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Skin color is the first thing you see when you see someone. Skin color has many uses, and the color of one’s skin can give you a general idea of the type of climate one’s ancestors evolved in. The lighter one’s skin is may tell you that their ancestors evolved in low UVB radiation, whereas the darker one’s skin is may tell you that their ancestors evolved in high UVB places. So this tells us that as migration occurred out of Africa, skin needed to lighten in order to synthesize vitamin D in low UVB climes. Note that I won’t make any claims about any skin color being an adaptation to any climate; I will just state that there is a strong association between UVB and skin color—the higher the UVB the darker the skin and the lower the UVB the lighter the skin.
The skin comprises about 16 percent of the human body, making it the body’s largest organ (D’Orazio et al, 2013). There are two layers to the skin, the dermis and epidermis. The outermost layer of skin—the epidermis—is the point of contact with the environment. So since this is the case, then the number of UVB rays in any given environment will dictate the color of one’s skin—in an ancestral manner.
So the most important factor in skin color is melanin, which is produced by melanocytes, but it accumulates in the keratinocytes of the stratum basale (the deepest layer of the five layers of the epidermis) and the stratum spinosum (the layer between the stratum granulosum and the stratum basale). Two forms of melanin exist: eumelanin (which is brownish black) and pheomelanin (which is reddish-yellow and contains sulfur).
In his textbook Anatomy and Physiology: The Unity of Form and Function, professor Ken Saladin writes:
People of different skin colors have essentially the same number of melanocytes, but in dark-skinned people, the melanocytes produce greater quantities of melanin, the melanin granules in the keratanocytes are more spread out than tightly clumped, and the melanin breaks down more slowly. Thus, melanized cells may be seen throughout the epidermis, from stratum basale to stratum corneum. In light-skinned people, the melanin is clumped near the keratinocyte nucleus, so it imparts less color to the cells. It also breaks down more rapidly, so little of it is seen beyond the stratum basale, if even there.
The amount of melanin in the skin also varies with exposure to ultraviolet (UV) rays of sunlight, which stimulates melanin synthesis and darken the skin. A sun-tan fades as melanin is degraded in older keratinocytes and as the keratinocytes migrate to the surface and exfoliate. (Saladin, 2010: 194)
Skin color is one of the most significant factors involved in colonizing a certain, new, area where the skin color the group has is not conducive to life in that clime. So, when the out of Africa migration occurred, skin color needed to lighten as to better confer survival in the new, colder climes. Though, there is an anomaly: Arctic peoples. Why is their skin dark—at least relative to other peoples who live or have lived in colder climates?
Think about life in the Arctic. It is pretty much all white. Food is scarce, and they eat a lot of animal fat and protein. Now, think about the ice. The ice reflects UV rays onto the skin of the Arctic people, making it not as light as, say, Europeans and East Asians.
A term I’ve heard a lot over the years is “Black don’t crack”, speaking to the fact that a lot of black people look young, even into old age. What, if any, is the physiologic reason behind this? For instance, Vashi, Maymone, and Kundu (2016) write:
Individuals with darker skin are overall thought to have firmer and smoother skin than individuals with lighter skin of the same age
Rawlings (2006) states that “Caucasians have an earlier onset and greater skin wrinkling and sagging signs than other skin types and in general increased pigmentary problems are seen in skin of colour although one large study reported that East Asians living in the U.S.A. had the least pigment spots.” Blacks have more corneosome layers than whites (21.8 cell layers compared to 16.7 cell layers). There is no difference in skin thickness between whites and blacks, so black skin is thought to be more compact with greater intercellular cohesion (see also La Ruche and Cesarini, 1992). Take transepidermal water loss (TEWL)—the total amount of water vapor lost through the skin and other appendages through non-sweating conditions. Since the Asian corneum is thinner, it takes fewer tape strippings to decrease TEWL compared to blacks who take more tape strippings, while whites are in the middle. (Though some studies note no difference).
So why does it seem that blacks, on average, age less than whites in the fact? I can think of one main thing: Their darker skin protects them from the effects of photoaging due to the melanocytes their skin produces. The opposite holds for whites—white skin produces fewer melanocytes and therefore is less protected against UV rays from the sun. Therefore lighter ethnic groups are more likely to have damaged skin compared to darker ethnic groups, and the main driver of this is the number of melanocytes produced by the skin. Rawlings (2006: 87) even writes that “Overall I would expect less signs of aging, i.e. maintenance of skin elasticity in darker skinned individuals [Negroids are reported to have an intrinsic sun protection factor (SPF) value of approximately 13].”
Rawlings also writes (pg 89):
In African Americans photoaging appears primarily in lighter complexioned individuals and usually does not appear until the late fifth or sixth decade of life.
There is another factor when it comes to skin: sweat glans. I have covered in the past the fact that Asians have fewer apocrine sweat glands than whites and blacks, while blacks produce more chloride in their sweat compared to whites. Prokop-Prigge et al (2017) state “that an individual’s ethnicity has a significant impact on human axillary odor production.” Blacks also have around 70 percent more lipids in their hair, while having larger sebaceous glands than whites.
So skin color dictates numerous changes in the skin which are associated with aging. Skin aging is associated with lighter-skin, whereas hyperpigmentation is associated with darker skin. Asians have lower TEWL, highest water content, and highest skin color lipid levels while the opposite is seen for blacks. Blacks have greater gland pore size, and increased apocrine and apoeccrine sweat glands along with greater sebum excretion. White skin has an earlier onset of aging, skin wrinkling and loss of elasticity. So there are differences in ethnic skin color and structure and function, and this causes the differences we notice between ethnies and how they age.
Campiche et al (2019) write:
There is differential manifestation of aging signs in different ethnic groups.
Our results show that Africans from the African continent show delayed signs of aging compared to Caucasians.
They found no differences in forehead wrinkles between Caucasians and Africans, though there was a difference in depth of forehead wrinkles. Blacks showed less advanced crow’s feet than whites, while also having less depth. There were no differences in mouth frown lines with the exception of depth and wrinkle surface and volume parameter, of which there was an increase in Caucasian subjects compared to African subjects. Though when it comes to the length, surface and vertical lines in African subjects they showed more advanced aging but there was no difference in depth between the races. Caucasians had bigger nasiolabial folds (smile or laugh lines) than Africans, regarding length, surface, depth and volume. Africans had deeper pores than Caucasians. Africans had a greater homogeneity than Caucasians when it came to skin color. (Note that the cohorts came from France and Mauritius.)
Campiche et al (2019: 12) write:
This is also in line with the fact that photoaging in African Americans does not appear until the late fifth or sixth decade of life.22 This may explain why aging in our Black African cohort from Mauritius is less pronounced than in the Caucasian cohort although the Black African cohort is older.
The difference in age between our Caucasian and Black African cohorts (median age 46 years vs 56 years) could bring into question the comparisons of the two cohorts. Nevertheless, we mostly found that Caucasians displayed more severe signs of aging than Black Africans which is in line with the common understanding that the onset of aging in fair skin starts earlier than in darkly pigmented skin and that there were differences in the appearance of lip lines and facial pores.
So differences between the two ethnic groups come down to facial site, and measurement parameter. This study further buttresses the point that, at least when it comes to certain ethnic groups, whites age faster than blacks—even when the whites are younger than blacks (46 compared to 56 years, respectively).
When it comes to skin color and desirability, though, we see something else: light skin being prized, whereas dark skin is shunned. Jablonski (2010: 188) writes:
As we have seen, for much of recent history and around the world, pale skin has been prized to such a degree that people have been willing to risk illness and disfugurement to obtain it.
[and also on pg 177]
Preferences for light skin have arisen independently in many cultures, and they have been reinforced when different “cultures of lightness” have come into contact. Because having lighter skin has often been associated with higher social status, success, and happiness, people over the ages have sought to become lighter by various means.
I won’t ruminate on the causes of this, I just wanted to make a note of it at the end of this piece on black and white skin color.
In sum, there are many interesting differences between black and white—and even Asian—skin. Better understanding of these kinds of differences will lead to better skin care for all races, and dermatologists can then use that information to give better case based on race/ethnicity/skin color to a certain individual. We know what causes differences in skin color between individuals and groups—melanocytes. We also know that skin color and UVB radiation are strongly related. We know that there are numerous differences in skin biology when comparing different peoples whose ancestors have evolved in different climates. So understanding these differences can and will lead to better healthcare for all populations.
