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What Happens When a Physiologist Looks into “HBD” Claims? A Case Study

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The Bajau spleen size and better-living-through-evolution story is also a reminder that since the dawn of the theory of evolution, humans have been incredibly creative in coming up with evolutionary and hence genetic narratives and explanations for just about every human trait that can be measured. This effort recycles from time to time and is again reaching a peak in an era when it is possible to quickly and cheaply “genotype” human populations. (Joyner, Boros, and Fink, 2018: 524-525)

Yesterday on Twitter Matt Yglesias—Vox blogger—tweeted out a 2018 paper in which the authors argue that ‘natural selection’ explained the bigger spleens of the Bajau and, consequently, how they could hold their breaths for such a long time (Ilardo et al, 2018). The main claim of the paper is that ‘natural selection’ ‘selected-for’ larger spleens which then increases how much oxygen can be stored. The point of the study was to find out if their exceptional diving abilities had a ‘genetic basis.’ Thankfully, though, a group of physiologists looked into the claims of Ilardo et al (2018) and found their main claims wanting (Joyner, Boros, and Fink, 2018). That’s how easy it is for selectionists: Notice a trait; then work backward and attempt to formulate the best story you can (see Smith, 2016).

These diving capabilities are similar to high-altitude hypoxia—indeed the authors assume that there was an adaptation for breath-hold diving. They compared some Bajau people (n=59) and close neighbors who did not—the Saluan (n=34)—really interact with the water environment. So, using a portable ultrasound machine, they photographed the spleens of the two groups and noted a “clear visual difference” between Bajau spleens and Saluan spleens. The Bajau had spleens about 40-50 cc bigger than the Saluan.

These results suggest a physiological difference between the Bajau and the Saluan that is not solely attributable to a plastic response of the spleen to diving activity. While other unknown environmental factors could potentially explain the observed difference between the groups, genetic factors remain a possibility.

So big spleens mean big breath-diving ability. And big spleens were an object of selection. So breath-diving was therefore selected for—so the just-so story goes. But, “a slightly larger spleen is almost certainly not the most important [part of diving] from a physiological perspective” (Joyner, Boros, and Fink, 2018: 524). They then found ‘genes for’ big spleens and they then formulated their just-so story. Accompanying evidence was the fact that deep-diving animals have bigger spleens, so since the Bajau have bigger spleens, this then would mean that the bigger spleens then allows for better breath-diving. Joyner, Boros, and Fink (2018: 525) write:

The general idea is that, like blood doping in cyclists, bigger spleens that contract would give the Bajau divers a boost of oxygen-carrying red cells that would make them more successful at underwater-based hunting and gathering. Thus, spleen size was selected for via evolution over the last 1,000 years or so. A few simple back-of-the-envelope calculations about oxygen stores are instructive. A 40 cc bigger spleen that was all red cells and contracted completely with diving might give the Bajau 20 milliliters of extra oxygen. That is about 1% or less of the oxygen stored in the body and lungs of healthy humans.

Joyner and colleagues then go on to note other ethnies who perform similar breath-dives, while also noting that the Bajau routinely perform dives at 5-10 meters for 30 seconds, which while impressive, is something that fit people can do if they train their lung capacity.

Of note, in the famous Japanese and Korean breath-hold divers who have been studied for decades, repeated descents of this depth and duration don’t cause oxygen levels in the blood to fall much (Schagatay, Lodin-Sundstrom, and Abrahamsson 2011; Stanek et al. 1993). Second, repeated dives of this duration with brief periods of rest only cause whole-body oxygen consumption to rise to the level seen during a brisk walk or slow jog (Craig and Medd 1968). This is hardly the sort of maximum efforts made by deep-diving seals, competitive breath-hold divers, and blood-doping cyclists. The extra oxygen from a slightly larger spleen could easily be generated by a slightly larger breath prior to starting the dive.

It is incredibly easy to think up just-so stories for anything you notice (e.g., my just-so story on Mesoamerican human sacrifices). The Bajau learn to do breath-dive like that—it is an acquired ability. ALL human traits are experience-dependent and plastic, but obviously not to the same degrees.

The spleen is a blood filter. Being a blood filter, if it can filter MORE blood by being bigger, then it will give the individual whose spleen it is an advantage at certain tasks. It sits upper-left part of the abdomen and is protected by the rib cage while also being a place for blood cell storage (Pernar and Tavakkoli, 2019). The spleen acts as a reservoir of oxygen storing “‘thick blood’ rich in cells” so that when the diving animal the oxygen levels are stressed, the body has the reservoir of extra oxygen (Milton, 2004). Esperson et al (2002) also note how the spleen acts as a reservoir of red blood cells, while the contraction of the spleen causes extra hemoglobin production after exposure to diving events.

When a diver submerges their body in the water, two things happen: bradycardia—slower heart rate and vasoconstriction—the narrowing of arteries. The increase in water pressure further causes blood shift—an extension of vasoconstriction which allows us to dive deeply and the spleen effect—meaning that the spleen of divers shrinks which then releases the stored RBCs into the body, allowing for prolonged diving. So, if we look at this in regard to the Bajau, their large spleen shrinks and since their spleen is large due to the number of RBCs it has, it would then follow that as they deep-dive the spleen would shrink (known as splenic contraction) causing the release of the RBCs into the body, allowing for the deep-diving phenotype. Thus, without the blood shift and spleen effect, divers would not be able to dive to such deep depths. (See Gooden, 1994.) The mammalian dive response has, also, been hypothesized to be a reflex to preserve life (Panneton, 2013).

Bajau and, for example, Tibetan environments are similar in that the Bajau spend time in low-oxygen environments (the water) and so do the Tibetans (the mountains). But the Tibetans are constantly exposed to this effect; the Bajau need to be in the water for this effect to occur.


Lastly, the “HBDers” in the comments on Yglesias’ tweet said the same ol’ predictable things. Such as “human spleen growth is complex and due to what the stereotypes of a group’s spleen size are”; “of course it’s true!”; “variation in spleen size within groups is greater than variation in spleen size within groups”; “spleens are a social construct”; “evolution only happened in humans below the neck”; etc. These are the same ol’ sayings that come out from “HBDers” whenever a finding like this comes out. And, you can tell that they are ignorant to the anatomy/physiology of this stuff. They just jump on anything that they can say “HBD is real!!” as if anyone denies that humans are biologically diverse (like when the Rushton retraction came ‘it doesn’t mean that HBD isn’t true!). They move and weave different definitions of ‘HBD’ to fit their needs.

Such storytelling can be done for any trait, as noted by Smith (2016). One can think up selectionist stories and competing ideas for the evolution of traits, but without a way of ajudicating between two stories. One of the best definitions of just-so stories I am aware of is from Not in Our Genes (Lewontin, Rose, and Kamin, 1984: 258-262) cited in Smith (2016). Just-so stories:

predicate a genetically determined contrast in the past…unstated assumption that genes may arise with any arbitrarily complicated action needed by the theory…insulated from any possibility of being contradicted by fact…. If one is allowed to invent genes with arbitrary complicated effects on phenotype and then to invent adaptive stories about the unrecoverable past of human history, all phenomena, real and imaginary, can be explained.

So what happens when a physiologist looks into “HBD” claims? They are found very, very wanting.

A Bad Week for “HBD”: Retractions

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I’ve been writing on this blog since June 15th, 2015. Back then, I held staunch hereditarian beliefs. Rushton’s views on testosterone were enticing to me, especially his theoretical article with Templer (Rushton and Templer, 2012). When I first read it I thought “Oh, justification for my prior beliefs about blacks and crime.” Then, when I started studying anatomy and physiology, I reread the paper and thought “Wow who gave the OK to publish this mess?”

So in February of 2018 I published a critique of the article, Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals? A Response to Rushton and Templer (2012). I critiqued many of the claims in their article; its biggest weakness completely handwaving the warnings of Ducrest et al (2008) that human populations “are therefore not expected to consistently exhibit the associations between melaninbased coloration and the physiological and behavioural traits reported in our study.” Rushton and Templer dodged this by saying that we should compare African and European crime rates and that we do, indeed, see that Africans commit more crimes than whites and Africans have darker skin than whites so this is sort of “preliminary evidence” for the relationship in human races.

However, unfortunately for Rushton, Cernovsky and Litmann (2019) reanlyzed the INTERPOL crime data:

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.

So, if we accept the INTERPOL data—as Rushton did—then we would be justified in saying that the proposed relationships and causal pathways do not hold.

Then at the end of October the Twitter account @evopsychgoogle wrote a long thread with a strong, in-depth critique of the arguments and sources in Rushton and Templer (2012). He then published his critique as a letter to the editor of Personality and Individual Differences (PaID). In the letter, he exposes the shoddy logic of Rushton and Templer, while showing their misreadings of sources and misunderstanding of pleiotropy. Their main point in the paper is that LHT may explain why dark-skinned individuals are more violent, mature faster, etc while they also argue that the melanocortin system is a physiological coordinator of LH traits and skin color.

Testosterone production is a simple bodily process—to quote myself from November, 2017:

There are five simple steps to testosterone production: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone) (Saladin, 2010: 137). Testosterone is a steroid and so there are no ‘genes for’ testosterone.

Cells in the testes need to take cholesterol and then convert it into testosterone with the luteinizing hormone. According to Rushton and Templer, the result of this bodily process is part of the reason why blacks are more violent than whites—they have higher levels of testosterone and testosterone causes aggression/violence. Surely, Rushton and Templer were aware of Rohrmann et al (2007) who showed no difference in testosterone between blacks and whites. Surely Rushton and Templer were aware of all of the research that I cited in what I would call my ‘master article’ on race, testosterone, prostate cancer, and aggression. Rushton and Templer, quite obviously on a review of the literature, are misleading their readers.

