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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.
How much admixture does it take for one race to no longer exist? The answer to the question is intuitive, and using Hardimon’s (2017) minimalist race concept, it is also easily answerable on logical grounds. For example, the answer to the question will show that the “one-drop rule” (that “one drop” of “black blood” makes one black) doesn’t make logical sense. These kinds of holdovers are from the racialist concept. Racialist races do not exist, therefore the concept of the “one-drop rule” does not either, since there are no facts of the matter the two concepts explain.
The maintenance of the races that current exist depend on, at the moment, social barriers to reproduction, such as racism, segregation, differences in culture and class, role segregation and racial discrimination. Thus, social isolation is important for the maintenance of the current races. Social isolation, like geographic isolation (i.e., oceans, mountains, deserts, etc.) impedes racial interbreeding and thus ensures the continuation of the genetic transmission of distinct patterns of visible physical features which correspond to geographic ancestry.
Social isolation mechanisms have been in effect for hundreds of years, which began with the advent of African slavery to the New World. Laws against miscegenation existed in some states (Phillips, Odunlami, and Bonham, 2007), which is part of the reason why it’s (an unspoken) taboo to racially intermarry and bear children with someone not of their own race. Due to this, the few interracial unions that did produce children were specifically barred—in the eyes of society—to only be able to have children with others of their same socialrace at the lower ends of the social hierarchy.
Social isolation mechanisms have ensured the continuation of human races after the discovery of the New World when the geographic isolation mechanisms began breaking down due to exploring new lands. These isolating mechanisms on the populace ensured little admixture in the European population, but compared to European Americans, African Americans have a higher percentage of the opposite admixture. Understanding racial admixture and the genetic transmission of distinct visible physical features which correspond to geographic ancestry is extremely important to understanding when races “disappear” due to inbreeding.
Therefore, social isolation—ever since 1492—and the laws/rules that came after the breakdowns of geographic isolation between races still ensured the existence of the races as we know them today. Social factors acted as de facto physical barriers that impeded the races from breeding, thusly keeping their visible physical features intact, which means keeping their racial phenotype intact since races are defined—most importantly—on the basis of visible physical features. Social isolation can, clearly, be just about as “strong” as geographic isolation, since the social repercussions of interracial unions may exile them from the groups they were in. Thus, people would be wary of interracial unions, even if—as it seems—our culture in America seems to be swaying towards inclusivity in regard to interracial relationships, people still generally associate with and date people who look like themselves and their parents (see below).
How Much Admixture?
How much admixture can one race take before said race ceases to exist? Since C 1 (a group is distinguished from another group on the basis of distinct visible physical features) doesn’t require sharp lines between said visible physical features, C 2 (members linked by peculiar ancestry) also doesn’t require that all of the ancestors of Rs (races) be Rs.
The best possible example for an answer to the question of “How much admixture?” is simple. Think of Europeans (a subrace of the Caucasian race). When Europeans interbreed with non-Europeans, they begin to lose their distinct pattern of visible physical features which correspond to their geographic ancestry. Thus, in the case of Europeans, the answer to the question of “How much admixture?”, meaning “How much interbreeding can the European subrace take before it is “bred out” of existence?” is, of course, not too much.
Think of a union between a black woman and white man (using the social race designation; their populationist race is African and Caucasian, respectively). The child the woman bears will share some of her physical features, but barely. The baby will look more like the non-European parent, but of course, a baby who is the product of the union between an African and European will share features with both parents, and thus, the baby can “roughly fit the pattern” of a minimalist race. We can easily explain this: mixed-race individuals can err, physically, to one minimalist race over another because they are the products of individuals who do fit the patterns (of visible physical features which correspond to geographic ancestry).
Contrary to the alarmist claims heard in the media and from the altright, trends in interracial marriages do not indicate that minimalist (populationist) races are coming to an end (in this case, the white (social) race).
It is true that in the modoern (post-1492) world there is vastlty more racial interbreeding than there was before 1492. And if one is referring to the very long run, then races are almost certainly on their way out. But it is one thing to say that the human races will cease to exist at some point in the distant future and quite another to say that they are likely to disappear anytime soon. It is by no means clear that we are in an epistemic position to make the latter claim.