Usain Bolt, Michael Phelps, and Caster Semenya: Should Semenya Take Drugs to Decrease Testosterone Levels?
In the past week in the world of sport, all the rage has been over mid- to long-distance runner Caster Semenya. Semenya has won the 800 m in 1:56.72 and setting world records in the 400, 800, and 1500 m with times of 50.74, 1:58.45 and 4:10.93 respectively. In 2012 and 2016, Semenya won the gold for the 800 m with times of 1:57.23 and 1:55.28 respectively. I won’t really discuss the anatomic and physiologic advantages today. What I will discuss, though, is the fact that Semenya has been told that she has to take drugs to decrease her testosterone levels or she cannot compete anymore. Semenya was told to decrease her testosterone levels or she could face a ban in the 800 m. The new rules state that:
Female athletes affected must take medication for six months before they can compete, and then maintain a lower testosterone level.
If a female athlete does not want to take medication, then they can compete in:
- International competitions in any discipline other than track events between 400m and a mile
- Any competition that is not an international competition
- The male classification at any competition, at any level, in any discipline
- Any intersex, or similar, classification
But Semenya has declined taking these drugs—so her future is up in the air. So, if Semenya—or any other athlete—has to take drugs to decrease their levels since it gives an unfair advantage, then, in my opinion, this may lead to changes in other sports as well.
Look at Michael Phelps. Michael Phelps has won a record 28, winning 23 medals at Rio in 2016. Phelps has a long, thin torso which decreases drag in the water. Phelps’ wing span is 6’7” while he is 6’4”—which is disproportionate to his height. He has the torso of a 6’8” person, which gives him a greater reach per stroke. His lower body is 5’10” which lowers the resistance against the water. He has large hands and feet (with flexible ankles), which help with paddling capacity (size 14 shoe; yours truly wears a size 13).
There is one more incredible thing about Phelps: He produces around 50 percent lower lactic acid. Think of the last time that you have run for some distance. The burning you feel in your legs is a build up of lactic acid. Lactic acid causes fatigue and also slows muscle contractions—this occurs through lactic acid passing through the bloodstream, becoming lactate. (Note that it does not necessarily cause fatigue; Brooks, 2001.) Phelps does not produce normal levels of lactic acid, and so he is ready to go again shortly after a bout of swimming.
Phelps said “In between the 200m free and the fly heats I have probably had in total about 10 minutes to myself.” A normal person’s muscles would be too fatigued and cramped. I would also assume that Phelps has an abundance of type I muscle fibers as well.
Now take Usain Bolt. The 100 m dash is, mostly, an anaerobic race. What this means is that mitochondrial respiration has minimal effect on the type of energy used during the event (Majumdar and Robergs, 2011). So during anaerobic events, there is no free oxygen to drive energy—the energy stored in the muscle is used to perform movement through a process called glycolysis. Sprinting is an intense exercise—fuel choice during exercise is determined by the intensity of said exercise. “A 100-meter sprint is powered by stored ATP, creatine phosphate, and anaerobic glycolysis of muscle glycogen.”
Now we can look at the physical advantages they have. Swimmers and runners, on average, have different centers of mass (Bejan, Jones, and Charles, 2010). In all actuality, Phelps and Bolt are the perfect example of this phenomenon. Winning runners have a West-African origin and winning runners are more likely to be white. These somatotypic differences between the two races influence why they excel in these two different sports.
Usain Bolt is 6’5”. Since he is that height, and he has long legs, he necessarily has a longer stride—Bolt is the perfect example of Bejan, Jones, and Charles’ (2010) paper. So take the average white sprinter of the same height as Bolt. Ceteris paribus, Bolt will have a higher center of mass than the white athlete due to his longer limbs and and smaller circumference. Krogman (1970) found that, in black and white youths of the same height, blacks had shorter trunks and longer limbs, which lends credence to the hypothesis.
Phelps is 6’4”. As noted above, he has a long torso and long limbs. Long torsos are conducive to a lower center of mass—what whites and Asians have, on average. So long torsos mean that one will have taller sitting heights than those with short torsos. This means that whites and Asians have taller sitting heights than blacks, who have shorter torsos. This average taller sitting height is conducive to the longer torsos which is why whites excel in swimming. Bejan, Jones, and Charles (2010) also note that, if it were not for the short stature of Asians, they would be better swimmers than whites.
In any case, the different centers of mass on average between blacks and whites are conducive to faster times in the sports they excel at. For whites, the three percent increase in center of mass means that there would be a 1.5 percent increase in winning speed and a 1.5 percent decrease in winning time in the case of swimming. The same holds for blacks, but in the case of running: their higher center of mass is conducive to a 1.5 percent increase in winning speed and also a 1.5 percent decrease in winning time, which would be a .15 second decrease, or from 10 s to 9.85 s—which is a large differential when it comes to sprinting. (Note that this phenomenon also holds for black women and white women—black women are better sprinters and white women are better swimmers. Asian women excel in the 100 m freestyle, but not Asian men for reasons discussed above.)
Now put this all together. If Phelps and Bolt have such advantages over their competition and they—supposedly—win due to them, then if Semenya has to decrease her T levels, why shouldn’t Phelps and Bolt decrease X, Y, or Z since they have physiologic/anatomic advantages as well? Why does no one talk about Semenya’s anatomic advantages over, say, white women and why only bring up Semenya’s testosterone levels? Forcing Semenya to decrease T levels will set a bad precedent in sport. What would stop a losing competitor from complaining that the winner—who keeps winning—has an “unfair” physiologic/anatomic advantage and must do X to change it? (Or say that the anatomic advantage they possess is “unfair” and they should be barred from competition?)
Here’s the thing: Watching sport, we want to see the best-of-the-best compete. Wouldn’t that logically imply that we want to see Semenya compete and not rid herself of her advantage? If Semenya’s physiologic advantage(s) is being discussed, why not Semenya’s anatomic advantages? It does not make sense to focus on one variable—as all variables interact to produce the athletic phenotype (Louis, 2004). Phelps and Bolt perfectly embody the results of Bejan, Jones, and Charles (2010)—they have, what I hope are—well-known advantages, and these advantages, on average, are stratified between race due to anatomic differences (see Gerace et al, 1994; Wagner and Heyward, 2000).
Phelps and Bolt have anatomic and physiologic advantages over their competition, just as Semenya does, just like any elite athlete, especially the winners compared to their competition. If Semenya is forced to decrease her testosterone levels, then this will set a horrible precedent for sport, and people may then clamor for Phelps and Bolt to do X, Y, and Z due to their physical advantages. For this reason, Semenya should not decrease her testosterone levels and should be allowed to compete in mid-distance running.
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.
Race and medicine is a tendentious topic. On one hand, you have people like sociologist Dorothy Roberts (2012) who argues against the use of race in a medical context, whereas philosopher of race Michael Hardimon thinks that we should not be exclusionists about race when it comes to medicine. If there are biological races, and there are salient genetic differences between them, then why should we disregard this when it comes to a medically relevant context? Surely Roberts would agree that we use her socio-political concept of race when it comes to medicine, but not treat them like biological races. Roberts is an anti-realist about biological races, whereas Hardimon is not—he recognizes that there is a minimalist and social aspect to race which are separate concepts.
In his book Rethinking Race: The Case for Deflationary Realism, Hardimon (2017, Chapter 8) discusses race and medicine after discussing and defending his different race concepts. If race is real—whether socially, biologically, or both—then why should we ignore it when it comes to medical contexts? It seems to me that many people would be hurt by such a denial of reality, and that’s what most people want to prevent, and which is the main reason why they deny that races exist, so it seems counterintuitive to me.
Hardimon (2017: 161-162; emphasis his) writes:
If, as seems to be the case, the study of medically relevant genetic variants among races is a legitamate project, then exclusionism about biological race in medical research—the view that there is no place for a biological concept of race in medical research—is false. There is a place for a biological concept of race in the study of medically relevant genetic variants among races. Inclusionism about biological race in medical research is true.