Thankfully this paper has only been cited 15 times in the past 8 years since it was published. Evolution, presumably, accounts for the differences in death, AIDS rate, testosterone, lower life expectancy, etc. One recent citation can be found in the textbook Race and Crime (Gabiddon and Greene, 2018, 5th edition) in a discussion about Rushton’s r/K selection theory and causes for Rushton’s proposed relationship. They write (pg 122-123):

As with all theories, there have been several criticisms of the r/K selection theory. First, Rushton generally underemphasizes sociological factors. Most of his cross-national comparisons point strictly to numbers, without taking into account variables such as socioeconomic status, and other important sociological variables (Whihte, 2018). Second, in the 21st century, there are few “pure” races, especially in the United States, as noted in Chapter 1. White sexual aggression against Black females during the slave era produces countless mixed-race offspring. Therefore, the rigorous adherence to the Black-White-Asian split is problematic. Finally, if Rushton;s theory were true, what would explain White aggression as early colonizers and their current involvement in wars and violence across the globe? In contrast to Rushton’s theory, Bradley (1978) argued that, as a result of migration to colder regions, since the beginning of humanity, Whites have been the global aggressors.

So, testosterone does not cause aggression and it does not cause crime; the melanocortin system does not work in such a way that works for Rushton and Templer’s theory (Cone, 2006).

Hilliard (2012: 73) stated that “No evidence shows that racism motivated Rushton” while Dutton (2018) stated the same, interviewing Rushton’s ex-wife (whom he had an illegitimate black son with). But, knowing what we know about testosterone and Rushton’s views on blacks and whites, knowing about his (false) views on testosterone and race (while citing old, flawed studies like Ross et al) we can call into question the claim that Rushton had no racial animus. @evopsychgoogle also brought up the fact that COIs and funding sources were not brought up (this being Rushton’s final paper before his death and the fact that he was the head of the Pioneer Fund at the time means we don’t have to ask where the funding came from). Rushton and Templer should have never been published in the first place.

Lastly, Clark et al (2020) argued that ‘intelligence’ as ‘measured‘ by ‘IQ tests’ modulates the relationship between religiosity and crime at a country-wide level. They, of course, used Lynn’s global ‘IQ’ data. Though, there were many critiques of the paper and the data used in it (see here, here, and here) and Clark et al decided to finally retract their paper due to the problems of Lynn’s dataset. So, if they retracted due to the problems with Lynn’s dataset, does that mean that other papers that relied on Lynn’s shoddy work (e.g., Richardson, 2004; Morse, 2008) should be retracted too? Ebbeson (2020) notes the flawed ‘IQ estimates’ used in Clark (2020), noting the small, unrepresentative child samples used, along with showing that their dataset leads to “notions” which “are incompatible with psychological science” so “all conclusions drawn from these data are invalid.”

Clark et allost confidence in their findings” since “the homicide data have limitations that call [their] findings into question” while “The IQ data … have much more serious issues.” “Serious” is an understatement. To quote Ebbeson (2020)

For example, in the ‘NIQ_QNWSAS’ dataset, several African, South Asian and Central American countries have an average IQ below 50, such as Nepal (national IQ: 43.0), Sierra Leone (national IQ: 45.1), Guatemala (national IQ: 47.7) and Gambia (national IQ: 49.8) These estimates would seem to suggest that a majority of the population in these countries are moderately, severely, or profoundly cognitively impaired. (cf. Table 1). This notion is incompatible with psychological science and there is no doubt that these estimates are wrong.

All in all, this is not a good week for “HBD”—Rushton is being exposed for the know-nothing about physiology that he is, and Lynn’s ‘national IQ’ numbers are getting the scrutiny they finally deserve. So, I hold, if Clark et al was retracted for those reasons, we need to retract ALL papers that relied on Lynn’s ‘national IQ data.’ People may cry ‘censorship! HBD is dead!’, but ‘HBD’ (what I would term psychological hereditarianism) has been long dead. Rushton and Templer’s paper should have never been published but it’s better late than never that it is finally getting retracted. If you’re saying that Rushton and Templer got retracted for “political reasons” then it’s clear that you did not read either of the two existing critiques of the paper.

My Citation Count

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I started this blog almost 5 years ago. Currently (excluding this one), there are 480 articles on this blog. Searching my blog name “notpoliticallycorrect.me” on Google Scholar leads to two citations—one on “IQ” and obesity and the other on inclusionism about race when it comes to medicine. These two cites pretty much perfectly show my views and their change in the past 5 years since the creation of this blog. I will discuss both papers that cited me in turn.


In the journal Social and Human Sciences. Domestic and Foreign Literature (a sociology journal), a 2016 article I published (back in my “HBD” days titled “Race, Obesity, Poverty, and IQ, writing:

income and education (which in the latter case presumably correlates with IQ levels). They have the highest prevalence of type 2 diabetes. In terms of ethnicity, overweight indicators are as follows: 67.3% for whites, 75.6% for African Americans and 77.9% for Latinos. Summing up all this, we obtain, in the words of the authors of the study, “politically incorrect conclusions”: African Americans and Hispanics are more at risk of living in poverty, have lower IQ, higher rates of obesity and a chance of developing diabetes; The main factor in these correlations is the IQ level (Race, obesity, poverty and IQ, 2016).

Almost four years later (after my views have undergone a significant change) I would draw different conclusions. Blacks are 51% more likely to be obese than whites (Lincoln, Abdou, and Lloyd, 2016) with the cause being a multitude of factors. Though it seems that black American men with more African ancestry may be protected against central adiposity (Klimentidis et al, 2016). Racial disparities in obesity are due to an interaction of a multitude of factors (Byrd, Toth, and Stanford, 2018). Interestingly, black kids with obesity don’t perceive themselves as obese (Lankarani and Assani, 2018), which, presumably, is due to higher rates of obesity in the black population. Black girls are more likely to have an earlier menarche than white giris (e.g., Freedman et al, 2000) and it is because black girls are more likely to be obese than white girls which is due to the effects of leptin being permissive for menarche, from the higher levels of body fat in black girls (Salsberry, Reagen, and Pajer, 2010).

We must look to social determinants of health to understand why certain non-white populations are more likely to be obese than others. Looking at “IQ” as causal for obesity—which I used to believe—obscures much more than it helps. We can look to epigenetic effects, for example, regarding biological explanations of obesity (Krueger and Reithner, 2016), for instance high BMI in black women being related to saliva-based DNA methylation, which is used as a marker for aging (Li et al, 2019). Even perceived racism (it does not have to be actual) can have physiologic effects on black women, heigtening cortisol levels, leading to a heigtened obesity risk (Mwendwa et al, 2016).

In any case, it’s cool that I got cited but uncool that it was something that I don’t believe anymore.


The second citation comes from Rossi (2020: 13) in the journal Social Science Information titled New avenues in epigenetic research about race: Online activism around reparations for slavery in the United States citing my article Race, Medicine, and Epigenetics: How the Social Becomes Biological:

Consequently, social scientists’ opinions about epigenetic research dealing with race and slavery have sometimes been scrutinized by blog authors. For example, the article untitled [sic] ‘Race, medicine, and epigenetics: How the social becomes biological’ published in 2019 on the blog Notpoliticallycorrect features a long discussion on whether race could be seen as a viable variable to discuss the epigenetics of trauma, especially relating to slavery in the US.14 After summarizing the views of legal scholar and sociologist Dorothy Roberts, who has argued repeatedly in her works against the use of the concept of race in biomedical sciences, the author sides with philosophers Michael Hardimon and Shannon Sullivan, who are both enthusiastic about the inclusion of race to discuss genetics and epigenetics:

Race and medicine is a tendentious topic. On one hand, you have people like sociologist Dorothy Roberts (2012) who argues against the use of race in a medical context, whereas philosopher of race Michael Hardimon thinks that we should not be exclusionists about race when it comes to medicine. If there are biological races, and there are salient genetic differences between them, then why should we disregard this when it comes to a medically relevant context? [. . .] So, we should not be exclusionists (like Roberts), we should be inclusionists (like Hardimon). [. . .] Furthermore, acknowledging the fact that the social dimensions of race can help us understand how racism manifests itself in biology (for a good intro to this see Sullivan’s (2015) book The Physiology of Racist and Sexist Oppression, for even if the ‘oppression’ is imagined, it can still have very real biological effects that could be passed onto the next generation – and it could particularly affect a developing fetus, too). It seems that there is a good argument that the effects of slavery could have been passed down through the generations manifesting itself in smaller bodies.

Relying also on Jasienska’s research, the author of this blog post therefore dismissed the idea that race should not be applied to the medical field, while using the words and legitimacy of humanities scholars such as Hardimon and Sullivan to back up their claims. These contributions show the way journalists and various blog authors write about epigenetics by mixing together scientific articles in various fields (the social sciences, philosophy, psychiatry, social work) in an effort to bring more legitimacy to the topic. This process highlights the ways in which lay circles produce new connections between various papers and texts dealing with epigenetics, no matter how different their fields of expertise may be.

This shows a very sharp contrast with my current views and my older views on race and obesity. Before, thinking that obesity was “determined” by IQ (e.g., Kanazawa, 2012; Kanazawa, 2014) was an error—people with low “IQs” are more likely to be in poverty and have less access to good foods, along with the abundance of fast food restaurants in areas with a higher concentration of blacks (James et al, 2014). Black women, for instance, have a lower RMR than white women (Gannon, DiPietro, and Poehlman, 2000)


These two articles of mine that were cited (on similar issues, no less) show the evolution of my views over the past four or so years in between the publication of the two articles on this blog. This is a good case study on how the one can view the aetiology of one thing completely different based on the types of views they previously held. The views of obesity and race I hold now are much more complex than the reductive “it’s genes/IQ” kind of guy that I used to be. A more holistic view of obesity disparities, factoring in access to food (food swamps/deserts), income, location etc is more informative than looking just to “IQ” or “genes for” obesity—because even if “genes for” obesity exist and even if “genes for” obesity are distributed unevenly across races, the predominant determinant of weight will be activity level/caloric consumption, which is based on SES and other factors—not “IQ” or “obesity genes.” The social does become biological, and it does have consequences for obesity disparities between and within races.