Contrary to what some writers suggest, recent trends in racial intermarriage in the United States do not indivate the imminent end of populationist (or minimalist) races. 5 The skyrocketing rates of intermarriage in this country notwithstanding, it remains true that the vast majority of Americans continue to marry within their own conventionally designated racial group. Despite the remarkable fact that the multiracial, multi-ethnic Americans have apparently become the fastest-growing demographic group in the United States, their numbers are still swamped by individuals who are members of a single continental-level minimalist races. 6 I don’t think that the significant fraction of DNA traceable to “Europeans” in most black Americans, and the small but real fraction of DNA traceable to “Africans” in white Americans, makes the end of the populationist (or minimalist) race significantly more imminent.
There is no evidence of which I am aware indicating that the rate at which racial interbreeding in the United States (or anywhere else) is occurring is one that would lead to the elimination of all racial differences—a situation in which no two groups could be distinguished on the basis of patterns of visible physical corresponding to differences in geographic ancestry—in the near future. To sum up: the increase frequency of encountering individuals of mixed racial ancestry does not mean that the concept of race is going to go out of business anytime soon. (Hardimon, 2017: 122)
Yaeger et al (2009) show that, in their sample, self-identification as African American is a reliable indicator of ancestry. Their findings also “suggest that self-reported race and ancestry can predict ancestral clusters, but do not reveal the extent of admixture.” Thus, self-identified race—even in the presence of admixture as is the case with African Americans—can show the racial category that an individual belongs to (based on their ancestry).
Hardimon (2017: 49) articulates a simple rule that employs the minimalist concept of race:
If both parents of an individual belong to one particular racial group R, that individual will belong to R.
What happens, however, if one parent belongs to R1 and the other parent belongs to R2. The minimalist concept of race does not say. Still less does it tell us what one’s race is if one’s grandparents belongs to an R1, another to R2, another to R3, and another to R4. This is a further respect in which the minimalist race concept is vague.
Particular conceptions of race (for example, the infamous “one-drop rule”) may specify the race of the individuals of “mixed” parentage, but the minimalist concept of race does not. The idea that a genune concept of race must specify the race of each individual is a hangover from the racialist race concept. Recall here that the minimalist racehood is not defined in terms of the characteristics of the individuals who belong to races. It is defined in terms of characteristics of groups.
So, the minimalist concept of race is vague, just like the populationist concept. But we can make one claim on the answer to the question “How much admixture?”: “Once a race loses its specific phenotype due to racial interbreeding, then the race ceases to exist.”
The one drop rule (also known as the law of hypodescent), is a form of racial essentialism (Perez and Hirschman, 2009), which states that “one drop” of another, inferior (on the basis of racialist races) race’s blood denotes him to the inferior race in the social hierarchy. The one drop rule was created back during the slave days and signified who could breed with who, on the basis of how “pure” their blood was. It was, and still is today, a way for race deniers to deny the existence of race.
The one-drop rule stated that anyone with one black ancestor was classified as black (Pauker et al, 2009). That is, his position on the socialrace hierarchy (a hierarchy since it’s based on the false racialist race concept) is based on the fact that he has one black ancestor. Due to this, and other differing amounts of admixture in certain ethnic groups and other social groups taken to be races, people have—fallaciously—stated that races do not exist since the unions of two separate races “erases” one, or both, of the races in question.
This rule helped to ensure the maintenance of populationist races, since society frowned upon interracial marriage. This, obviously, was a social custom. The Jim Crow laws helped to ensure the maintenance of the physical characteristics of the races in question, though the laws were enacted to ensure the “racial purity” (whatever that is) of the European race, it helped to ensure lower amounts of admixture in black Americans. Thus, black Americans would be expected to self-identify as black (Liebler and Zacher, 2017).
Liebler and Zacher (2017)‘s data “supports the notion that this “rule” has some power even today, as there are almost 30 times as many people reporting that they are racially black with American Indian ancestry (weighted N=522,607) as there are people reporting American Indian race with black ancestry (weighted N=16,226).” Bryc et al (2015) show that, despite the expectations of the one drop rule “individuals identify roughly with the majority of their genetic ancestry.”