So, we should not be exclusionists (like Roberts), we should be inclusionists (like Hardimon). Sure, some critics would argue that we should be looking at the individual and not their racial or ethnic group. But consider this: Imagine that an individual has something wrong and standard tests do not find out what it is. The doctor then decides that the patient has X disease. They then treat X disease, and then find out that they have Y disease that a certain ethnic group is more likely to have. In this case, accepting the reality of biological races and its usefulness in medical research would have caught this disease earlier and the patient would have gotten the help they needed much, much sooner.
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.
We should, of course, use the concepts of socialrace when discussing the medical effects of racism (i.e., psychosocial stress) and the minimalist/populationist race concepts when discussing the medically relevant race-related genetic diseases. Being eliminativist about race doesn’t make sense—since if we deny that race exists at all and do not use the term at all anymore, there would be higher mortality for these “populations.” Thus, we should use both of Hardimon’s terms in regard to medicine and racial differences in health outcomes as both concepts can and will show us how and why diseases are more likely to appear in certain racial groups; we should not be eliminativists/exclusionists about race, we should be inclusionists.
Hardimon discusses how racism can manifest itself as health differences, and how this can have epigenetic effects. He writes (pg 155-156):
As philosopher Shannon Sullivan explains, another way in which racism may be shown to influence health is by causing epigenetic changes in the genotype. It is known that changes in gene expression can have durable and even transgenerational effects on health, passing from parents to their children and their children’s children. This suggests that the biological dimensions of racism can replicate themselves across more than one generation through epigenetic mechanisms. Epigenetics, the scientific study of such changes, explains how the process of transgenerational biological replication of ill health can occur without changes in the underlying DNA sequence.
If such changes to the DNA sequences can be transmitted to the next generation in the developmental system, then that means that the social can—and does—has an effect on our biology and that it can be passed down through subsequent generations. It is simple to explain why this makes sense: for if the developing organism was not plastic, and genes could not change based on what occurs in the environment for the fetus or the organism itself, then how could organisms survive when the environment changes if the “genetic code” of the genome were fixed and not malleable? For example, Jasienska (2009) argues that:
… the low birth weight of contemporary African Americans not only results from the difference in present exposure to lifestyle factors known to affect fetal development but also from conditions experienced during the period of slavery. Slaves had poor nutritional status during all stages of life because of the inadequate dietary intake accompanied by high energetic costs of physical work and infectious diseases. The concept of ‘‘fetal programming’’ suggests that physiology and metabolism including growth and fat accumulation of the developing fetus, and, thus its birth weight, depend on intergenerational signal of environmental quality passed through generations of matrilinear ancestors.
If the environmental quality—i.e., current environmental quality—is “known” by the developing fetus through cues from the mother’s nutrition, stress etc, then a smaller body size may be adaptive in that certain environment and the organism may survive with fewer resources due to smaller body size. In any case, I will discuss this in the future but it was just an example of a possible epigenetic modification on current slaves. I, personally, have noticed that a lot of blacks are really skinny and have really low body fat—who knows, maybe this could be part of the reason why?
This is something that sociologist Maurizio Meloni (2018) calls “the postgenomic body”—the fact that biology is malleable through what occurs in our social lives. So not only is the human brain plastic, but so is the epigenome and microbiome, which is affected by diet and lifestyle—along with what we do and what occurs to us in our social lives. So our social lives, in effect, can become embodied in our epigenome and passed down to subsequent generations. Similar points are also argued by Ulijaszek, Mann, and Elton (2012). (Also see my article Nutrition, Development, Epigenetics, and Physical Plasticity.)So in effect, environments are inherited too, and so, therefore, the environments that we find ourselves in are, in effect, passed down through the generations. Meloni (2018) writes:
On the other hand, by re-embedding the individual within a wider lineage of ancestral experiences and reconfiguring it as a holobiontic assemblage, it may literally dissolve the subject of emancipation. Moreover, the power of biological heredity may be so expanded (as it includes potentially any single ancestral experience) to become stronger than in any previous genetic view. Finally, the several iterations of plasticity that emerge from this genealogy appear so deeply racialized and gendered that it is difficult to quickly turn them into an inherently emancipatory concept. Even as a concept, plasticity has an inertial weight and viscosity that is the task of the genealogist to excavate and bring into view.
Thus, current biological states can be “tagged” and therefore be epigenetically transmitted to future generations. Think about it in this way: if epigenetic tags can be transmitted to the next generation then it would be presumed that that environment—or a similar one—would be what newer generations would be born in. Thus, the plasticity of the organism would help it in life, especially the immediate plasticity of the organism in the womb. Likewise, Kuzawa and Sweet (2008) argue:
that environmentally responsive phenotypic plasticity, in combination with the better-studied acute and chronic effects of social-environmental exposures, provides a more parsimonious explanation than genetics for the persistence of CVD disparities between members of socially imposed racial categories.
Of course, if we look at race as both a biological and social category (i.e., Spencer, 2014), then this is not surprising that differences in disease acquisition can persist “between members of socially imposed racial categories.” Phenotypic plasticity is the big thing here, as noted by many authors who write about epigenetics. If the organism is plastic (if it can be malleable and change depending on external environmental cues), then disease states can—theoretically—be epigenetically passed to future generations. This is just like Jasienska’s (2009, 2013, Chapter 5) argument that the organism—in this case, the fetus—can respond to the environmental quality that it is developing in and, therefore, differences in anatomy and physiology can and do occur based on the plasticity of the organism.
Lastly, Jan Badke, author of Above the Gene, Beyond Biology: Toward a Philosophy of Epigenetics (Baedke, 2018), argues that, since the gene-centered view of biology has been upended (i.e., Jablonka and Lamb, 2005; Noble, 2006, 2011, 2012, 2017) for a postgenomic view (Richardson and Stevens, 2015). Genes are not closed off from the environment; all organisms, including humans, are open systems and so, there are relationships between the environment, developmental system, and the genome which affect the developing organism. Baedke and Delgado (2019) argue that the “colonial shadow … biologicizes as well as racializes social-cultural differences among human groups.” Since every race faces specific life challenges in its environment, therefore, each race shows a “unique social status that is closely linked to its biological status.” Thus, differing environments, such as access to different foods (i.e., the effects of obesifying foods) and discrimination can and are passed down epigenetically. Baedke and Delgado (2019: 9) argue that:
… both racial frameworks nutrition plays a crucial role. It is a key pathway over which sociocultural and environmental difference are embodied as racial difference. Thus, belonging to a particular race means having a particular biosocial status, since races include two poles – a social status (e.g., class, socio-economic status) and a biological status (disease susceptibility) – which are closely interlinked. Against this background, human populations in Mexico become an exemplar of types of bodies that are not only relocated to a destabilizing modernized world in which they suffer from socio-economic deprivation. What is more, they become paradigmatic primitive bodies that are unbalanced, biologically deprived, and sick. In short, in these recent epigenetic studies poor places and lifestyles determine poor bodies, and vice versa.
In sum, accepting the reality of race—both in a minimalist/populationist biological manner and social manner—can and will help us better understand disease acquisition and differing levels of certain diseases between races. Recognizing the minimalist/populationist concepts of race will allow us to discover genetic differences between races that contribute to variation in different diseases—since genes do not alone outright cause diseases (Kampourakis, 2017: 19). Being eliminativist/exclusionist about race does not make sense, and it would cause much more harm than good when it comes to racial disease acquisition and mortality rates.
Furthermore, acknowledging the fact that the social dimensions of race can help us understand how racism manifests itself in biology (for a good intro to this see Sullivan’s (2015) book The Physiology of Racist and Sexist Oppression, for even if the “oppression” is imagined, it can still have very real biological effects that could be passed onto the next generation—and it could particularly affect a developing fetus, too). It seems that there is a good argument that the effects of slavery could have been passed down through the generations manifesting itself in smaller bodies; these effects also could have possibly manifested itself in regard to obesity in Latin America post-colonialism. Gravlee (2009) and Kaplan (2010) also argue that the social, too, manifests itself in biology.
(For further information on how the social can and does become biological see Meloni’s (2019) book Impressionable Biologies: From the Archaeology of Plasticity to the Sociology of Epigenetics, along with Meloni (2014)‘s paper How biology became social, and what it means for social theory. Reading Baedke’s and Meloni’s arguments on plasticity and epigenetics should be required before discussing these concepts.)
I’m watching Mystery Diagnosis right now, and I heard the narrator say that lupus is three times more common in African Americans than Caucasian Americans. (The woman was black.) So let’s look into it.