Davide Piffer on Italians

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The other day on Twitter, Davide Piffer made the claim that North and South Italians are “two different races” and that the North is “governed by morons from the South.” What would make him say that North and South Italians “are two different races”? Well, a new study was just published which looked into the genetic divergence of North and South Italians. It seems that Piffer is saying that the fact that North and South Italians are genetically distinct means that they are races. But this is an error in reasoning—it is fallacious to believe that just because two groups are genetically distinct that they are therefore races.

Sazzini et al (2020) show evidence that North and South Italians genetically diverged after the last glacial maximum (LGM). They state that there was “adaptive evolution” at “insulin-related loci” from Italian regions with temperate climates. The state that climatic factors differentiated those from the North and those from the South. The “adaptations” that those in the North have protect them from:

… we proposed climate-related selective pressures as potential factors having influenced adaptive evolution at insulin-related genes especially in the ancestors of Northern Italians. By regulating glucose homeostasis, adiposity, and thermogenesis in response to high-calorie diets adopted to cope with energetically demanding environmental conditions, these adaptive events might have also contributed to make people from Northern Italy less prone to develop T2D and obesity despite the challenging nutritional context imposed by modern lifestyles. Conversely, possible adaptations against pathogens and modulation of melanogenesis in response to high UV radiation are supposed to have played a role in reduced susceptibility of people from Southern Italy respectively to immunoglobulin-A nephropathy and skin cancers. Finally, multiple adaptive processes evolved by the overall Italian population, but having resulted more pronounced in people from the southern regions of the peninsula, were found to have the potential to secondarily modulate the longevity phenotype. Therefore, by pinpointing genetic determinants underlying biological adaptation of Italian population clusters in response to locally diverging environmental contexts, the present study succeeded in disclosing also valuable biomedical implications of such evolutionary events.

What they did was select 39 unrelated genomes, representative of the known genetic differences in Italian the Italian population, and then compare the differences 35 populations from all over Europe. They found divergence between the two occurred between 12 and 19 kya—they presume that the so-called “adaptations” for North Italians, being “adapted” to lower temperatures and higher-kcal food, and the so-called “adaptations” for South Italians being adapted to warmer climes, so they have “genes to protect against” skin cancer and pathogens—while gene variants ‘related’ to longer life were also showed changes in those genes.

The press release, though, cautions against adaptive conclusions:

The authors caution that although correlations may be drawn between evolutionary adaptations and current disease prevalence among populations, they are unable to prove causation, or rule out the possibility that more recent gene flow from populations exposed to diverse environmental conditions outside of Italy may have also contributed to the different genetic signatures seen between northern and southern Italians today.

While this is an interesting study (and it does need to reign back its ‘adaptive conclusions’), it does not show that North and South Italians are different races. If they are different races, how does it go? Is there a single North Italian race and a single South Italian race? Or are North Italians Caucasian, while South Italians would be African? Are there 5, 6, or 7 races in Piffer’s racial schema?

Like all hereditarians, he just assumes the existence of race—if this and that population are genetically distinct, then they must be races. Wow, how compelling an argument to show that races exist. But if North and South Italians are a different race on the basis of genetic differentiation, then so are East and West Germans (Nelis et al, 2009), North and South Germans (Heath et al, 2008), Southeast and Northwest Dutch (Lao et al, 2013), North and South Dutch (Byrne et al, 2020), Northern and Southern Swedes (Humphreys et al, 2011), East and West Fins (Kerminen et al, 2017), etc. Using genetic differentiation as a basis to show which population is or is not a race logically leads one down this path. Why not 7 billion races? Each individual is unique? Oh, wait: He would say something about “breeding populations” probably—and that’d be good because he would then be stating conditions for racehood, not just assuming their existence on the basis of genetic differentiation. Though, the claim would still fail.

Piffer has let his mask slip before—back in March he called immigrants to Italy “gorillas”, then saying that “Gorillas are nobler” because they would not take beds from the sick, since this was when Corona was really heating up in Italy. This is similar to what the “World’s Smartest Man” Christopher Langan said about gorillas and immigration. There seems to be a relationship between idiotic sayings about gorillas and immigration and racism… hmm…

In any case, the fact that North and South Italians are genetically distinct populations in no way, shape, or form, is evidence that they are different races. For if it is, then there are many, many races—even in countries with the same group of people, if we are to understand race how Piffer seems to understand it (any type of genomic differentiation between populations makes them races). So is each family on earth a different race? This is the kind of conclusion that Piffer’s lazy thinking leads to. Piffer is just like Murray—if populations cluster in genomic analyses then those population clusters are races. Two hereditarians—two assumptions that fail, since if we take them to their logical conclusion, there are more races than is traditionally stated. Piffer, it seems, just sees a group he is clearly biased agains (South Italians), sees they are distinct genomically from the North, and then says “Aha! these morons from the South who are governing us are just a different race than we are!” Clinal differences in skin color, too, don’t ‘prove’ that North and South Italians are a different race.

Too bad for Piffer, reality is different than in his own biased world. Italy is over two thousand years old—and the people in the North and the South belong to the same race. Piffer’s ‘research’ into the “IQs” of North and South Italians (Lynn, 2010; Piffer and Lynn, 2014; see Cornoldi et al, 2010; D’Amico et al, 2011; Robinson, Saggino, and Tommasi, 2011; Danielle and Malanima, 2011; Cornoldi, Giofre, and Martini, 2013; in any case, is (and has been) suspect—but now we know that he has other motivations than just iScience!

(Note: The Italianthro blog has a ton of information on Italy, its peopling, “IQ”, and other things. Check the blog out.)

Consanguinity in Different Cultures

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Bans against consanguinity have been around for thousands, of years, though they differ by degree and culture. The Greeks had no single name for it, a similar term not appearing until around the 9th century—for instance, classic Athenian law stated that children of the same father could marry—i.e., a half-brother and half-sister (Ager, 2005). But what were some of the original reasons why they were banned—eugenic considerations or cultural/closeness reasons? Why were people banned from having a partner that was too close to them? Throughout history, different cultures obviously had different practices. The Roman Catholic Church, Pharaonic and Ptolemic Egypt, ancient Iran, all had different practices, for different reasons, on close marriage to relatives. The ban on first-cousin marriage appeared in American law around the time of the Civil War—clearly, then, the cousin-marriage ban in America was not based on the eugenics movement, though it was eugenic in nature (Paul and Spencer, 2008). Though there was debate on the matter during the Progressive Era (Wilson).

Gene and Wilcaux (2009: 115-116) write:

Schneider addressed sexual and matrimonial prohibitions among the Yapese in an early article (1957), but he developed his approach in a volume devoted to the subject of incest (1976). It was in the latter that he presented his culturalist views on the topic, making the important point that ‘the most frequent confusion found in the literature in my experience is the confusion between the question of the origin of the prohibition on incest and the question of why it is maintained long after the conditions which may account for its origin have passed’(Schneider 1976: 156). He went on to argue that ‘the incest prohibition is not universal’, supporting this affirmation with the cases of brother–sister marriages of Pharaonic and Ptolemaic Egypt, the ‘apparent lack’ of an incest prohibition in ancient Iran, and the marriages between members of the royal family of Hawaii as analysed by Marshall Sahlins (Schneider 1976: 154). None of these relations would be considered as incestuous for the native people. He also insisted on the inclusion of kin other than nuclear kin in the different prohibitions that Europeans identify as incestuous, on the importance of elements such as food for determining who a person can and cannot have sexual relations with and on cases in which incest includes non-sexual behaviour. He then proposed equating incest with the idea of acting ‘ungrammatically’ in a given cultural code (Schneider 1976: 167). Thus, for Schneider, a priori definitions of incest based on a Western tendency to relate kinship to sexual intercourse and the birth of a child should be avoided. Rather, he argued, we should adopt a cultural and symbolic approach towards each case. [See also Scheidel, 1997 for more information on sibling and half-sibling marriage in Roman Egypt. They did this to keep the throne in the family; Galton, 1998]

But the Romans were the first to dissuade consanguineous marriages when Emperor Claudius married his niece Agrippina in the middle of the 1st century. Then, in the middle of the fifth century, which the Roman Catholic Church eventually picked up, with the Pope citing passages in Leviticus to justify the banning of marriages with close kin (Bittles, 2009). (I should bring up the ‘Hajnal line’ now, but I’ll save that for an article by itself. In the meantime, read Steinbach, Kuhnt, and Knull, 2016 where they show that by taking marriage rate, divorce rate, step-families, and single-parent prevalence into account, we cannot use the ‘Hajnal line’ to explain differences between East and West Europe”; see also who argue that Szolyysek and Ogorek, 2019 who show that when regional populations cluster on familial traits that they lie outside of the ‘line’, which calls into questions the conclusions of Hajnal and his acolytes.)

When it comes to these cases, the ban on close marriages was not to have healthy children—and therefore attempt to prevent the types of problems that arise through the marriage of a close relative if they conceive a child—the ban was to avoid relationships that lacked difference on a bio-social level. One example here would be in certain Muslim communities. Children who shared the same wet nurse—a nurse who breastfeeds for parents—were banned from having any kind of relations later in life as they were known as ‘milk-siblings’:

Children who have been regularly breastfed (three to five or more times) by the same woman are considered “milk-siblings” and are prohibited from marrying each other. It is forbidden for a man to marry his milk mother (wet nurse) or for a woman to marry her milk mother’s husband.