Most people in one sample that had less than 20 percent African ancestry identified as white. In the US, “Latinos” (a social-race) were estimated to have 65.1 percent European, 6.2 percent African, and 18.6 percent Native American DNA. Overall, 3.5 percent of European Americans had 1 percent or more African ancestry, while 1.4 percent of self-reported European Americans had were estimated to carry at least 2 percent African ancestry (Bryc et al, 2015).
Importantlty, Guo et al (2014) write:
The one-drop rule represents an important case in which social context trumps bio-ancestry. When asked to classify into a single race, most individuals with 30 % to 60 % African ancestry self-report as black; virtually all respondents with >60 % African ancestry self-classify as black. In contrast, a substantially higher proportion of European ancestry is “required” to self-classify or to be classified by an interviewer as white than the proportion of African ancestry necessary to self-classify or be classified as black. However, when given the option of identifying as multiracial, the majority of individuals with 40 % to 60 % African ancestry in both ROOM and Add Health and substantial proportions of individuals with >60 % African ancestry in ROOM stopped self-classifying as only black and primarily chose a multiracial classification.
“The infamous one-drop rule is peculiar to this country [America] but it is a feature of the American conception of race, not the minimalist concept of race.” (Hardimon, 2017: 56) The one-drop rule is a clear tell to how the socialrace concept acts. It is an essentialist concept, which means that it is necessarily racialist—since “one drop” of black blood makes one black—according to the rule.
The Maintenance of Races
It is possible that one society could take social measures to ensure the existence of their specific racial phenotype (that is, the existence of their minimalist race or subrace). Such a society would have to grapple with the moral and ethical underpinnings of such measures to ensure the maintenance of their phenotype (see Glannon, 2001’s book Genes and Future People for an extensive review of the moral, political, social, and ethical implications of human genetic engineering). This could also include genetic modification, though sound arguments exist that show that the way most people view genetic modification depends on a “strong view” of genetic determinism, which is false (Resnick and Vorhaus, 2006). However, it is possible that, through the will of the people in the society, that social isolation can lead to a de facto “physical” isolation through the social norms of the society in question.
However, since the races as they currently are are in no danger of non-existence, such measures, while they would (presumably) work, do not need to be taken. Such measures, though, do not need to be taken, since most people want to court with others who look like themselves, and those who are more likely to look like themselves are people of their own ethny, which is to say, people of their own populationist race. Thus, social measures to ensure the maintenance of races do not need to be taken.
As noted above, certain concepts from the days of the one drop rule are still in effect today, as a holdover from the days of Jim Crow and before. Some of these holdover concepts, though, help to maintain the races we know today. However, there is a possibility that our populationist races, too, have benefits socially constructed. Hardimon (2017: 126) writes (emphases his):
If populationist races exist, the role human action plays in their maintenance is rather more pronounced then the role it played in their genesis. Insofar as social norms and practices prohibiting or discouraging intermarriage have been the primary mechanisms preventing racial interbreeding since 1492, the maintenance of the separation has been intentional: this outcome is the very point of the discriminatory activity and practices in question. There is thus an especially strong sense in which, if populationist races exist, populationist race has been socially constructed since 1492.
Hardimon (2017: 126) goes on to say that the maintenance of populationist races “is not a natural process outside of human control”, nor is it “immutable or inalterable“, while “its existence is not an invariant, unchangeable,”natural” fact” and “The continued existence of populationist races, if it is a fact, is a fact within our power to change.” Thus, if populationist races exist (and they do), they exist by virtue of existing in nature.
So the races are not in danger of non-existence anytime soon, since the percentage of interracial unions are not too high compared to those who marry within their populationist races. The maintenance of populationist races comes down to—and will come down to, as long as humans are around—to social policies, whether enacted by state/country governments or the people themselves, sans any laws on miscegenation.