Lupus is a long-term autoimmune disease where the body’s immune system becomes hyperactive and attacks healthy tissue. It can damage any part of the body, skin cells, joints, organs. Many symptoms of lupus exist, like kidney inflammation, swelling, and damage to the blood, heart, joints, and lungs. No cure exists for lupus, though there are ways to minimize inflammation through diet and lifestyle.
Lupus is two to three times more likely to occur in women of color—blacks, Hispanics/Latinos, Native Americans, and others—compared to white Americans. Somers et al (2014) state that lupus affects 1 in 537 black women, “with black patients experiencing earlier age at diagnosis, >2-fold increases in SLE incidence and prevalence, and increased proportions of renal disease and progression to ESRD as compared to white patients.” However, Somers et al (2016) note that medical records may be poor or missing while the reliability of diagnosis is low for non-whites and non-blacks. They also note that race and ethny data in the US is based on self-ID for the parents and child on the birth certificate, but self-ID has almost a perfect relationship with geographic ancestry (i.e., race) (Tang et al, 2005).
Guillermo et al (2017: 7) write that:
Ethnicity is a biological and social construct, including not only genetic ancestry, but also cultural characteristics (language, religion, values, social behaviors, country of origin) yet it is an arbitrary definition . Race is oftentimes used interchangeable with ethnicity but it mainly refers to the biological features of groups of people. Given that there are differences in the clinical characteristics and prognosis among different populations, it is worth evaluating the impact of race/ethnicity in SLE. Genetic ancestry influences the risk for the incidence of SLE; for example, Amerindian ancestry is associated with an increased number of risk alleles for SLE , and also with an early age at onset , Amerindian and African ancestry are associated with a higher risk for kidney involvement [122,123] and European ancestry with a lower risk .
First, let’s look at ref , which is McKenzie and Crowcroft (1994), who Guillermo et al (2017) cite as saying that ethnicity is “an arbitrary definition.” They note that some researchers use Blumenbach’s terms (see Spencer, 2014). They claim that modern definitions class Asians as Caucasian or black … what? They state that modern definitions classify Asians as black because “all disadvantaged groups [are] “black populations,”
[since] the experience of racism is paramount.” This is ridiculous on so many levels.
In any case, Southern Europeans are more likely to have a higher risk of renal involvement, and antibody production but along with that a lower risk of discoid rash whereas Western Europeans while Ashkenazi Jews “seem to be protected from neurologic manifestations” (see Richman et al, 2009). Asians and Native Americans in Canada are less likely to have manifestations than Africans; a type of lupus known as cutaneous vasculitis is more common in Native Americans from Canada, while Asians from Canada had a lower rate of serotisis and arthritis compared to Caucasians, Native Americans and African descendants (Peschken et al, 2015). However, Peschken et al (2015) note that while ethnicity was not that strong a predictor of damage accrual, low income was.
Kidney involvement is a major factor in the development of lupus (Bagamant and Fu, 2009), while it is more frequent in “Hispanics”, African-descendants, and Asians. Further, “Hispanics” and blacks are more likely to have end-stage renal failure than whites (Ricardo et al, 2015). When it comes to lupus nephritis—inflammation of the kidneys caused by lupus—“Hispanics” also have a better response to mycophenolate mofetil, which is an immunosuppressive drug that prevents organ rejection (Appel et al, 2009). After the onset of the disease, the disease declines slowly in “Hispanics”, then Africans, and finally fastest in whites. There also seems to be an SES factor in the aetiology of the disease. Sule and Petri (2005) write that “Socioeconomic status can have a major impact on SLE disease manifestations and mortality, independent of ethnicity“, while saying that association with SES is all over the place, with there being no relationship with SES and lupus acquisition.
Vila et al (2003) studied “Hispanics” from Texas and Puerto Rico. They noted that those from Texas accrued more damage than those from Puerto Rico. This is not surprising. “Hispanics” are not a homogenous group (they are a socialrace with no minimalist correlate, they have differing admixture from all over; “Hispanics” can be of any race. Vila et al (2007: 362) note that:
This diversity appears to be areflection of the great variability that exists between these populations with regards to their genetic, environmental and sociodemographic backgrounds.
“Hispanics” from the southeast part of America are different ethnically than those from the southeast.
Blacks and “Hispanics” have a higher rate of mortality than whites, but these differences disappear once SES is accounted for (Ward, Pyun, and Studenski, 1995; Kasitanon, Magder, and Petri, 2006; Fernandez et al, 2007). There could be some genetic differences between races/ethnies that contribute to disease differences between them. But as Kampourakis (2017: 19) notes in his book Making Sense of Genes:
… genes do not alone produce characters or disease but contribute to their variation. This means that genes can account for variation in characters but cannot alone explain their origin.
In sum, there is a wide range of differences between races and ethnies when it comes to lupus. Is the main cause environmental or genetic? Neither, as genes and environment interact to form disease (and any other) phenotypes. So if one at-risk minority group has a low SES, that may be a risk factor. The fact that there are ethnic differences in response to autoimmune drugs when it comes to certain forms of lupus is interesting. The wide range of ethnic differences in the acquisition of the disease is interesting, with Ashkenazi Jews seemingly protected from the disease. In any case, there are racial/ethnic differences in the acquisition of this disease and to better treat those with this disease—and any other—we need to be realists about race, whether it’s biological or social, since there are very real disease and mortality outcomes between them.
JP Rushton’s career was pretty much nothing but peddling bullshit. In the beginning of his career, he was a social learning theorist. He published a book Altruism, Socialization, and Society (Rushton, 1980). I bought the book a few years back when I was still a hardcore Rushton defender to see what he wrote about before he started pushing IQ and evolutionary theories about human races and I thought it was pretty good. In any case, Rushton got a lot wrong. So much so, that his career was, in my opinion, wasted peddling bullshit. Rushton was shown to be wrong time and time again on r/K theory and cold winter theory; Rushton was shown to be wrong time and time again on his crime theorizing; and Rushton’s and Jensen’s papers on the causes of the black-white IQ gap rest on a misunderstanding of heritability. In this piece, I will cover those three subjects.
Recently, two new papers have appeared that have a bone to pick with Rushton: One by Flynn (2019) and the other by Cernovsky and Litman (2019). Flynn discusses Rushton’s claims on the method of correlated vectors, his cold winter theory (that Asians and Europeans were subjected to harsher climates which led to higher levels of intelligence and therefore IQ) and his misuse of regression to the mean. He also discussed how the black-white IQ gap is environmental in nature (which is the logical position to hold, since IQ tests are tests of middle-class knowledge and skills (Richardson, 2002) and they are not construct valid).
Cold Winters Theory
Rushton theorized that, due to exposure to harsher environments, that Europeans and East Asians evolved to be more intelligent than Africans who stayed in the, what I assume to be, less harsh environments of Africa (Rushton, 1985). This is Rushton’s “Differential K theory.” Flynn (2019) writes that he “can supply an evolutionary scenario for almost any pattern of current IQ scores.” And of course, one can do that with any evolutionary adaptive hypothesis.
Even Frost (2019) admits that “there is no unified evolutionary theory of human intelligence, other than the general theory of evolution by natural selection.” But since “natural selection” is not a mechanism (Fodor, 2008; Fodor and Piattelli-Palmarini, 2010), then it cannot explain the evolution of intelligence differences, nevermind the fact that, mostly, these claims are pushed by differences in non-construct valid IQ test scores.
In any case, Rushton’s theory is a just-so story.
Judith Anderson (1991) refuted Rushton’s hypothesis on ecological grounds. Rushton asserted that Africans were r-selected whereas Asians and Europeans were more K-selected. Rushton, however, did not even use alpha-selection, which is selection for competitive ability. So r- and K selection is based on density-independence and density-dependence. K-selection is expected to favor genotypes that persist at high densities—increasing K—whereas r-selection is expected to favor genotypes that increase more quickly at low densities—increasing r. Alpha-selection can also occur at high or low population densities but is more likely in high densities. Though alpha-selection “favours genotypes that, owing to their negative effects on others, often reduce the growth rate and the maximum population size” (Anderson, 1991: 52). I further discussed the huge flaws with Rushton’s r/K model here. So Rushton’s theory fails on those grounds, along with many others.