In Leviticus 18:6-18, Deuteronomy 22:30, and Deuteronomy 27:2-23 the authors spake against marriage with close (blood) relatives while in Leviticus 20:11-21 along with the prohibitions against relations with blood kin, even your uncle’s wife was out of the question (the unrelated wife). When it comes to the Roman Catholic Church banning cousin marriage, however, there is a debate as to what the impetus for the ban was: was it due to eugenic considerations or to ban the marriage of two close individuals, no matter their relatedness status? MacKellar and Bechtel (2014: 62) write:

It is likely, however, that the basis for this prohibition on consanguinity [in the Roman Catholic Church] was not a concern for eugenic considerations. The condemnation of affinity, such as marrying a step-daughter (cannon 1092) and marrying an adopted child or sibling (cannon 1094) implies that these codes were again drafted on the basis of avoiding sexual relationships between people who were considered too similar or who had something ‘overly in common.’

Parkes (2005) notes that even marriage between a godparent and godchild was banned in Christian communities. I grew up Roman Catholic and I, too, would not marry my Godmother (who is my fourth cousin). MacKellar and Bechtel (2014: 63) do note that the Christian Church even banned relationships between, say, student and teacher to prevent “sexual corruption and abuse. These sexual restrictions were not, therefore, drafted to protect progeny from inheritable disorders but were similar to those that prevent relationships between teachers and their pupils or doctors with their patients. These relationships were prohibited even though it may have been certain that no child would ever be born.

Chinese cousin marriage prohibitions are interesting. First cousins could marry eac other if they did not have the same surname but if they had the same surname they were barred from marriage, as Wong (2017) notes that “The old Chinese system is a patriarchal system, where children take the surname of the father. In this patriarchal system, first cousins of the same surname could not marry. First cousins, with different surnames, could marry.”

Many Asian ethnies have the same or similar surnames. So, on that basis, it is interesting to note that in Korea, for example, much cultural shame is brought on people who choose to marry and have the same last name. It is so taboo that family and friends question their loved ones who date a person with their same last name. The New York Times has an interesting story from the mid-90s about Koreans and dating/marrying an individual with the same last name:

It should be a time of celebration. K. H. Lee and his girlfriend have fallen in love and want to get married soon to start a new life together.

But Mr. Lee, a 31-year-old civil servant, and his fiancee face a battle against Korean history that threatens to bring their love to ruin: they have the same last name. Even his friends disapprove of his plans.

“I can feel them asking, ‘Do you really have to do this?'” said Mr. Lee, who, who would not disclose his full given name or his girlfriend’s because the issue is so delicate. “Even if it were allowed by law, if the relatives found out, the whole family would be shamed because we have a strong sense of face.” Not being able to marry a person with the same family name is a special burden in South Korea, where 22 percent of South Korea’s 44 million people are named Kim. The figure leaps to 55 percent after adding in Park, Lee, Choi, and Chong.

The NYT story also notes an interesting bit of Korean folklore about this ban:

According to folklore, the practice was brought over from China in the 14th century, after a Korean messenger, named Lee, visited China. His Chinese host asked him his wife’s name, and upon hearing that it was also Lee, the Chinese supposedly replied: “Ah! You’re not an aristocrat. You’re a commoner!” When the messenger returned, he relayed the story to the Korean emperor, who immediately declared a ban against same-clan marriages.

Dating people with the same last name in South Korea is such a taboo that some people even attempt to find out their perspective SO’s last name discretely. The practice, to them is cultural as of now since presumably, marriage and children with one with the same last name won’t lead to any birth defects.


We have been marrying/conceiving children with close relatives since time immemorial. Though, different peoples have different reasons for shunning consanguineous marriages—some cultural, some biological, some both. The Greeks banned it in some instances, but allowed it in others. In Islam, children who are “milk-siblings” cannot marry. Asians (who are likely to share names with their own ethny, and even sometimes another Asian of a different ethny) have some interesting considerations on cousin marriages—it being so engrained in their culture that some will not talk to someone if they share their last name. The considerations of banning consanguineous marriages by the Church, though, could go both ways—it could be due to banning marriages between people who are ‘related’ socially, and not genetically.

The history of cousin marriage—along with the banning/allowing it throughout history, along with how different peoples handle the situation shows exactly how humans individuate through culture.

Sudden Infant Death Syndrome (SIDS): How A Genetic Determinist Theory Cost Infant Lives

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Sudden Infant Death Syndrome (SIDS) has a long history—almost as long as human civilization (Raven, 2018). The term was coined in 1969 to bring attention to children who died in the postnatal period (Kinney and Thach, 2012; Duncan and Byard, 2018). About 95 percent of SIDS cases occur within the first 6 months of life, happening around the 4-6 months mark (Fleming, Blair, and Pease, 2015). The syndrome is associated with the sleep period, presumed to have begun with the transition from sleep to waking (Kinney and Thach, 2012) The prone sleeping position, along with smoking, is said to increase the incidence of SIDS (Ramirez, Ramirez, and Anderson, 2018). Due to a campaign in the mid-90s, though (called the back-to-sleep campaign), it has been estimated that SIDS deaths have decreased by 50 percent, saving thousands of infant lives (Kinney and Thach, 2012).

But, those infants who die from SIDS may also have a problem with the part of their brain that controls waking/sleeping:

Infants who die from SIDS may have a problem with the part of the brain that helps control breathing and waking during sleep. If a baby is breathing stale air and not getting enough oxygen, the brain usually triggers the baby to wake up and cry to get more oxygen.

So, if a baby’s brain is not getting enough oxygen, its brain will have it wake up and cry in an attempt to rid itself of “stale oxygen”—this is one other purpose that crying serves—which then gets the baby more oxygen to its brain.

Buchanan (2019) hypothesizes that reduced Co2 is a cause for SIDS—being that Co2 induces arousal from sleep. Buchanan (2019: 4-5) writes:

As can be imagined, acute rises in CO2 levels occur when an individual is unable to expel CO2, such as in the setting of an airway obstruction that might occur when an individual is lying prone in a crib or bed perhaps with a pillow and bedclothes covering the nose and mouth. It has been proposed that such a rise in CO2 would activate arousal circuitry in a normal baby to wake the baby up, cause them to cry out, summoning a caregiver who would come to their aid, and ostensibly correct the airway blockage to allow resumption of normal breathing [16,20,31]. It has been proposed, among other possibilities, that there is an impaired CO2-arousal system in SIDS-susceptible babies such that when they rebreathe CO2 as described above, they do not arouse, and thus do not cry out, and the blockage is not corrected [16,32]. They thus become acidotic and hypoxic and ultimately succumb.

So, if a babe’s airway gets blocked, for instance by a pillow or toy, they wake, cry out for attention and their caregiver comes to solve the problem or they change their laying position. But in SIDS cases, this does not occur. Why? Buchanan argues that those who succumb to sudden deaths like SIDS have screwy serotonin receptors—they ensure that blood oxygen and CO2 levels are healthy. But some of these infants may have brains that don’t allow them to detect the CO2 and blood oxygen levels—when the body may be suffocating. SIDS victims are usually found face-down in their cribs. But, there are no biomarkers for SIDS (Haynes, 2018). The SIDS diagnosis is only given after all other causes of death are ruled out—this is why SIDS is so mysterious. Genetic mutations have been posited as a cause (Männikkö et al, 2018), as has a pregnant mother smoking during pregancy, leading to a doubled risk of SIDS (Anderson et al, 2019).

But the best prevention against SIDS is nonprone sleeping—having the baby sleep on its back. The efficacy of this approach since the 1990ss has been noted (Gibson et al, 1992; de Luca and Hinide, 2016) while “Achieving recommended prenatal care and infant vaccinations, as well as reductions in maternal tobacco and substance use, has the potential to further reduce rates of SIDS and should be given as much attention as safe sleep advice in SIDS risk reduction campaigns” (Hauck and Tanabe, 2017: e289). The back-to-sleep program, though, has been associated with a decrease in motor development from the infant sending time in the supine position along with the strong possibility of developing plagiocephaly—which causes a “flat head” due to being placed in similar positions while the infant’s skull is soft and still developing (Miller et al, 2011). It has also been estimated that if it was known that the advice to place infants on their stomachs to sleep led to SIDS, then we “might have prevented over 10 000 infant deaths in the UK and at least 50 000 in Europe, the USA, and Australasia” (Gilbert et al, 2005: 884).

But the history of SIDS in America is a lot more sinister—rather than children dying from ‘natural causes’ (SIDS), in the 1970s, it was hypothesized by one SIDS researcher that SIDS was ‘genetic’ and ‘transmissible’ on the basis of one family who, unfortunately, had experienced this tragedy more than once.

This leads us to the story of Waneta Hoyt, who is the subject of this article.

Hoyt and Steinschneider: Genes vs environment

Horrible tragedies befell a woman from New York named Waneta Hoyt—five of her children had mysteriously died due to SIDS between the years of 1965-1971.

Waneta killed her first child, Eric who was three-months-old. SIDS is a diagnosis that is arrived at through a process of elimination—rule out all other causes at a young age (under 1) and the cause is then SIDS. But, the thing is, when an autopsy is performed on the infant, there is no difference between what would be said to be SIDS deaths and a light smothering.

After Waneta murdered her first child, she was cold and distant but it was not noticed. It was reported that she would never hold her children as a loving mother would, keeping them quite far from her. But it wasn’t until three years later that she, again, murdered. But this time it was two of her children—her two-year-old son and six-week-old daughter. The murders that Waneta were committing were wrongfully diagnosed as being due to SIDS.

This caught the attention of renowned SIDS researcher Alfred Steinschneider who had a clinic in which he specialized in caring for infants who were thought to be high-risk for SIDS. Steinschneider wanted to watch Waneta’s fourth child in his sleeping ward, in an attempt to prevent what he thought was due to SIDS. So, when he heard of Waneta’s story, he reached out to her to monitor her daughter, Molly.

