defers to the OMB, and the OMB refers to race as “sets of” categories which then correspond to five clusters found by Rosenberg et al’s (2002) analysis, race (what Spencer, 2014 terms “Blumenbachian populations”) must exist, though “race” is both socially constructed and biologically real.
Put another way, Spencer’s (2014) argument could also be:
P1) The US meaning of “race” is a referent, which refers to the discourse used by the US Census Bureau; the US Census Bureau refers to the discourse used by the Office of Management and Budget (OMB).
P2) The referent of “race”, in US ontology, refers to a set of human population groups, not a biological kind (sets of human population groups as denoted by the OMB), which refer to “Africans”, “Caucasians”, “East Asians”, “Native Americans”, and Pacific Islanders/Oceanians.
P3) The US meaning of race is both biologically real and socially constructed; Americans refer to real, existing groups when they talk about race.
C) If the US meaning of race is a referent which refers to the discourse used by the US Census Bureau and they refer to the OMB who discuss “sets of” population groups, then when Americans talk about race they talk about Blumenbachian partitions, since race is both biologically real and socially constructed.
The claim “Race exists” is now established. Note how Argument (1) establishes the claim that “races” are real, existing groups who are phenotypically distinct populations with differing geographic ancestry. Note how Argument (2) establishes the claim that populationist race = minimalist race and that “races” are a group of populations that exhibit a distinctive pattern of genetically transmitted phenotypic characters which then correspond to that group’s geographic ancestry who belong to a biological line of descent which was initiated by a geographically separated and reproductively isolated founding population. (This definition of “race” a subdivision of Homo sapiens is the best I’ve come across so far.) Finally, note how Argument (3) establishes the claim that race, in the American sense, is both biologically real and socially constructed. All three arguments are sound and logically valid.
Now, which groups fall into which of the five racial categories?
Caucasians denote a wide-range of groups; Europeans, MENA (Middle Eastern/North African) peoples, Indians are a very diverse group, racially speaking, with “Caucasoids”, “Mongoloids” and “Australoids” (Australoids would mean Pacific Islander/Oceanian) (see Kashyap et al, 2006 for an overview of ethnic, linguistic and geographic affiliations of Indians in the study). Ashkenazi Jews are taken to be a specific race in today’s modern racial ontology, however, Ashkenazi Jews do not exhibit a distinctive pattern of genetically transmitted phenotypic characters which then correspond to their geographic ancestry; they do represent a “geographically isolated and reproductively isolated founding population”, but the fact that they do not exhibit a distinctive pattern of genetically transmitted phenotypic characters means they are not a race, according to Arguments (1) and (2). Ashkenazi Jews are Caucasian, and not their own race. Of course, skin color does not denote race, it is only one marker to use to infer which groups are races.
Africans comprise all of Sub-Saharan Africa. Africa has the most genetic diversity in the human species (see Campbell and Tishkoff, 2010). Africans, in general, have long, slim bodies with a broad nose, dark skin, kinky hair (lip size is different based on the ethny in question). There are over 3,000 different ethnic groups in Africa, who all comprise the same race. Now, since Africans have the most genetic diversity this does not necessarily mean that they are so phenotypically distinct that there are tens, hundreds, thousands of races on the continent. One only needs to refer back to Arguments (1) and (2) to see that brash claims that “all Xs are Ys” don’t make any sense—especially with the arguments laid out above.
East Asians denote a minimalist and populationist race (Arguments (1) and (2)) and Blumenbachian partition (Argument (3)). East Asians denote, obviously, those that derive from East Asia (Chinese, Japanese, Koreans, Vietnamese). These peoples are relatively short, on average, have a distinct yellow-ish tint to their skin (which is why they are sometimes called “yellow”), epicanthic folds and shorter limbs (more likely to have the endomorphic phenotype).
Native Americans are derived from a Siberian population that crossed the Bering Land Bridge about 14kya. They then spread throughout the Americas, becoming the “Natives” we know today. They are what used to be termed “red” people, due to their skin color. Native Americans are derived from Siberians, who share affinities with East Asians. (This will be discussed in further depth below.) They have black hair, and dark-ish skin. Populations that lived in the Americans pre-1492 expansion are part of the Native American racial grouping.
The last racial grouping are Pacific Islanders. Spencer (2014: 1032) writes that we can define Oceanians (Pacific Islanders):
as the most inclusive human population born from East Asians in Oceania (Sahul and the Pacific Islands) and from the original human inhabitants of Oceania. Since Sahul was a single landmass composed of present-day Australia, New Guinea, and Tasmania 50,000–60,000 years ago, when humans first inhabited it, and since we know that the original human inhabitants of Oceania interbred to create modern Oceanians, and since temporal parts of populations are genealogically connected, it should be the case that most Oceanians have genealogical connections to the original peoples of some Pacific island. The only Oceanians who will not will be individuals who became Oceanian from interbreeding alone and Oceanians descended from indigenous peoples of Sahul but not indigenous peoples of a Pacific island (e.g., Aboriginal Australians). The final source of evidence comes from counterfactual cases. [Pacific Islanders and Australian Aborigines share a deep ancestry, see McEvoy et al, 2010.]