When it came to race, Rushton was a lumper, not a splitter. What I mean by these terms is simple: lumpers lump together Native Americans with East Asians and Pacific Islanders with Africans while splitters split them into further divisions. Why was Rushton a lumper? Because it fit more with his theory, of course. I remember back when I was a Rushton-ist, and I was, too, a lumper, that to explain away the low IQs of Native Americans—and in turn their achievements—was that they still had their intelligence from the cold winters and that’s when they did their achievements. Then, as they spent more time in hotter climates, they became dumber. In any case, there is no justification for lumping Native Americans with East Asians. Looking through Rushton’s book, he gives no justification for his lumping, so I can only assume that it is bias on his part. Now I will justify the claim that splitting is better than lumping. (Rushton also gave no definition of race, and according to Cernovsky and Litman (2019: 54), Rushton “failed to provide any scientific definition of race …”
Race is both a social and biological construct. I can justify the claim that Natives and East Asians are distinct races in one way here: ask both groups if the other is the same race. What do you think the answer will be? Now, onto genetics.
Spencer (2014) discusses the results from Tishkoff et al (2009), saying that when they added 134 ethnic groups to the ones found in the HDGP sample of 52, the K=5 partition clustered Caucasians, Mongoloids, and three distinct sets of Africans. Mongoloids, in this case, being East Asians, Native Americans, and Oceanians. But Tishkoff et al oversampled African ethnic groups. This, though, does not undercut my argument: of course when you oversample ethnic groups you will get the result of Tishkoff et al (2009) and since Africans were oversampled, the populations more genetically similar were grouped into the same cluster, which, of course, does not mean they are the same race.
Census racial discourse is just national racial discourse. The census uses defers to the OMB to define race. How does the OMB define race? The OMB defines “race” as “sets of” populations. Race in US racial discourse designates a set of population groups, thus, race is a particular, not a kind.
I can then invoke Hardimon’s (2017) argument for the existence of minimalist races:
1 There are differences in patterns of visible physical features which correspond to geographic ancestry.
2 These patterns are exhibited between real groups.
3 These groups that exhibit these physical patterns by geographic ancestry satisfy conditions of minimalist race.
C Race exists.
Now we can say:
1 If Native Americans and East Asians are phenotypically distinct, then they are different races.
2 Native Americans and East Asians are phenotypically distinct.
C Therefore Native Americans and East Asians are different races.
Rushton arbitrarily excluded data that did not fit his theory. How dishonest. Cernovsky and Litman (2019) write:
When Rushton presented crime statistics derived from 2 Interpol Yearbooks as allegedly supporting his thesis that Negroids are more crime inclined than Caucasoids, he arbitrarily excluded disconfirmatory data sets. When all data from the same two Interpol Yearbooks are re-calculated, most of the statistically significant trends in the data are in the direction opposite to Rushton’s beliefs: Negroids had lower crime rates than Caucasoids with respect to sexual offenses, rapes, theft, and violent theft or robbery, with most correlation coefficients exceeding .60. While we do not place much credence in such Interpol statistics as they only reproduce information provided by government officials of different countries, our re-analysis indicated that Rushton excluded data that would discredit his theory.
Further throwing a wrench into Rushton’s assertions is his claim that Mongoloids constitutes both East Asians and Native Americans. Well, Central America has some of the highest crime rates in the world—even higher than in some African countries. What is the ad-hoc justification for explaining away this anomaly if they truly are the same race? If they are the same race, why is the crime rate so much higher in Central America? Surely, Rushton’s defenders would claim something along the lines of recent evolution towards X, Y, and Z. But then I would say, then on what basis are they the same race? No matter what Rushton’s defenders say, they are boxed into a corner.
Lastly, Rushton and Jensen (2005) argued, on the basis of heritability estimates, and twin studies, that the black-white IQ gap is largely genetic in nature. But there are a few problems. They rely largely on a slew of trans-racial adoption studies, all of which have been called into question (Thomas, 2017). IQ tests, furthermore, are not construct valid (Richardson and Norgate, 2015; Richardson, 2017). Heritability estimates also fail. This is because, in non-controlled environments these stats do not tell us much, if anything (Moore and Shenk, 2016). Likewise, Guo (2000: 299) concurs, writing “it can be argued that the term ‘heritability’, which carries a strong conviction or connotation of something ‘heritable’ in everyday sense, is no longer suitable for use in human genetics and its use should be discontinued.” (For more arguments against heritability, read Behavior Genetics and the Fallacy of Nature vs Nurture.)
Rushton and Jensen (2005) also relied on the use of twin studies, however, all of the assumptions that researchers use to attempt to immunize their arguments from refutation are circular and ad hoc; they also agree that MZs experience more similar environments than DZs, too (Joseph et al, 2014; Joseph, 2016, see a summary here; Richardson, 2017). In any case, the fact that G and E interact means that heritability estimates are, in effect, useless in humans. Farm animals are bred in highly controlled environments; humans are not. Thus, we cannot—and should not—accept the results of twin studies; they cannot tell us whether or not genes are responsible for any behavioral trait.
There was a lot that Rushton got wrong. His cold winters theory is a just-so story; East Asians and Native Americans are not the same race; heritability estimates are not a measure of how much genes have to do with phenotypic variation within or between groups; IQ tests are not construct valid; r/K selection theory was slayed as early as 1991 and then again in 2002 (Graves, 2002); twin studies are not informative when it comes to how much genes influence traits, they only measure environmental similarity; and finally, Rushton omitted data that did not fit his hypothesis on racial differences in crime.
It’s sad to think that one can spend a career—about 25 years—spewing nothing but pseudoscience. One of the only things I agree with him on is that races are real—but when it comes to the nuances, I disagree with him, because there are five races, not three. Rushton got a lot wrong, and I do not know why anyone would defend him, even when these glaring errors are pointed out. (For a good look into Rushton’s lies, see Dutton’s (2018) book J. Philippe Rushton: A Life History Perspective and my mini-review on the book.)
I was watching the show Ancient Aliens a while back (I don’t believe it, it’s great for a good laugh now and then, though) and I recall them “theorizing” that Asians are aliens—specifically due to the Dropa stones. So I was searching Google for some information on it, and I discovered this article Race, Citizenship, and the Politics of Alien Abduction; Or, Why Aliens do not Abduct Asian Americans (Tromly, 2017).
Tromly argues that alien abductions are a specific cultural—national—phenomenon and that certain groups, mainly Asian Americans, are excluded from these so-called abductions. Surely, most readers are familiar with the most famous of all alien abductions—the case of Betty and Barney Hill (Barney Hill was a black man). One night, they were driving down the road. And all of a sudden, they woke up in their car and many hours had elapsed (a concept known as “missing time“). They then went to a hypnotizer and underwent hypnosis. They then described many experiments that the aliens carried out on them. In any case, I’m not going to discuss the so-called abduction here, but this is one case—one of the most famous—of a minority being abducted.
Tromly argues that the notion of alien visitors elicits collectivity in humans—that, of course, all national, racial, and social differences would be put aside in the event of a hostile alien invasion and we would attempt to quell the alien threat. Think War of the Worlds. Indeed, Stephen Hawking argued that we should not attempt to contact aliens. His reasoning was simple: When Europeans came to the Americas in the late 1400s, with their superior technology, they subjugated the natives. Of course, if aliens from far, far away came to earth, they would be far more technologically superior to us—leaps and bounds ahead of the technological superiority when Europeans and Native Americans are compared. So this type of alien invasion, Tromley argues, would spur humans’ “species-consciousness”
Tromly (2017: 278) writes:
According to this paradigm, abductees are traumatized to the point that nationality becomes irrelevant. Describing the trauma of his own abduction in his bestselling book Communion, Whitley Strieber writes, “I was reduced to raw biological response. It was as if my forebrain had been separated from the rest of my system, and all that remained was a primitive creature, in effect the ape out of which we evolved long ago” (18).
So, Tromly then cites psychiatrist John Mack who argues that abductees are not self-selected and that they come from all walks of life. He is pretty much saying that, to the aliens, there is no one type of person that is more desireable to the aliens and therefore no one group is more worthy of visitation than any other. Further, he is arguing that, whatever differences exist between these diverse people, they are equal in one thing: their visitations by alien visitors.