The nurses at Steinschneider’s clinic, though, became suspicious of Waneta when she was at the clinic since she was cold and distant to Molly—she would not show her any affection. Steinschneider’s nurses emphatically told Steinschneider that it was Waneta who was murdering her children. Steinschneider shot back, and sent Molly home anyway. In an interview on the television program Deadly Women called Mothers Who Kill, one of the nurses who watched Molly before she was discharged by Steinschneider said:

And then about a quarter to eleven when we were getting ready to go off duty I said ‘Joyce, what do you think, do you think she’s still alive?’ Of course when I came on duty the next day she was dead.

This is wonderfully noted by Firstman and Talman in their book on Waneta’s case The Death of Innocents (1996):

Forty-eight hours later, on Thursday, June 4, Steinschneider scheduled Molly for her third discharge. By now, the nurses were speaking more openly about their suspicions. “I just know something’s going to happen,” Corrine Dower said to Thelma. “One of these times she’s going to do it.” Corrine was scornful of Steinschneider. “If he had any brains at all he would have seen that she didn’t want the baby,” she would say years later. “You can tell in the grocery store if a person cares about their child. We were just disgusted with Steinschneider.” (book excerpt from How Two Baby Deaths Led to a Misguided SIDS Theory)

Presumably, since this was Waneta’s fourth time experiencing the tragedy of SIDS, Steinschneider did not think that Waneta could be involved—but his nurses knew the truth. It was when Waneta had her fifth child that Steinschneider thought he would make his breakthrough in his research. Steinschneider was so convinced that the baby’s were dying due to SIDS, and he thought that if he could monitor Waneta’s new baby as much as possible, that he may figure out why babies die from SIDS.

Steinschneider believes that SIDS is hereditary—passed on through genes. The fifth child was watched at Steinschneider’s clinic and when Steinschneider discharged him—in an attempt to prove his theory—his nurses protested. Then, shortly after, Waneta called Steinschneider saying that it had happened again—her fifth child had mysteriously died.

After the death of Waneta’s fifth child, Steinschneider published his paper Prolonged Apnea and the Sudden Infant Death Syndrome: Clinical and Laboratory Observations arguing that SIDS was caused largely by hereditary sleep apnea (Steinschneider, 1972). By 1997, Steinschneider’s paper was the most-cited paper in the SIDS literature (Bergman, 1997). It was due to Steinschneider’s research, though, that parents began using sleep monitors to monitor their children’s sleep so they could be alerted in case their child had sleep apnea.

Steinschneider cared more about his research and theory of SIDS and sleep apnea over what was striking him right in the face—Waneta was responsible for the deaths of her five children. Steinschneider’s 1972 paper was cited and used for 22 years, until it was found upon an in-depth look into Steinschneider’s paper that what was clear to Steinschneider’s nurses and not him was true—Waneta was responsible for the deaths of her children. Steinschneider’s paper, in any case, concluded that SIDS is a genetic disorder and it was thusly inherited. And Waneta’s case, it seems, lent credence to his hypothesis. Steinschneider gave Waneta the perfect alibi—her woes were caused by a genetic disease and there was nothing that could have been done to prevent it.

Waneta was convicted in 1995 of five counts of murder and sentenced to 75 years in prison—therefore refuting Steinschneider’s theory. Three years after her sentence, though, Waneta died in prison of cancer. The case of Waneta Hoyt allowed mothers to kill their children in this specific way (a light smothering) for almost a quarter of a century.

Hickey, O’Brien, and Lighty (1996) write:

Norton saw history repeating itself in the reluctance of many factors to face the fact that some deaths attributed to SIDS were homicides. She agreed with the bulk of SIDS research, which pointed to apnea, or the cessation of breathing, as the final pathway to death. But there were many causes of apnea, not all of them natural. An adult could place a hand or a pillow over an infant’s nose and mouth and stop the child from breathing. The pressure needed to smother an infant often left no telltale signs, Norton explained.

“There is no way for the pathologist at autopsy to distinguish between homicidal smothering and SIDS,” she concluded.

Norton worried that homicides were being passed off as SIDS because many doctors held the erroneous belief that SIDS ran in families. They ignored large-scale studies that had shown no genetic tendency toward SIDS. Flouting conventional wisdom, Norton warned that the sudden, unexplained death of a SIDS victim’s sibling should be treated as a possible homicide.

When Waneta was convicted, letters to the editor were sent about Steinschneider’s paper. The short correction to the paper chronicles, interestingly, a letter to the editor of the journal Pediatrics, who published the Steinschneider paper

“But the paper indicated a more sinister possibility to Dr. John F. Hick of Minnesota. In a letter to the journal, he wrote that the case offered “circumstantial evidence suggesting a critical role for the mother in the death of her children.” (See below.)

But his warning was dismissed, until Mr. Fitzpatrick read the paper 15 years later.

“The medical records described two happy, healthy, perfectly normal kids,” he said. “It convinced me that these children were murdered.”

Hick’s letter to Pediatrics says:

In reporting two siblings who succumbed to “sudden infant death syndrome,” Steinschneider exposes an unparalleled family chronicle of infant death.’ Of five children, four died in early infancy and the other died without explanation at age 28 months. Prolonged apnea is proposed as the common denominator in the deaths, yet the author leaves many questions relevant to the fate of these children unanswered.

In her signed confession, Waneta said that she smothered her five children because their screaming made her “feel useless”, though Waneta later stated that she only said that to stop the police from questioning her. Steinschneider, like another motivated-reasoner J.P. Rushton, ignored data that did not fit his theory of sleep-apnea-induced-SIDS—specifically how Waneta acted around her children while at his clinic and the thoughts of his own nursing staff telling him not to discharge the Hoyt infants.

Waneta recalled her strangling of her children—specifically Julie:

”They just kept crying and crying. . . . I just picked up Julie and I put her into my arm, in between my arm and my neck like this . . . and I just kept squeezing and squeezing and squeezing.”

Steinschneider’s testimony during Waneta’s trial, however, is very interesting. Reported by the New York Times, Steinschneider attempted to defend his patient Waneta against claims that she had murdered her children:

Autopsies were done,” he said, speaking of Molly. “They could not find a known cause of death.”

This, Dr. Steinschneider said, “by definition” is SIDS.

But under intense cross-examination. Dr. Steinschneider conceded that he could not remember — and did not record — crucial details from the medical histories of the two infants, whom he had hospitalized for observation soon after birth. In each case, the parents had reported that the baby was having difficulty breathing and that its older siblings had died mysteriously.

The doctor also acknowledged concluding that Molly and Noah had died of SIDS without knowing how thoroughly the authorities had probed the “death scene” for evidence of other causes, including murder.

It is said—even by the prosecutor on her case—that Waneta suffered from Munchausen by proxy (Firstman and Talan, 1996)—which is the intentional cause of illness, usually on children, in order for the mother to elicit sympathy for others (Gehlawat et al, 2015). In cases like this, mothers who have the Munchausen syndrome will suffocate their children and then rush them to the hospital—they get the satisfaction of inflicting pain and then the satisfaction of getting cared for for the so-called mysterious death of their baby. One study of 51 sleep apnea monitorings found that about 40 percent of the program treated infants who had apnea that seemed to be induced by the parent; this was inferred from the fact that once the infants were admitted to the hospital, the doctors found no signs of apnea (Light and Sheridan, 1990).

One doctor even took it upon himself to place cameras in his practice in order to monitor parents that were suspected of abusing their children. Thirty-nine infants were monitored—thirty-three infants were being abused by their parents, what’s more is that some of the infants in this study who were identified in the video also had a sibling who mysteriously died from SIDS (Southall et al, 1997). What the study shows is that these parents were suffocating their children, causing their breathing problems and that they most likely have gotten away with infanticide before. Another case involved a mother taking her daughter to eleven different hospitals, but none of them found anything wrong with the girl and she ended up dying under suspicious circumstances (Hassler, Zamorski, and Weirich, 2007).

Conclusion

We now know that Steinschneider ignored contrary evidence to his theory of genetically-induced sleep apnea causing SIDS which apparently ran in families, and since he brushed off his nursing staff telling him that Waneta was acting strangely around her two children that he had admitted into his clinic, he could have saved their lives. But Steinschneider’s genetic determinist theory was more important than seeing what was clear as day to his staff and even others who read his 1972 paper—a mother was strangling her own infants.

SIDS has a long history, dating back to biblical times. But, in the modern-era, erroneous theories on the causes of SIDS were pushed while other, more obvious causes were disregarded in favor of a grand genetic theory of SIDS causation. Waneta and Steinschneider both helped each other out: Steinschneider (unknowingly) helped Waneta evade detection for 22 years while Waneta lent credence to the hypothesis that Steinschneider was developing. The fact that, at the time of their first meeting, three of Waneta’s children had died in almost the same fashion pointed to a genetic, inherited cause in Steinschneider’s eyes.

At the time of publication of The Death of Innocents, Steinschneider still continues to defend his now-discredited theory and still lobbies for the use of infant sleep monitors. Of course, since he testified FOR Waneta, despite the mounting evidence against her, he could be seen as an accomplice, however weakly. But this case shows one thing that should be well-known—researchers become attached to their pet hypotheses/theories and will ignore contrary evidence if it is brought to their attention. Firstman and Talman estimate that between 5 and 10 percent of SIDS cases are actually homicides. (But see Milroy and Kepron, 2017.)

Steinschneider created the SIDS disease on the basis of Waneta’s story—and a multi-million dollar industry then appeared due to his paper—it’s all to save infants, buy these sleep apnea monitors. But there were two children that Steinschneider did not—could not—save: He could have saved those babies, if not for his genetic determinist beliefs on SIDS causation. Had Steinshneider looked at the more obvious answer to the problem which was right in front of his face, he may have seen that Waneta suffered from Munchausen by Proxy, and, as evidenced from the references above, those who suffer from the disease act out exactly how Waneta did—by strangling their children with the cause of death being blamed on SIDS.