It has been said that we are attracted to people “who look like us“, “who look like our parents“, and “‘who are more similar to ourselves“. This means—NECESSARILY—that people are more likely to be attracted to people of their own race/ethnic group. People “who look like us” are co-ethnics and people of the same racial background; people who “look like our parents”, are, again, people who would share the same geographic ancestry. Since the physical features that delineate races are genetically transmitted from parent to offspring, then, people are more likely to be attracted to people of their same race. Finally, “people more similar to ourselves” doesn’t necessarily mean “people more racially/ethnically similar to ourselves”, since, of course, there are many other things that individuals have in common other than their race/ethnic group. However, it has been established that we are attracted more to people who share more similar genes than ourselves (Rushton,1997, 1998; Sebro et al, 2017). Thus, logically, since we are attracted to people who look like ourselves and our parents, we are attracted to people of our own ethnicity/race, as a matter of fact.
The question “How much admixture does it take for one race to no longer exist” is answered simply once the term “RACE” is defined: the amount of admixture it takes for one race to be “bred out” of existence is proportional to the amount of admixture it takes for one race’s physical features which correspond to geographic ancestry which are exhibited by the real group in question (this case being a subrace of a minimalist/populationist race). Europeans can’t take “much”, if any, other admixture, otherwise the traits that make Europeans European (which are, of course, not mutually exclusive to them, but the traits they—and their ethnies—exhibit are distinct) will disappear and so one of the Caucasian subraces will disappear as well. Social isolation, at the moment, is maintaining the races as we know them—and will far into the foreseeable future (there is no evidence that they will disappear anytime soon). “Violations” of the one drop rule abound, but they mean little to the minimalist/populationist concepts of race since the visible physical features which distinguish the races remain intact.
The fact that people are more attracted to people who look like themselves and their parents is an implicit way of saying that people are more attracted to people who are physically similar to themselves—that is, racially/ethnically similar to themselves—and shows that the races will not be going anywhere for the foreseeable future.
Human races will continue to exist as long as the social barriers that impede racial interbreeding remain. (Of course, if these social barriers did not exist, a majority of people still would court people who look like themselves and their families.) This is evidence that, contra social laws that impede or frown upon interracial marriages, we do not need such laws/rules because people stick to their own anyway. Therefore, the races are not in danger of disappearing anytime soon.
Everyone wants to know the keys to athletic success, however, as I have argued in the past, to understand elite athletic performance, we must understand how the system works in concert with everything—especially in the environments the biological system finds itself in. To reduce factors down to genes, or training, or X or Y does not make sense; to look at what makes an elite athlete, the method of reductionism, while it does allow us to identify certain differences between athletes, it does not allow us to appreciate the full-range of how and why elite athletes differ in their sport of choice. One large meta-analysis has been done on the effects of a few genotypes on elite athletic performance, and it shows us what we already know (blacks are more likely to have the genotype associated with power performance—so why are there no black Strongmen or any competitors in the World’s Strongest Man?). A few studies and one meta-analysis exist, attempting to get to the bottom of the genetics of elite athletic performance and, while it of course plays a factor, as I have argued in the past, we must take a systems view of the matter.
One 2013 study found that a functional polymorphism in the angiotensinogen (ATG) region was 2 to 3 times more common in elite power athletes than in (non-athlete) controls and elite endurance athletes (Zarebska et al, 2013). This sample tested was Polish, n = 223, 156 males, 67 females, and then they further broke down their athletic sample into tiers. They tested 100 power athletes (29 100-400 m runners; 22 powerlifters; 20 weightlifters; 14 throwers and 15 jumpers) and 123 endurance athletes (4 tri-athletes; 6 race walkers; 14 road cyclists; 6 15 to 50 m cross-country skiers; 12 marathon runners; 53 rowers; 17 3 to 10 km runners; and 11 800 to 1500 m swimmers).
Zarebska et al (2013) attempted to replicate previous associations found in other studies (Buxens et al, 2009) most notably the association with the M235T polymorphism in the AGT (angiotensinogen) gene. Zarebska et al’s (2013) main finding was that there was a higher representation of elite power athletes with the CC and C alleles of the M235T polymorphism compared with endurance athletes and controls, which suggests that the C allele of the M235T gene “may be associated with a predisposition to power-oriented
events” (Zarebska et al, 2013: 2901).