Tromly (2017: 280) then writes:
Lowe argues that this ideal of political membership comes at the cost of specific individuation: “In being represented as citizen within the political sphere… the subject is ‘split off’ from the unrepresentable histories of situated embodiment that contradict the abstract form of citizenship” (2). These inadmissible “particularities” include “race, national origin, locality, and embodiment [that] remain largely invisible within the political sphere” (2). It is useful to revisit Mack’s presentation of the abduction community in light of Lowe’s observations, because his catalogue of abductees is typical of the discourse in that it defines abductees solely in terms of class and profession—in effect, Mack’s example of the diversity of abductees is underwritten by an assumption of sameness. Because he fails to mention other types of difference on the assumption that they are irrelevant, Mack excludes these differences and, ironically, his demonstration of the diversity of the abductee community becomes subtly exclusionary.
Alien abduction, if you keep up with this kind of thing, is pretty obviously racially exclusive: most abductees are white Americans. Though, of course, believers in alien abductions claim that this accurately reflects the racial demographics of America—with whites being the majority racial group.
Tromly then describes a re-telling of the Betty and Barney Hill saga, where the couple he describes are still an inter-racial couple, but the wife remembers the alien abduction, whereas the husband recalls does not remember it, he recalls the night as normal. This story is written by Asian American writer Peter Ho. So when the wife sees a blue alien light, the husband sees blue police lights—implying that alien abductions and police stops are, in a way, coeval. The wife wants to tell the story—the abduction story—since it can be looked at in a broader national context whereas the husband does not want to—since what he recalls of that night was not a night of alien abduction but a night of being stopped by the police. Eventually, the husband gives in to his wife, who was continuously nagging him to “remember’ the abduction. So he “recalled” one under hypnosis, and a completely different one while he dreamed.
Tromly (2017: 287) writes:
The significance of the Asian American abductee’s absence is shaped, in part, by how abduction in general is understood. Accepting accounts of abduction as true accounts of events that have taken place would require hypothesizing about why aliens might be more interested in some ethnicities than others. To understand accounts of abduction as imagined stories that emerge from anxiety, hysteria, or trauma might suggest that these narratives are not a useful avenue for the expression of the concerns of Asian Americans. … Of course, linguistic barriers may be a reason that a certain segment of the Asian American community cannot participate in the textual spread of the abduction phenomenon. (Many abductees recall repressed memories of abduction after reading texts by Hopkins or Strieber.) However, a more compelling reason for their exclusion is that Asian Americans, or the associations they typically bear in popular discourse, disrupt the logic of the abduction narrative.
Great point! What if the aliens can only telepathically communicate with English-speaking people, therefore they are the only ones that get abucted—and not Asian Americans?
Tellingly, Asianness is sometimes used to mark the otherness of extraterrestrial aliens—Strieber, for example, describes the otherworldly features of an alien with whom he comes in contact through a comparison with “Asian” features: “its eyes are slanted, more than an Oriental’s eyes” (60).9 However, rather than focusing on the possible racial connotations of physical descriptions of aliens, it is more productive to examine the similarities between descriptions of alien characteristics and long-standing Asian American stereotypes. Whether they are conceptualized as a threat to humanity or an advanced and enlightened race, aliens that abduct are almost always described as being deliberate, dispassionate, and, needless to say, technologically adept.
Of course, this is where the observation from Ancient Aliens comes from: popular accounts of the aliens are that they are short, physically weak and frail-looking, and, most notably, have slanted eyes. Asians fit this description, too. So, one can see the parallel here: Asians are technologically adapt, as are the aliens. Asians, too, are looked at as being an enlightened race. This, too, pushes the Asian stereotypes—the “yellow peril” stereotype—where Asians want to come to America and take American resources, and the “model minority”—the claim that Asians are what other minorities should strive to be—because they excel “through technological sophistication, emotionless drive” (Tromly, 2017: 288), while they are extremely productive, what I assume aliens would be like.
In any case, it seems that alien abductees are actually more likely to be white. I was watching Ancient Aliens last April and they were discussing certain characteristics of abductees—pretty much like Tromly was, without mentioning race. What they mentioned, though, was pretty funny: abductees were more likely to have rH negative blood along with having a higher percentage of green and hazel eyes. I took two pictures of the screen when it came on:
Wow, how interesting, what a disparity. So it seems, that along with not targetting minorities at the same rate as whites, they are targeting a group of people that are more likely to have green eyes and rH negative blood. Then, someone appeared on the screen and then stated that since hazel and green eyes and RH negative blood are due to mutations, that the aliens either created it or they have a special interest in it. They were talking about a “genetic component” to alien abductions. Seems like even being abducted by aliens is “genetic”, too. Wow, what isn’t “genetic” nowadays?
This article wasn’t that serious; I just found this today and read it, and I had a few laughs. While it is interesting that only white Americans seem to be the subjects of alien abductions and the like—and minorities seem to be overlooked—I don’t think it’s anything like Tromly says. Though obviously, I would say that since the aliens are not abducting Asian Americans and aliens look similar to Asians (small bodies, almond-shaped eyes, and weak and frail-looking bodies) and it is hypothesized by Ancient Astronaut “theorists” that aliens are humans from the future, the conclusion is simple to see: these aliens abducting humans are Asians from the future and they’re not abducting Asians because they are looking for different genes and other physiological and anatomic differences, and since they are descended from Asians then why would they abduct them? Checkmate, Ancient Aliens deniers.
Barnett argues in The Waning of Materialism that for any pair of conscious beings, it is impossible for that pair itself to be conscious. I punch myself and feel pain; You punch yourself and feel pain. But our pair wouldn’t feel a thing. Thus, pairs of people are incapable of experiencing pain. This is what Barnett call’s “The Datum.” He posits six explanations for explaining “The Datum”:
(1) Pairs of people lack a sufficient number of sufficient parts; (2) Pairs of people lack immediate parts of standing in the right sorts of relations to the other and the environment; (3) pairs of people lack the immediate parts of the right kinds of nature; (4) pairs of people are not structures, they are unstructured collections of two parts; (5) some combination of 1-4; and (6) pairs of people are not simple.
Let’s take (1): Imagine that each human on earth is in severe pain, while the collection of people is experiencing pure bliss. This is untenable. Thus, no matter how large, a collection of people cannot be the subject of experience. So pairs of people do not have a sufficient number of immediate parts and thusly do not explain “The Datum.”
Now let’s take (2): Let’s say that scientists shrink you and I down into someone else’s brain, me being the left hemisphere and you being the right hemisphere. Then someone punches the person we have been implanted as their hemispheres; they then react. We then stimulate neurons and the person defends themselves, putting their hands up in defense. We do just what that person’s hemispheres would have done. So we function just like a regular brain. So now you and I have a new relation: is it conscious? You and I may remain conscious, but arethe pair conscious? No. Thus, pairs of people lack the right parts necessary to stand in the right sorts of relations to themselves and the environment and therefore do not explain “The Datum.”
Now let’s take (3): Let’s say I tell you that I have two objects—(a) and (b)—in mind. You, clearly, need more information to conclude that (a) and (b) are conscious, but you don’t need more information to conclude that the pair—comprised of (a) and (b)—is conscious. We know a priori that pairs of things are not conscious; pairs of, say, TVs, rocks, shoes, beds, are not conscious. So, that any pair—(a) and (b)—may be conscious is absurd is not evidence that the two alone are not conscious.
Now let’s take (4): We can know by reflection that the pair comprising (a) and (b) are not conscious. We know a priori that pairs of things are collections while conscious beings are structures. Collections exist iff whenever the comprisal of what makes up the collections exist; a structure of things exists iff the things in question exist in relation to a certain structure. So consider the atoms in the threads in my pillow as a collection and my pillow as a structure. So if we were to disperse the atoms in the thread making up my pillow out into space, the atoms would still exist but my pillow would not. So are pairs of people incapable of having experience because they are not structures? Let’s now return to (2), when you and I were placed in someone’s brain as their hemispheres. So unlike the pair, the system (brain) is a structure and it would cease to exist if you and I were removed from the individual’s brain, though the pair that you and I form would not. However, the system of people is not a candidate for the subject of experience than the pair that constitutes the system. So the idea that pairs of people are incapable of experience since they are not structures does not explain “The Datum.”