The Hoyt-Steinschneider case is a warning—don’t jump so quickly to implicate heredity in the ontology of X, especially when other, more obvious, tells are right there in front of you.

Gould, Bradbury, and Evolutionary Contingency

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I have been an avid reader and interested in astronomy/space ever since I could remember. I remember really loving Stephen Hawking and his documentaries on black holes. I would read anything I could find on constellations and stars. From there I went on to reading sci-fi. I then recall seeing The Martian Chronicles by Ray Bradbury and from then on I had become interested in sci-fi writing. But, as I grew older, I drifted away from sci-fi and now only read non-fiction. Then when I got older I got into ‘HBD’ (chronicled here) and along with it evolution—but, unlike other ‘HBDers’ I became enamored with the work of Gould, while some of my favorite books come from him. Gould wrote a lot about evolutionary contingency—the degree to which an outcome could be different. Evolutionary contingency is a big topic in philosophy of biology, and Bradbury has a great short story on this type of contingency.

Ray Bradbury is an interesting author—one who has many short stories and regular books. One of my favorite stories from Bradbury is one called A Sound of Thunder which chronicled a time machine company who let people go back in time to hunt any animal they’d like—if you want to take down the ancestor of a whale before it became aquatic, just name the place and they will send you there. They were told to only stay on the path laid out by the time machine company—animals they could shoot were marked with red paint, presumably those animals would have died anyway so killing them would not change any outcomes. The text from Bradbury is worth quoting in full, as it wonderfully captures the thought of evolutionary contingency:

He indicated a metal path that struck off into green wilderness, over streaming swamp, among giant ferns and palms. “And that,” he said, “is the Path, laid by Time Safari for your use, It floats six inches above the earth. Doesn’t touch so much as one grass blade, flower, or tree. It’s an anti-gravity metal. Its purpose is to keep you from touching this world of the past in any way. Stay on the Path. Don’t go off it. I repeat. Don’t go off. For any reason! If you fall off, there’s a penalty. And don’t shoot any animal we don’t okay.”

“Why?” asked Eckels.

They sat in the ancient wilderness. Far birds’ cries blew on a wind, and the smell of tar and an old salt sea, moist grasses, and flowers the color of blood.

“We don’t want to change the Future. We don’t belong here in the Past. The government doesn’t like us here. We have to pay big graft to keep our franchise. A Time Machine is finicky business. Not knowing it, we might kill an important animal, a small bird, a roach, a flower even, thus destroying an important link in a growing species.”

“That’s not clear,” said Eckels.

“All right,” Travis continued, “say we accidentally kill one mouse here. That means all the future families of this one particular mouse are destroyed, right?”

“Right”

“And all the families of the families of the families of that one mouse! With a stamp of your foot, you annihilate first one, then a dozen, then a thousand, a million, a billion possible mice!”

“So they’re dead,” said Eckels. “So what?”

“So what?” Travis snorted quietly. “Well, what about the foxes that’ll need those mice to survive? For want of ten mice, a fox dies. For want of ten foxes a lion starves. For want of a lion, all manner of insects, vultures, infinite billions of life forms are thrown into chaos and destruction. Eventually it all boils down to this: fifty-nine million years later, a caveman, one of a dozen on the entire world, goes hunting wild boar or saber-toothed tiger for food. But you, friend, have stepped on all the tigers in that region. By stepping on one single mouse. So the caveman starves. And the caveman, please note, is not just any expendable man, no! He is an entire future nation. From his loins would have sprung ten sons. From their loins one hundred sons, and thus onward to a civilization. Destroy this one man, and you destroy a race, a people, an entire history of life. It is comparable to slaying some of Adam’s grandchildren. The stomp of your foot, on one mouse, could start an earthquake, the effects of which could shake our earth and destinies down through Time, to their very foundations. With the death of that one caveman, a billion others yet unborn are throttled in the womb. Perhaps Rome never rises on its seven hills. Perhaps Europe is forever a dark forest, and only Asia waxes healthy and teeming. Step on a mouse and you crush the Pyramids. Step on a mouse and you leave your print, like a Grand Canyon, across Eternity. Queen Elizabeth might never be born, Washington might not cross the Delaware, there might never be a United States at all. So be careful. Stay on the Path. Never step off!”

“I see,” said Eckels. “Then it wouldn’t pay for us even to touch the grass?”

“Correct. Crushing certain plants could add up infinitesimally. A little error here would multiply in sixty million years, all out of proportion. Of course maybe our theory is wrong. Maybe Time can’t be changed by us. Or maybe it can be changed only in little subtle ways. A dead mouse here makes an insect imbalance there, a population disproportion later, a bad harvest further on, a depression, mass starvation, and finally, a change in social temperament in far-flung countries. Something much more subtle, like that. Perhaps only a soft breath, a whisper, a hair, pollen on the air, such a slight, slight change that unless you looked close you wouldn’t see it. Who knows? Who really can say he knows? We don’t know. We’re guessing. But until we do know for certain whether our messing around in Time can make a big roar or a little rustle in history, we’re being careful. This Machine, this Path, your clothing and bodies, were sterilized, as you know, before the journey. We wear these oxygen helmets so we can’t introduce our bacteria into an ancient atmosphere.”

This passage from Bradbury wonderfully illustrates evolutionary—historical—contingency. Things could have been different—this is the basis of the contingency argument. The universe does not repeat itself—if we were to replay the tape of life we would get a completely different outcome—Lane (2015) states maybe octopi would rule the earth? We could replay the tape of life, have it go exactly as it did to lead up to today, change ONE SEEMINGLY MINISCULE THING (say, stepping on a bug that did not die) which would then cascade throughout history leading to a change in the future. Evolution is full of passive trends, with no indication that—for example with body plans—that there is a drive to become more complex—it is passive (Gould, 1996: 207):

All the tests provide evidence for a passive trend and no drive to complexity. McShea found twenty-four cases of significant increases or decreases in comparing the range of modern descendants with an ancestor (out of a potential sample of ninety comparisons, or five groups of mammals, each with six variables measured in each of three ways; for the other comparison, average descendants did not differ significantly from ancestors). Interestingly, thirteen of these significant changes led to decreases in complexity, while only nine showed an increase. (The difference between thirteen and nine is not statistically significant, but I am wryly amused, given all traditional expectation in the other direction, that more comparisons show increasing rather than decreasing complexity.

Gould first put forth his contingency argument in Wonderful Life—any replay would be different then the next. Gould critiqued the increasing complexity claim, arguing that diversification is always accompanied by decimation—once a mass extinction (say, an asteroid impact) occurs, there will then be subsequent diversification after the decimation.

We have no idea why certain organisms persisted over others after periods of decimation—and ‘adaptation’ to environments cannot be the whole story. Out of all of Gould’s writing that I have read in my life, this passage is one of my favorites as it perfectly captures the problem at hand:

Wind the tape of life back to Burgess times, and let it play again. If Pikaia does not survive in the replay, we are wiped out of future history—all of us, from shark to robin to orangutan. And I don’t think that any handicapper, given Burgess evidence as known today, would have granted very favorable odds for the persistence of Pikaia.

And so, if you wish to ask the question of the ages—why do humans exist?—a major part of the answer, touching those aspects of the issue that science can treat at all, must be: because Pikaia survived the Burgess decimation. This response does not cite a single law of nature; it embodies no statement about predictable evolutionary pathways, no calculation of probabilities based on general rules of anatomy or ecology. The survival of Pikaia was a contingency of “just history.” I do not think that any “higher” answer can be given, and I cannot imagine that any resolution could be more fascinating. We are the offspring of history, and must establish our own paths in this most diverse and interesting of conceivable universes—one indifferent to our suffering, and therefore offering us maximal freedom to thrive, or to fail, in our own chosen way. (Gould, 1989: 323)


Contingency is about counterfactuals—what could have happened, what could have been, or what would have been had some certain condition changed, with everything before that occurring as usual. Bradbury’s A Sound of Thunder wonderfully illustrates the contingency of the evolutionary process—change one seemingly small, minuscule thing in the past and this could snowball and cascade to huge changes in the future—we may never have existed or we would have existed but have been radically different. If we could go back in time and, say, crush a butterfly and see the changes it would have made, we could say that the event that caused the future to change was the crushing of that butterfly—this could have, eventually, led to the non-existence of a certain group of people or a certain group of animals which would have radically changed the outcome of the world—both the natural and human world.

So, if we could replay life’s tape from the very beginning, I do believe that life as we know it would be different—for if we played it from the beginning, we could have a scenario as described by Bradbury—everything could go exactly the same with one small seemingly minuscule change snowballing into a world that we would barely recognize.

A History of the “Race” Concept

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The concept of “race” stretches back as long as human civilization. The concept of “racism” also stretches back just as far with it—they seem to be intertwined. There is a consensus, though, the term was constructed during the European Age of Exploration. This claim though, is false. The concept actually goes back at least 5,000 years. By looking at the art and reading the myths of these ancient civilizations, we can see that the social constructivist claim about race—that it is a recent creation—is false. They also described their physical features and also attempted to explain behavioral differences between races based on the limited knowledge they had in their day.

Sarich and Miele (2004) state that the PBS documentary on race—which is largely the main reason why they wrote their book Race: The Reality of Human Difference—claimed that race is a human invention and that since we create it we can then “unmake it.” We can look at art from ancient civilizations and see that they did sort people into groups based on their skin color and other physical characters. Each civilization, of course, thought itself and its racial features to be ‘superior’ to the others they encountered. The ancients used the set of observable features to describe what we now call “races.”

India

Our first trip on this long journey to understand the history of race is India. The earliest hints of what would become the caste system were written around 5kya. In the Rig Veda, a description of the Arya(n) invasion in the Indus valley where a dark-skinned people lived. The god of the Arya(n)s Indra “is described as “blowing away with supernatural might from earth and from the heavens the black skin which Indra hates” (Gossett, 1997: 3-4). They also called these dark-skinned people “Anasahs” which meant “the noseless people.” They then describe Indra killing all of the dark-skinned people and conquering the Indus for the Arya.