A group is in race X, if and only if they share a pattern of visible physical features and common geographic ancestry. If they do not share a pattern of visible physical features which correspond to common geographic ancestry then they do not constitute a race. Keep this in mind for the next two sections.
Are Oceanians black?
One claim that gets tossed around a lot (by black nationalists) is the claim that Oceanians are black due to their skin color, certain phenotypic traits. But this could just as easily be explained by convergent evolution, not that they are, necessarily, the same racial grouping. If this were true, then Australian Aborigines would be black, by proxy, since Australian Aborigines and Oceanian are the same race. The claim, though, holds no water. Just because two groups “look similar” (which I do not see), it does not follow that they are the same race, since other conditions need to be met in order to establish the claim that two separate groups belong to the same race.
Are Native Americans Mongoloid?
Lastly is the claim that Native Americans do not denote an actual racial grouping, they are either Mongoloid or a sub-race of Mongoloids.
Many authors throughout history have presumed that Native Americans were Mongoloid. Franz Boas, for example, said that the Maya Indians were Mongoloid, and that, American populations had features the most similar to Mongoloids, so they are thusly Mongoloid. Wikipedia has a great overview of the history of the “Mongoloid” terminology, with examples from authors throughout history. But that is irrelevant. Native Americans genetically transmit heritable phenotypic characters which correspond with their geographic ancestry and are genetically and geographically isolated population groups.
Although the claim that “Native Americans are Mongoloid” has been echoed for hundreds of years, a simple argument can be erected to take care of the claim:
P1) If Native Americans were East Asian/Mongoloid, then they would look East Asian/Mongoloid.
P2) Native Americans don’t look East Asian/Mongoloid, they have a distinct phenotype which corresponds to their geographic ancestry (See Hardimon’s minimalist/populationist race concepts).
C) Therefore, Native Americans are not East Asian/Mongoloid.
Establishing the claim that Native Americans are not East Asian/Mongoloid is simple. Some authors may make the claim that since they look similar (whatever that means, they don’t look similar to me), that they, therefore according to Arguments (1) and (2) they are a separate race and not a sub-race of East Asians/Mongoloids; Argument (3) further establishes the claim that they are a separate race on the basis that they form a distinct cluster in clustering analyses (Rosenberg et al, 2002) and since, Americans defer to the US Census Beureau and the US Census Beureau defers to the OMB who discusses sets of populations, then when Americans talk about race they talk about Native Americans as separate from East Asians/Mongoloids, since, according to Arguments (1) and (2) they have a distinct phenotype.
Generally, they have distinct skin colors (of course, skin color does not equal race, but it is a big tell), they have similar black, straight hair. But they are, in my opinion, just too phenotypically distinct to call them the same race as Mongoloids/East Asians. For the claim “Native Americans and Mongoloids/East Asians” to be true, they would need to satisfy P1 in Argument (1) and P4 in Argument (2). Native Americans do not satisfy P1 in Argument (1) nor do they satisfy P4 in Argument (2). Therefore, Native Americans are not Mongoloid/East Asian.
The claim “Race exists and is a biological reality” is clearly established by three sound, valid arguments—two from Hardimon (2017; chapters 2-6) and one from Spencer (2014). These arguments show, using the latest of genetic clustering studies, that races, as classicly defined, do indeed, exist and that our old views of race hundreds of years ago were, largely, correct. These arguments establish the existence of the old folk-racial categories. Races have distinct phenotypes which are genetically transmitted and are correlated with geographic ancestry. Some may make certain claims that “Oceanians are black” or “Native Americans are Mongoloid”, but these claims do not hold. These two groups in question are phenotypically distinct, and they come from unique geographic locations, therefore they are not a part of the races that some purport them to be.
Racial differences in body fat are clear to the naked eye: black women are more likely to carry more body fat than white women; Mexican American women are more likely to carry more body fat than white women, too. Different races/ethnies/genders of these races/ethnies have different formulas to assess body fat through the use of skin-folds. The sites to grasp the skin is different based on gender and race.
Body mass index (BMI) and waist circumference is overestimated in blacks, which means that they need different formulas to assess their BMI and adiposity/lean mass. Race-specific formulas/methods are needed to assess body fat and, along with it, disease risk, since blacks are more likely to be obese (black women, at least, it’s different with black American men with more African ancestry, see below). The fact of the matter is, when matched on a slew of variables, blacks had lower total and abdominal fat mass than whites.
This is even noted in Asian, black and white prepubertal children. He et al (2002) show that sex differences in body fat distribution are present in children who have yet to reach puberty and the differences in body fat in Asians is different than that from blacks and whites which also varies by sex. Asian girls had greater gynoid fat by DXA scan only, with girls having greater gynoid fat than boys. Asian girls had lower adjusted extremity fat and gynoid fat compared to white and black girls. Though, Asian boys had a lower adjusted extremity by fat as shown by DXA (a gold standard in body fat measurement) when compared to whites, but greater gynoid fat than whites and blacks.