Now let’s take (5): Maybe “The Datum” is not explained by (1)-(4). Maybe some combination of the 4 explains “The Datum.” Maybe pairs of people aren’t conscious because it is a collection which results from the existence of two people; maybe a conscious being is a structure comprised of many cells, organs, standing with one another and the environment they are in certain causal dependent relations. So human bodies which are physical structures that are comprised of organs, cells, blood, etc, are conscious; the differences between human bodies are captured in (1)-(4); the four hypotheses do not explain “The Datum” alone; so some combination of (1)-(4) must explain “The Datum.” So let’s go back to (1). If we consider 7 billion people—and not a pair—then we know that no matter the number of people, that collection is not, itself, conscious. Now take (2), but on a larger—societal—level. If everyone in that society has a similar goal and aims for those goals, are they conscious? No; the claim that they are is absurd. Sure, the society functions just as human brain functions, but is that society—itself—conscious? No. Now take (3), but imagine that every neuron in your head was replaced by a mini-man. Thus, if we shift our attention to the number of mini-men in the head to the structure they comprise, it does not make any difference: (1)-(3) does not explain “The Datum.” Finally, let’s take (4). Imagine that your brain was sliced in half and dispersed into vats. Then those hemispheres are halved—while radio transmitters are placed in your hemispheres (preserving communication with the CNS)—and so on and so forth, until each of your neurons sits in its own individual vat. Now imagine that each neuron is paired up with an individual and the neuron gets a break, with the individual then carrying out the function of the specific neuron, Now, what concerns us is whether or not ‘you’ are identical to the scattered parts of what used to comprise ‘you’ and the system that controls your body. Certain times, billions of people operating billions of radio transmitters are operating the system; other days its billions of neurons operating billions of radio transmitters. So these billions of objects which still interact with your nervous system interact with your nervous system just like your brain used to when it was confined to its skull. So whether or not these billions of people that comprise your radio transmitters that control your scattered neurons is irrelevant; what matters is whether the system itself is a subject of experience—and it is not. So no combination of (1)-(4) explains “The Datum.”
Now, finally, let’s take (6): Are pairs of people not qualified from being conscious because they aren’t simple? In all 4 of the hypotheses, composite entities are presented and we ask whether or not the entity may be conscious. Whether or not the entity in question has 2, 100, 100,000, 100,000,000,000 parts is irrelevant. What does matter—however—is whether or not the posited entities presented are a composite. So there is absurdity in the idea that they are identical to a subject of any experience. The only hypotheses that rival this preceding explanation are (1)-(4), but they are inadequate. So simplicity best explains “The Datum.”
So conscious beings must be simple. We are not simple particles, so Barnett’s argument is an argument against materialism. So correlations between our mental states and our brain states do not give reason to identify ourselves with our brains. Therefore we are not our brains.
I am simple. I contain no proper parts (there is no such thing as “half an *I*”). However, my brain contains proper parts. Therefore I am not my brain.
(Ir)RationalWiki (IW) is a Wikipedia-style website, where anyone can edit or create an article on whatever they’d like. They are a left-leaning website, so they, of course, don’t like what they consider to be “right-wingers.” Many “HBDers” have IW articles on them, notable hbdchick, JayMan (though it seems like his article was deleted), Emil Kirkegaard, Anatoly Karlin, and even a new one on the philosopher of biology Nathan Cofnas (see his response here). When I discovered my own article on IW, I laughed, since it grouped me in with “Frogs and Swastikas, AltRight.” Well, I think that the “Pepe the frog” meme is idiotic and childish, and I’m not a Nazi (National Socialist).
In any case, I recently looked at the page and discovered that they finally edited it to reflect my new views. My views changed around April/May 2017 due to two books: DNA is not Destiny: The Remarkable, Completely Misunderstood Relationship Between You and Your Genes (Heine, 2017) and Genes, Brains, and Human Potential: The Science and Ideology of Intelligence (Richardson, 2017). I would say that before reading these two books that I was a “genetic determinist.” However, Richardson’s work lead me to the work of Denis Noble, Jablonka and Lamb, Susan Oyama, and David Moore and the philosophy of developmental systems theory (DST). My deterministic views (and outdated views on genes and the physiological system) were then cured.
In any case, here is what the new edit says about me now:
RaceRealist started out as a supporter of hereditarianism racist theories about IQ and a fanboy of Richard Lynn and Arthur Jensen, but later to his credit rejected these views. Instead however of giving up all his racialist beliefs, he still defends racialism, albeit minus the IQ pseudoscience. The latter has led to him to be criticised as still being a racist but using a deceptive motte and bailey strategy of trying to present himself as a more moderate non-hereditarian “race realist” when he still retains the old racist IQ beliefs about inferior black people in private. Furthermore, despite claiming to have changed his views on the latter – all his old pro-hereditarianism posts on his blog are still up alongside background photos of white supremacists.
The first sentence is true; I did start out as supporter of hereditarianism. When I discovered the work of people like Rushton, Lynn, Kanazawa, and Jensen I thought “Wow, this all makes so much sense and explains why our societies are stratified the way they are.” Though, as mentioned above, I did change my views.
Yes, I do “still defend racialism”, but a softer, non-hereditarian view of human races (Spencer, 2014, Hardimon 2017). These types of arguments about race are non-hereditarian, non-hierarchical. I do agree that “IQ science” is psuedoscience, but the claim that “I still retain [my] old racist IQ beliefs about inferior black people in private” are completely unfounded. How does whoever wrote this know what views I hold in private? Further, they claimed that I “rejected [those] views” in reference to hereditarianism (Jensenism) but then they say that “I still retain [my] old racist IQ beliefs about inferior black people in private”? How does that make any sense?
Further, I have explicitly stated that the terms “superior” and “inferior” are strictly anatomic terms and, outside of that context, make no sense. The head is superior to the feet; the feet is inferior to the head. It seems that the author of this did not read my article Blumenbachian Partitions and Minimalist Races where I explicitly state:
Biological racial realism (the fact that race exists as a biological reality) is true, however, just like with Hardimon’s minimalist races, they do not denote “superiority”, “inferiority” for one race over another. Most importantly, Blumenbachian populations do not denote those terms because the genetic evidence that is used to support the Blumenbachian partition use noncoding DNA. (It should also be noted that the terms “superior” and “inferior” are nonsensical, when used outside of their anatomic contexts. The head is the most superior part of the human body, the feet are the most inferior part of the human body. This is the only time these terms make sense, thus, using the terms outside of this context makes no sense.)
Yes I have changed my “views on the latter [hereditarianism]”, and no, I will not remove my “old pro-hereditarianism posts” on my blog. I leave them up to show the evolution of my views over time. My blog is almost four years old, and half of the time I was a staunch hereditarian/genetic determinist and the other half I discarded those views and embraced the philosophy of DST.
In any case, the race debate is a philosophical, not biological, one; genetic variation exists between human populations which no one denies. The question “What is race?” is strictly a philosophical question and so, after that question is answered, it follows that the argument about the existence of race is then philosophical. Holding views on racial realism (the claim that our racial categories pick out real kinds in nature; Smith, 2015; 43). Therefore, the views that I hold on race are not scientific, but philosophical.
Re my views on immigration: yes I did write that non-western people are abnormal to our societies (fun fact: I wrote that as a paper for an Abnormal Psychology course, and I got an A). I do still hold that immigration should be restricted/completely halted, though it should not be based on IQ testing, as I once argued in the past. I agree that these views that I once held are idiotic. Looking back at what I wrote and used to believe in the past, I believed a lot of bullshit and pseudoscience. I openly admit that my former prejudices drove my old beliefs. However, as noted earlier (and in the past), I rejected those kinds of genetic determinist “racist” views after discovering the philosophy of DST and reading Richardson and Heine.
A final note on my politics: I support closed borders, I support capitalism and I am a nationalist. I don’t care about what people do in private, just don’t bring it out on the streets. I would say that I am somewhat of a libertarian, and while I do hold some “AltRight” views, I would not self-identify as an alt-righter.
In sum, (Ir)RationalWiki is a joke of a website with how they attack individuals who do use their real names. I’m just some anon guy with a blog and Twitter account. They libel people with mined quotes and don’t reflect their views correctly. In any case, yes my views have changed, and no, it’s not some “cover” for my old views. I do not still hold those same beliefs “in private” (how would whoever wrote this know what views I hold in private? It’s idiotic). I’m not “AltRight”, nor have I ever been.