Elite power athletes were more likely to possess the CC genotype; 40 percent of power athletes had the genotype whereas 13 percent of endurance had it and 18 percent of non-athletes had it. So power athletes were more than three times as likely to have the CC genotype, compared to endurance athletes and twice as likely to have it compared to non-athletes. On the other hand, one copy of the C allele was found in 55 percent of the power athletes whereas, for the endurance athletes and non-athletes, the C allele was found in about 40 percent of individuals. (Further, in the elite anaerobic athlete, explosive power was consistently found to be a difference maker in predicting elite sporting performance; Lorenz et al, 2013.)
Now we come to the more interesting parts: ethnic differences in the M235T polymorphism. Zarebska et al (2013: 2901-2902) write:
The M235T allele distribution varies widely according to the subject’s ethnic origin: the T235 allele is by far the most frequent in Africans (;0.90) and in African-Americans (;0.80). It is also high in the Japanese population (0.65–0.75). The T235 (C4027) allele distribution of the control participants in our study was lower (0.40) but was similar to that reported among Spanish Caucasians (0.41), as were the sports specialties of both the power athletes (throwers, sprinters, and jumpers) and endurance athletes (marathon runners, 3- to 10-km runners, and road cyclists), thus mirroring the aforementioned studies.
Zarebska et al (2013: 2902) conclude that their study—along with the study they replicated—supports the hypothesis that the C allele of the M235T polymorphism in the AGT gene may confer a competitive advantage in power-oriented sports, which is partly mediated through ANGII production in the skeletal muscles. Mechanisms can explain the mediation of ANGII production in skeletal muscles, such as a direct skeletal muscle hypertrophic effect, along with the redistribution of between muscle blood flow between type I (slow twitch) and II fibers (fast twitch), which would then augment power and speed. However, it is interesting to note that Zarebska et al (2013) did not find any differences between “top-elite” level athletes who had won medals in international competitions compared to elite-level athletes who were not medalists.
The big deal about this gene is that the AGT gene is part of the renin-angiotensin system which is partly responsible for blood pressure and body salt regulation (Hall, 1991; Schweda, 2014). There seems to be an ethnic difference in this polymorphism, and, according to Zarebska et al (2013), African Americans and Africans are more likely to have the polymorphisms that are associated with elite power performance.
There is also a meta-analysis on genotyping and elite power athlete performance (Weyerstrab et al, 2017). Weyerstrab et al (2017) meta-analyzed 36 studies which attempted to find associations between genotype and athletic ability. One of the polymorphisms studied was the famous ACTN3. It has been noted that, when conditions are right (i.e., the right morphology), the combined effects of morphology along with the contractile properties of the individual muscle fibers contribute to the enhanced performance of those with the RR ACTN3 genotype (Broos et al, 2016), while Ma et al (2013) also lend credence to the idea that genetics influences sporting performance. This is, in fact, the most-replicated association in regard to elite sporting performance: we know the mechanism behind how muscle fibers contract; we know how the fibers contract and the morphology needed to maximize the effectiveness of said fast twitch fibers (type II fibers). (Blacks have a higher proportion of type II fibers [see Caeser and Henry, 2015 for a review].)
Weyerstrab et al (2017) meta-analyzed 35 articles, finding significant associations with genotype and elite power performance. They found that ten polymorphisms were significantly associated with power athlete states. Their most interesting findings, though, were on race. Weyerstrab et al (2017: 6) write:
Results of this meta-analysis show that US African American carriers of the ACE AG genotype (rs4363) were more than two times more likely to become a power athlete compared to carriers of the ACE preferential genotype for power athlete status (AA) in this population.
“Power athlete” does not necessarily have to mean “strength athlete” as in powerlifters or weightlifters (more on weightlifters below).
Lastly, the AGT M235T polymorphism, while associated with other power movements, was not associated with elite weightlifting performance (Ben-Zaken et al, 2018). As noted above, this polymorphism was observed in other power athletes, and since these movements are largely similar (short, explosive movements), one would rightly reason that this association should hold for weightlifters, too. However, this is not what we find.