Vickery, Cureton, and Collins, (1988), Wagner and Heyward (2000), and Robson, Bazin, and Soderstrom (1971) show that there are considerable body composition differences between blacks and whites. These differences in body composition come down to diet, of course, but there is also a genetic/physiologic component there as well. Combining the known fact that skin-fold testing is not conducive to a good estimate, black American men with more African ancestry are less likely to be obese.
Vickery, Cureton, and Collins (1988) argue that, if accurate estimates of body fat percentages are to be obtained, race-specific formulas need to be developed and used as independent variables to assess racial differences in body fat percentage. Differences in muscularity don’t seem to account for these skinfold differences, nor does greater mesomorphy. One possible explanation for differences in skinfold thickness is that blacks may store most of their body fat subcutaneously. (See Wagner and Heyward, 2000 for a review on fat patterning and body composition in blacks and whites.)
The often-used Durnin-Womersley formula which is used to predict body fat just from skin folds. However, “The 1974 DW equations did not predict %BF(DXA) uniformly in all races or ethnicities” (Davidson et al, 2011). Truesdale et al (2016) even show that numerous formulas used to estimate percent body fat are flawed, even some formulas used on different races. Most of the equations tested showed starkly different conclusions. But, this is based on NHANES data and the only data they provide regarding skin-folds is the tricep and subscapular skinfold so there may still be more problems with all of the equations used to assess body fat percentage between races. (Also see Cooper, 2010.)
Klimentidis et al (2016) show that black men—but not black women—seem to be protected against obesity and central adiposity (fat gain around the midsection) and that race negatively correlated with adiposity. The combo of male gender and West African ancestry predicted low levels of adiposity compared to black Americans with less African ancestry. Furthermore, since black men and women have—theoretically—the same SES, then cultural/social factors would not play as large a role as genetic factors in explaining the differences in adiposity between black men and black women. Black men with more African ancestry had a lower WHR and less central adiposity than black men with less African ancestry. If we assume that they had similar levels of SES and lived in similar neighborhoods, there is only one reason why this would be the case.
Klimentidis et al (2016) write:
One interpretation is that AAs are exposed to environmental and/or cultural factors that predispose them to greater obesity than EAs. Possibly, some of the genes that are inherited as part of their West-African ancestry are protective against obesity, thereby “canceling out” the obesifying effects of environment/culture, but only in men. Another interpretation is that genetic protection is afforded to all individuals of African descent, but this protection is overwhelmed by cultural and/or other factors in women.
Black men do, as is popularly believed, prefer bigger women over smaller women. For example, Freedman et al (2004) showed that black American men were more likely to prefer bigger women. Black American men “are more willing to idealize a woman
of a heavier body size, with more curves, than do their White American counterparts” (Freedman et al, 2004: 197). It is then hypothesized that black American men find these figures attractive (figures with “more curves” (Freedman et al, 2004: 197)) to protect against eating pathologies, such as anorexia and bulimia. So, it has been established that black men have thinner skin folds than whites which leads to skewed lean mass/body fat readings and black men with more African ancestry are less likely to be obese. These average differences between races, of course, contribute to differing disease acquisition.
I have covered differences in body fat in a few Asian ethnies and have come to the obvious conclusion: Asians, at the same height, weight etc as whites and blacks, will have more adipose tissue on their bodies. They, too, like blacks and whites, have different areas that need to be assessed for skin folds to estimate body fat.
Henriques (2016: 29) has a table on the equations for calculating estimated body density from skin fold measures from various populations. Of interest are the ones on blacks or ‘Hispanics‘, blacks or athletes and blacks and whites. (The table is provided from NSCA, 2008 so the references are not in the back of the text.)
For black and ‘Hispanic’ women aged 18-55 years, the sites to use for skin-folds are the chest, abdomen, triceps, subscapular, suprailiac, midaxillary, and the thigh. For blacks or athletes aged 18-61 years, the sites to use are the same as before (but a different equation is used for body fat estimation). For white women or anorexic women aged 18-55, the sites used are just triceps, suprailiac and the thigh. For black and white boys aged 6-17, only the triceps and the calf is used. It is the same for black and white girls, but, again, a different formula is used to assess body fat (Henriques, 2016: 29).
Morrison et al (2012) showed that white girls had a higher percent body fat when compared to black girls at ages 9-12 but every age after, black girls had higher percent body fat (which is related to earlier menarche in black girls since they have higher levels of body fat which means earlier puberty; Kaplowitz, 2008). Black girls, though, had higher levels of fat in their subscapular skin folds than white girls at all ages.
So, it seems, there are population-/race-specific formulas that need to be created to better assess body fat percentage in different races/ethnies and not assume that one formula/way of assessing body fat should be used for all racial/ethnic groups. According to the literature (some reviewed here and in Wagner and Heyward, 2000), these types of formulas are sorely needed to better assess health markers in certain populations. These differences in body fat percentage and distribution then have real health consequences for the races/ethnies in question.