I’ve written on steroid use between blacks and whites last year, but it was a smaller part of an article concerning the misconceptions people have on steroids and what they do (responding to the hysteria that the media and the like discuss with their claims of “roid rage”). I cited some studies showing that blacks use more drugs than whites; that blacks are more likely to lie about drug-use than whites; and that blacks are more likely to use steroids than whites (indeed, minorities were twice as likely to use steroids compared to whites in one study). (It is also worth noting that “roid rage” is a myth; AAS use is associated with other drug use, which explains the relationship. See Lundholm et al, 2015. For further information on this matter, see the documentary Bigger, Stronger, Faster.)
Steroids are synthetic hormones—lab-made hormones that mimic the so-called “male hormone” testosterone. Though the term “steroid” is misleading; what is being discussed are androgenic anabolic steroids (AAS), since, for example, estrogen is a steroid and does not have the muscle-building and recovery properties of AAS. The term “anabolic” refers to muscle-building whereas the term “androgenic” refers to the increase in male sexual characters. AAS abuse is associated with tendon ruptures, a lower incidence of prostate hypertrophy, anxiety, depression, and a decreased libido (Bagge et al, 2017). Furthermore, the negative effects of AAS (ab)use cause cardiovascular problems, dyslipedemia—which may impact vascular functioning, ventricular arrhythmias while training, hypertension, etc. (Goldman and Basaria, 2018). Further negative effects include raised cholesterol, hair thinning, sterility, and decreased hormone levels. Croaker (2017) notes that AAS use is prevalent throughout high school and collegiate sports, though “When the desired outcome is achieved, the results are always short lived.”
Individuals use steroids for myriad reasons—despite the well-known adverse effects. A few considered are: (1) to become better at sports; (2) to increase muscle mass (which then relates to increased recovery time so the individual can train more); and (3) they are administered a script by their primary care doctor because their testosterone levels are low for their age range. In any case, in this article, I will discuss (1) and (2).
Whichever way the racial differences in AAS use go, we can all agree on one thing: in young men, they most likely want to become better athletes. AAS use is associated with shorter recovery times (
How can you tell if any individual is using steroids? It’s very simple. An increase in upper-body mass, most notably the shoulders and traps. The reason for this is that there are more androgen receptors in the shoulders and so they respond better to the flood of synthetic hormone.
AAS (ab)use is pretty prevalent throughout America. For example, Blashill et al (2017) write that “Black, Hispanic, and White sexual minority boys reported misuse at approximately 25%, 20%, and 9%, respectively.” “Sexual minorities” refers to sexual identity and the sex of the sexual partner. “Whites” were those who said they were not “Hispanic” and were white; “blacks” were those who said that they were not “Hispanic” and were black; while “Hispanics” were those who identified as a “Hispanic” ethnicity while marking down another race. (Note that “white” and “black” are socialraces.)
The (ab)use of AAS particularly affects homosexual minorities. Blashill et al (2017) write:
Sexual orientation health disparities in anabolic steroid misuse disproportionally affect Black and Hispanic sexual minority adolescent boys …
Blashill et al (2017) conclude from the results of their study that the (ab)use of AAS by sexual minorities may be due to “muscularity-oriented body image concerns.” I have heard (albeit, anecdotally) that a lot of homosexuals use AAS in order to look good so they would fall under (2).
The Child Trends Data Bank writes that “There are no significant differences in use of steroids in the past 12 months when comparing whites, blacks, and Hispanics.”
Hua and Braddock (2008: 29) write that “White males reported higher prevalence of steroid use than Black males, and sport participation served as a protective factor, but only for Black males.” They conclude that:
Specifically, our results show that sport participation served as a protective factor, but only for Black males. Sports active black male adolescents reported lower rates of steroid use than Black males who were not involved in sports.
So, it seems that sport participation is protective for blacks in regard to steroid use. However, black males lie about drug use more than white males, and so, I don’t see why we should accept the conclusions of this study. I also find it hard to believe that sport participation would be protective against AAS use. Intuitively, you would expect it to cause more AAS use.
The Journal of Ethics states that AAS (ab)use was higher in white (6.2%) and “Hispanic” students (7.2%) than black students (3.6%).
Irving et al (2002) state that 2.1% of white males 7.6 percent of black males, 6.1% of “Hispanic” males, 14.8% of Hmong males, 7.9% of “other Asian”, 3.1% of Native Americans, and 11.3% of mixed race males reported AAS use. Whereas 0.5% of white females, 4.3% of black girls, 0.9% of “Hispanic” girls, 8.9% of Hmong girls, 3% of “other Asian” girls, 4.7% of Native American girls, and 4.1% of mixed race girls used steroids. Here is table 1 from Irving et al (2002):
Low SES individuals were more likely to (ab)use AAS than high SES individuals in both sexes. Middle schoolers were more likely than high schoolers. (Where are they getting the AAS? Their parents? Older siblings?)
Irving et al noted that the male AAS users were least satisfied with their shoulders (we can’t all be so lucky). Fortunately for them, as noted above, the shoulders have the most androgen receptors in the body and so their shoulders will grow. However, other than not being satisfied with their shoulders, body image was not associated with AAS use in males. Female AAS users, more so than non-AAS users, were more likely to report that they used AAS to for “weight and shape.” Further, sport players were more likely than non-sport players to use AAS—as expected. In a nutshell, AAS use is associated with poor markers of physical health—most importantly because many individuals wanted to lose weight (most likely fat mass). It should be noted that those who were dissatisfied with their bodies were less knowledgable about nutrition, so to amleiorate some of this, nutrition should be taught earlier in schools.
I can’t think of any reasons why, however, Hmong males and females would be using AAS more than other ethnies. However, Irving et al (2002: 251) write:
One finding regarding the demographic characteristics of steroid users in our sample is worth noting. Steroid use was more common in non-Caucasian respondents (both male and female), with particularly high rates among Hmong participants. Initially, we were puzzled by this result and questioned its validity. However, in consultation with community informants from social service agencies that work with southeast Asian youth in the Minneapolis/St. Paul area, we were told by some informants that the “word on the street” was the Hmong youth were attempting to “bulk up” physically, by working out and using steroids. One possible explanation for this finding is that, as fairly recent immigrants (most Hmong immigrated to the U.S. in the past 20 years), Hmong youth may be “bulking up” to gain status in a culture that emphasizes physical appearance, including weight, shape, and physical strength. This interpretation is supported by anthropological research wherein exposure to western ideals of beauty and eating habits is followed by increases in weight and shape preoccupation and disordered eating practices among individuals from non-western cultures. On the other hand, it is possible that Hmong youth may have misinterpreted the question.
So if the Hmong did not misunderstand the question, it is possible, for example, that they were getting bullied (due to being new immigrants) and decided to take AAS in order to get bigger to stop the bullying.
Stilger et al (1999) note that (my emphasis):
Of the 873 high school football players participating in the study, 54 (6.3%) reported having used or currently using AAS. Caucasians represented 85% of all subjects in the survey. Nine percent were African-American while the remainder (6%) consisted of Hispanics, Asian, and other. Of the AAS users, 74% were Caucasian, 13% African American, 7% Hispanic, and 3% Asian, x2 (4,854 4) 4.203, p 4 .38. The study also indicated that minorities are twice as likely to use AAS as opposed to Caucasians. Cross tabulated results indicate that 11.2% of all minorities use/used AAS as opposed to 6.5% of all Caucasians (data not displayed).
Lastly, Green et al (2001) note that whites and blacks used AAS at the same rate, though the n = 10,850 Caucasians while for African Americans the n = 1,883.
However, unless a study notes that the participants’ blood was assayed, why should we believe the results when it’s been noted that blacks underreport and lie about drug use more than whites (Bauman and Ennett (1994); Ledgerwood et al, 2008; Lu et al, 2001)?
In sum, many studies report different results. I would say that the difference is due to cultural/social differences based on where the studies were carried out. The mixed results of these studies points to one thing: AAS use is prevalent throughout school life, and since it starts so young with many people, older siblings seem to be getting it for them. Sexual minorities are more likely to use than whites and this seems to come down to body image; Hmong seem more likely to use than non-Hmong; and the racial differences seem to hold with females as well.