Weightlifting, compared to other explosive, power sports, is different. The beginning of the lifts take explosive power, but during the ascent of the lift, the lifter moves the weight slower, which is due to biomechanics and a heavy load. Ben-Zaken et al (2018) studied 47 weightlifters (38 male, 9 female) and 86 controls. Every athlete that was studied competed in national and international meets on a regular basis. Thirty of the weightlifters were also classified as “elite”, which entails participating in and winning national and international competitions such as the Olympics and the European and World Championships).
Ben-Zaken et al (2018) did find that weightlifters had a higher prevalence of the AGT 235T polymorphism when compared to controls, though there was no difference in the prevalence of this polymorphism when elite and national-level competitors were compared, which “[suggests] that this polymorphism cannot determine or predict elite competitive weightlifting performance” (Ben-Zaken et al, 2018: 38). Of course, a favorable genetic profile is important for sporting success, though, despite the higher prevalence of AGT in weightlifters compared to controls, this could not explain the difference between national and elite-level competitors. Other polymorphisms could, of course, contribute to weightlifting success, variables “such as training experience, superior equipment and facilities, adequate nutrition, greater familial support, and motivational factors, are crucial for top-level sports development as well” (Ben-Zaken et al, 2018: 39).
I should also comment on Anatoly Karlin’s new article The (Physical) Strength of Nations. I don’t disagree with his main overall point; I only disagree that grip strength is a good measure of overall strength—even though it does follow the expected patterns. Racial differences in grip strength exist, as I have covered in the past. Furthermore, there are associations between muscle strength and longevity, with stronger men being more likely to live longer, fuller lives (Ruiz et al, 2008; Volkalis, Haille, and Meisinger, 2015; Garcia-Hermosa, et al, 2018) so, of course, strength training can only be seen as a net positive, especially in regard to living a longer and fuller life. Hand grip strength does have a high correlation with overall strength (Wind et al, 2010; Trosclair et al, 2011). While handgrip strength can tell you a whole lot about your overall health (Lee et al, 2016), of course, there is no better proxy than actually doing the lifts/exercises to ascertain one’s level of strength.
There are replicated genetic associations between explosive, powerful athletic performance, along with even the understanding of the causal mechanisms behind the polymorphisms and their carry-over to power sports. We know that if morphology is right and the individual has the RR ACTN3 genotype, that they will exceed in explosive sports. We know the causal pathways of ACTN3 and how it leads to differences in sprinting competitions. It should be worth noting that, while we do know a lot more about the genomics of sports than we did 20, even 10 years ago, current genetic testing has zero predictive power in regard to talent identification (Pitsladis et al, 2013).
So, of course, for parents and coaches who wonder about the athletic potential of their children and students, the best way to gauge whether or not they will excel in athletics is…to have them compete and compare them to other kids. Even if the genetics aspect of elite power performance is fully unlocked one day (which I doubt it will be), the best way to ascertain whether or not one will excel in a sport is to put them to the test and see what happens. We are in our infancy in understanding the genomics of sporting performance, but when we do understand which genotypes are more prevalent in regard to certain sports (and of course the interactions of the genotype with the environment and genes), then we can better understand how and why others are better in certain sports.
The genomics of elite sporting performance is very interesting; however, the answer that reductionists want to see will not appear: genes are difference makers (Sterelny and Griffith, 1999), not causes, and along with a whole slew of other environmental and mental factors (Lippi, Favaloro, and Guidi 2008), along with a favorable genetic profile with sufficient training (and everything else that comes along with it) are needed for the athlete to reach their maximum athletic potential (see Guth and Roth, 2013). Genetic and environmental differences between individuals and groups most definitely explain differences in elite sporting performance, though elucidating what causes what and the mechanisms that cause the studied trait in question will be tough.
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.
These studies, while they attempt to show us how genetic factors cause differences at the elite level in power sports, they will not tell the whole story, because we must look at the whole system, not reduce it down to the sum of its parts (Shenk, 2011: chapter 5). While blacks are more likely to have these polymorphisms that are associated with elite power athlete performance, this does not obviously carry over to strongman and powerlifting competition.