Sarich and Miele (2004: 47-48) note that the peoples that Indra hated were called Dasas—broad-nosed worshippers of the phallus. Even when Alexander the Great’s army reached India and described the Indians in the south of the country as some of the darkest people they have seen, they still made the distinction between Indians and Africans—by their hair type—so this tells us that race is more than ‘skin deep’ to the Greeks. Race, then, was known for thousands of years BEFORE the Age of Exploration.

Ancient China

We can look to ancient China, too, to see instances of racial descriptions and then racism along with it. For instance, a Chinese writer described yellow-haired, blue-eyed people from a distant province, “who greatly resembeled monkeys from whom they are descended” (Gossett, 1997: 4). Another Chinese legend describes differences between themselves and a brabarian tribe. A Chinese emperor stated that he would give his daughter to whomever slayed the chieftan he was having problems with. Then, the palace dog comes back with the head of the chieftan. The emperor did not go back on his word; he gave the dog his daughter and the resulting children were “fond of living in high altitudes and averse to plains” (Gossett, 1997: 4).

Like other civilizations, the ancient Han Chinese regarded other groups they came into contact with as barbarians. They were especially taken aback by the odd appearance of one group, the Yuehzi, because of their hairy, white, ruddy skin and their prominent noses, which the Chinese likened to those of monkeys.

[…]

The Han Chinese applied the term “Hu” to barbarians like the Yuehzi who had “deep eye sockets, prominent noses, and beards.” But they did not apply it to the Qiang, another barbarian group, who had a Mongoloid appearance and among whom some of the Yuezhi lived. Both groups were denigrated as uncivilized and inferior to the Chinese, but the Qiang were deemed to belong to the same racial stock, whereas the Yuezhi were viewed as being part of a very different stock, not only barbarian but ugly and monkey-like to boot.

Egypt

The Egyptians used a color-coding system—red (themselves), yellow (for their eastern enemies), black (Africans), and white (those from the north). The Eygptians also accurately depicted Africans as early as the third century BCE, describing them exactly how 19th-century European anthropologists would. Below is a picture of how the Egyptians depicted these groups.

raceegypt

There is, also, an interesting bit about colorism—discrimination based on skin color—here:

Color prejudice, says one writer, depended on which ethnic group held sway. When the lighter-skinned Egyptians were dominant they referred to the darker group as “the evil race of Ish.” On the other hand, when the darker-skinned Egyptians were in power, they resorted to calling the lighter-skinned people “the pale, degraded race of Arvad.” (Gossett, 1997: 4)

Jews

The Jews are some of the oldest peoples on earth, so they should then have some stories about their encounters with different races. One of the oldest, thought to be first, racist sayings was asked by the prophet Jeremiah who said “Can the Ethiopian change his skin or the leopard his spots?” The Jews are said to have ‘invented’ anti-black racism (Gossett, 1997: 5; Sarich and Miele, 2004), but this has been contested (Goldenberg, 1998). Take the full text from Gossett on Ham:

The most famous example of racism among the Jews is found in the legends which greew up concerning Ham, the son of Noah. The account in Genesis tells us of Ham’s expressing contempt for his father because Noah had become drunk and was lying in a naked stupor. Noah’s other sons had covered their father’s nakedness, averting their eyes. Noah blessed the descendants of Shem and Japeth, his other sons, but cursed the descendants of Ham. There is some confusion in the account in Genesis because it is not clear whether the curse was to be visited upon Ham or upon Canaan, Ham being a later insertion. Nothng is said in Genesis about the descendants of either Ham or Canaan being Negroes. This idea is not found untl the oral traditions of the Jews were collected in the Babylonian Talmud from the second century to the sixth centry A.D. In this source, the descendants of Ham are said to be cursed by being black. In the Talmud, there are several contradictory legends concerning Ham—onoe that God forbade anyone to have sexual relations on the Ark and Ham disobeyed this command. Another story is that Ham was cursed with blackness because he resented the fact that his father desired to have a fourth son. To prevent the birth of a rival heir, Ham is said to have castrated his father. Elsewhere in the Talmud, Ham’s descendants are depicted as being led into captivity with their buttocks uncovered as a sign of degredation.

Greeks and Romans

The Greeks and the Romans are really interesting. Being near the intersection of the Medditerranean, they would have seen many different races of people—and this is reflected in their art and legends. The Greek myth of Phaethon, for example, shows that the Greeks knew that skin color was a function of climate.

In the story, Phaethon asked his father to drive the sun chariot, using it only for the day. He could not control the chariot so it came to close to the earth in some regions, burning the people there while for the people in the north he drove too far away from the earth, ligtening their skin. Greek and Roman myths, in fact, show exactly how things change and that if we had a different reference point—like the Greeks and Romans did—we would then create different theories of ‘intelligence’:

“The nations inhabiting the cold places and those of Europe are full of spirit but somewhat deficient in intelligence and skill, so that they continue comparatively free, but lacking in political organization and the capacity to rule their neighbors. The peoples of Asia on the other hand are intelligent and skillful in temperament, but lack spirit, so that they are in continuous subjection and slavery. But the Greek race participates in both characters, just as it occupies the middle position geographically, for it is both spirited and intelligent; hence it continues to be free and to have very good political institutions, and to be capable of ruling all mankind if it attains constitutional unity.” (Pol. 1327b23-33, my italics)

Views of direct environmental influence and the porosity of bodies to these effects also entered the military machines of ancient empires, like that of the Romans. Offices such as Vegetius (De re militari, I/2) suggested avoiding recruiting troops from cold climates as they had too much blood and, hence, inadequate intelligence. Instead, he argued, troops from temperate climates be recruited, as they possess the right amount of blood, ensuring their fitness for camp discipline (Irby, 2016). Delicate and effemenizing land was also to be abandoned as soon as possible, according Manilius and Caesar (ibid). Probably the most famous geopolitical dictum of antiquity reflects exactly this plastic power of laces: “soft lands breed soft men”, according to the claim that Herodotus attributed to Cyrus. (Meloni, 2017: 41-42)

The Roman historian Vitruvius “attributed the keen intelligence of his countrymen to the rarity of the atmosphere and to the heat. The less fortunate northern peoples, “being enveloped in a dense atmosphere, and chilled by moisture from the obstructing air … have but a sluggish intelligence”” (Gossett, 1997: 7). How convenient—people at the time thought they were ‘superior’ to others and then attempted to justify it on the basis of environmental—eventually evolutionary—differences. However, the Greek theory of humors. Such accounts, though, only speak to how the Greeks thought that the environment shaped individuals, not shared traits of the group. Such differences were thought to be almost immediately reversible. They believed that one could take a person who grew up in another environment who, therefore, had a different temperment which could be changed by switching his environment.

Thus if there were, say, a microregion of Germany where “Asiatic” environmental conditions prevailed, a person who settled in that microregion would end up with Asian attributes. Thus, humoral accounts of human diversity focused on the way environments shape individuals, rather than the way populations share traits. (Smith, 2016: 85)

The Greeks and the Romans, ironically, seemed to be really big on environmentalism—the thesis that environment drives the proliferation of traits and that changing the environment can change ones phenotypic traits. While this is not wholly true, there is a kernel of truth here.

Sarich and Miele (2004: 51) describe different ancient scholar’s writings on their observations of racial differences:

The most detailed surviving description of the racially denning characteristics of black Africans from the classical world appears in The Moretum, a poem attributed to Virgil (circa 1st century AD). A female character named Scybale. is described as “African in race—her hair tightly curled, lips thick, color dark, chest broad, breasts pendulous, belly somewhat pinched, legs thick, and feet broad and ample.” In his book Blacks in Antiquity: Ethiopians in the Greco-Roman Experience, Frank M. Snowden comared the description with portrayls by twentieth-century anthropologists E. A Hootn and M. J Herskovits. For example, Hootn described the “outstanding features of the ancient specialized Negro division of manking” as “narrow heads and wide noses, thick lips and thin legs, protruding jaws and receding chins, integument rich in pigment but poor in hairy growth, flat feet and round foreheads, tiny curls and big smiles.”

Snowden concluded: “While the author of The Moretum was writing poetry, not anthropology,” his description of the distinguishing racial characteristics of black Africans “is good anthropology; in fact, the ancient and modern phraseology is so similar that the modern might be considered a translation of the ancient” (emphasis added).

Native Americans

I’m sure most have heard the popular ‘myth’ that God burnt blacks by cooking them too long. Come to find out, there is a real basis for this myth. The Native Americans thought that white people weren’t baked enough, blacks were baked too much and they were—like Goldilocks—juuuuust right:

Earthmaker made the world with trees and fields, with rivers, lakes, and springs, and with hills and valleys. It was beautiful. However, there weren’t any humans, and so one day he decided to make some.

He scooped out a hole in a stream bank and lined the hole with stones to make a hearth, and he built a fire there. Then he took some clay and made a small figure that he put in the hearth. While it baked, he took some twigs and made tongs. When he pulled the figure out of the fire and had let it cool, he moved its limbs and breathed life into it, and it walked away. Earthmaker nonetheless realized that it was only half-baked. That figure became the white people.

Earthmaker decided to try again, and so he made another figure and put it on the hearth. This time he took a nap under a tree while the figure baked, and he slept longer than he intended. When he pulled the second figure out of the fire and had let it cool, he moved its limbs and breathed life into it, and it walked away. Earthmaker realized that this figure was overbaked, and it became the black people.

Earthmaker decided to try one more time. He cleaned the ashes out of the hearth and built a new fire. Then he scooped up some clay and cleaned it of any twigs or leaves, so that it was pure. He made a little figure and put it on the hearth, and this time he sat by the hearth and watched carefully as the figure baked. When this figure was done, he pulled it out of the fire and let it cool. Then he moved its limbs and breathed life into it, and it walked away. This figure was baked just right, and it became the red people. (A Potawatomi Story)

Islam

The first peoples to describe Africans in a racist manner was not Europeans, it was the Arabs—Islamics. They held slaves long before Europeans; they even castrated their slaves. Jahiz of Basra described Africans as “people of black color, flat noses, kinky hair.”…despite their dimness, their boundless stupidity, their crude prceptions and their evil dispositions” is how Jahiz of Basra described Africans. Ibn Khaldun stated “The only people who accept slavery are the Negroes, owing to their low degree of humanity and their proximity to the animal stage.” Nasir al-Din Tusi stated “Many have observed that the ape is more teachable than the Zanji [African].” (All quotes from Sarich and Miele, 2004: 60).

Conclusion

What this little tour of the concept of race throughout history tells us one thing: The concept ‘race’ is not a European invention—races were not socially constructed in 1492. They were constructed thousands of years in the past by many different peoples who had different explanations for the racial differences they had observed. While some of them, for their time, are great explanations for the observed differences, there was an element of racial prejudice, even all of those thousands of years ago. Yes, race is partly socially constructed (as evidenced here) but that social construction has a real, biological basis behind it.

It is obvious that the concept of ‘race’ and ‘racism’ went hand-in-hand all throughout antiquity. It is only today, it seems, that we can attempt to use the concept of race without having any ‘racist’ undertones. Though, the tour we went on proves one thing: race exists and was known to have existed for thousands of years.

Transracialism

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Rachael Dolezal attracted media attention in 2015 since she, as a white women, presented and ‘acted’ what Americans would describe as (the socialrace) “black.” She was the former chapter president for the NAACP (National Association for the Advancement of Colored People) and former Africana studies instructor; when it was discovered that she had two white parents she resigned from the chapter. Her white parents then came out and said that she was “passing as black.” And, from looking at her appearance, one would be hardpressed to say that she did NOT look black and that she DID NOT attempt to make her appearance LOOK what the average American would describe as (the socialrace) “black.” In any case, though, the controversy is an interesting one: should she be able to self-identify as black, even though none of her (recent) ancestors derive from the African continent? I will discuss Quayshawn Spencer’s (2019) take on the Dolezal controversy then I will discuss my own thoughts on the matter.

The earliest use of the term “transracialism” I can find is from 2004, from Overall (2004) who states that transracialism is the “use of surgery to assist individuals to “cross” from being a member of one race to being a member of another” and that, if it is “morally acceptable” for one to have a surgery to have the sex they feel they should be, then it should be morally acceptable for one to have a surgery to change their race. (With this, I am reminded of the South Park episode where Kyle wanted to be black and play basketball so he went and got a “Negroscopy.”) Others, though, argue that transracialism does not exist (Botts, 2018). In any case, transracialism can be defined as the feeling of being a race other than what society has said your race is—even though, by attempting to “pass” as another race, society may see the individual in question as “black”, for example.

If one is black in America then, surely, there is a high chance that they have experienced what it is like TO BE, black in America, socially. In this specific case, has Dolezal ever experienced any sort of racial discrimination based on how she looks and presents herself, as a black woman? She claims to have been the victim of anti-black hate crimes by police, went to a HBCU (historically black college university) and, as stated, has changed her appearance in order to give off the “aura” that she is black, by tightly curling her and lightly tanning her skin—what black Americans would term a “high-yellow.” Her ex-husband is black. She ticks off the “black/African American” box on job applications. So, knowing all of this about Dolezal, and how she presents herself to the public, is she “black” socially?

“I was actually identified when I was doing human rights work in north Idaho as first transracial” Dolezal, 2015

When Dolezal filed anti-black hate crimes with the Spokane police, she was asked about her experience and then the reporter asked her if she was black. Dolezal responded by then ending the interview. Then, ABC found her birth parents who admitted that she was true of Caucasian (European) descent. Case closed? But wait: Dolezal eventually admitted that she was indeed born white, even though she used the terms “black” and “African American” to describe herself.

One debate was about whether Dolezal could accurately claim to be racially Black without posessing what was called Black ancestry in the conversation. 50 Furthermore, this debate was at least partially motivated by a genuine concern about whether Dolezal was taking away educational or employment opportunities that were intended for people with Black ancestry. For example, during Dolezal’s interview on The Real, co-host Loni Love said that she didn’t care about how Dolezal racially identified, but she did care about whether Dolezal marked ‘Black’ on her college applications because that act could have taken away scholarship money from a student with Black ancestry. 51 Interestingly, Dolezal said that Howard’s college application didn’t ask about race, but she did say that she marked ‘Black’ on her job application to Spokane’s Office of Police Ombudsman Commission. Furthermore, Dolezal said she marked ‘Black’ because “we all have human origins in Africa.” (Spencer, 2019: 252)

However, even though Dolezal may be “black-passing”, under her carefully constructed persona, she does look like a typical white American woman—indeed, I have seen many white women with hair like hers (not all had their hair done to look that way, either). In a 2015 interview, her adopted brother said that what Dolezal was doing was “blackface.” He recalls:

“She told me not to blow her cover about the fact that she had this secret life or alternate identity,” Ezra Dolezal said Saturday. “She told me not to tell anybody about Montana or her family over there. She said she was starting a new life … and this one person over there was actually going to be her black father.”

Let’s say that Dolezal did do this; she ‘constructed’ herself a fake ‘family’ where she has a black mother, black father and black siblings. She then goes out with them and the public sees them together. Rachael, by extension of being with her family, is now treated as “black”—since being “black” in America is social—is she now “black”? BUT, Dolezal seemed to be using “white privilege” when she would attempt to “black-pass” when convenient while “white-pass” when convenient—for instance, when she sued Brown for discriminating against her because she is white! Did she mark “black” on this application and then sue for being discriminated against for being white?

An example of this debate can be found once again during Dolezal’s interview on The Real. In that interview, co-host Tamar Braxton expressed exactly [the concern that Dolezal is a ‘race-shifter’] when she asked whether Dolezal thought she had “walked the walk of a Black woman.” Interestingly, Dolezal responded, “Absolutely,” and followed that up with, “the police mark ‘Black’ on my traffic tickets.” (Spencer, 2019: 253)

But it is easy to show that Dolezal’s claim about us all having African ancestry so there is nothing wrong with her putting “black” on employment forms and whatnot—racial membership is about “genomic ancestry, not ancestry simpliciter” (Spencer, 2019: 277, note 52). All living humans have African ancestry but not all living humans have genomic African ancestry. While the social is involved in OMB race theory, other conditions need to hold for one to be a member of a race.

Those that appear and present themselves as white are still considered black (Ginsberg, 1996; Hobbs, 2016). One could, for example, imagine an extremely light-skinned black—say like Beyonce—and ALMOST say “Oh, she’s white”, but something is off about the appearance, she does not look what the average American would term WHITE and so, after more inspection, she is—rightly—deemed ‘black.’ Thus, just because one presents themselves as a certain race, this does not mean that they ARE or BECOME that race. Race is NOT like a costume that one can choose to dress in and take it off at the end of the day—and while RACE is, partly, about one’s lived experiences in a racialized society, it is also about how society treats the individual they have deemed to be a certain race as well. While people are torn on Dolezal, the fact remains that she has altered her appearance considerably enough to “pass for” black.

‘White-passing blacks’, of course, have a ton of white (European) ancestry—which is how they can have light skin while still keep certain prominent ‘black’ features, such as the lips and nose. One story of a family that ‘white-passed’ is given in A Chosen Exile:

In California, the young woman passed as white. She married a white man, and they had children who never knew they had black blood. Then, one day, years later, her phone rang.

It was the woman’s mother with distressing news: Her father was dying, and she needed to return home immediately to tell him goodbye.

The cousin replied, “I can’t. I’m a white woman now.”

She missed her father’s funeral, and never saw her mother or siblings again.

Did this woman all of a sudden become white since she disavowed her family since she is “a white woman now?” If society treats her as ‘white’, is she white, disregarding her racial ancestry? Using Hardimon’s (2017) socialrace, yes, she would then be ‘white’ in America—but she, biologically, would still be ‘black.’

Asian eyes, white eyes?

Stories like this make me think back to a book I read in the seventh grade called Goodbye Vietnam (Whelan, 1993). From what I recall in the book all those years ago, the Vietnamese girl described Asians getting surgeries to change their eyelids (called a blepharoplasty) so they can ‘white-pass’, which would be ‘transracialism’ under Overall’s (2004) definition. Take this story from a plastic surgeon:

Millard first considered altering the human eye while reconstructing eyebrows for burn victims. He began to keenly study the eye, socket, and folds, musing how to change it from “Oriental to Occidental.”

Upon researching the operation, Millard found that surgeons in Japan, Hong Kong, and even Korea were already performing double-eyelid procedures for both medical and cosmetic reasons. Unable to find any publications about the surgery that were written in English, Millard devised his own operation. He decided to raise the nasal bridge and widen the eyes to reduce the “Asian-ness” of his patient’s visage. Millard first transplanted cartilage to the nose. He then tore the inner fold of the eyelid, removed fat resting above the eye, and sutured folds of skin together, creating a double eyelid. The interpreter was pleased with Millard’s work, and reported that after the operation, his ethnicity was often mistaken for Italian or Mexican.

For example, Kaw (1993: 75) writes that “the attempts by Asian American women to get the double-eyelid surgery “is an attempt to escape persisting racial prejudice that correlates their stereotyped genetic physical features (“small, slanty” eyes and a “flat” nose) with negative behavioral characteristics, such as passivity, dullness, and a lack of sociability.” The first writings of such a surgery in Asia, though, was in the 18th century, long before a strong European presence on the continent (Nguyen, Hsu, and Din, 2009) but I’m sure one can say that they saw Europeans over the ages and attempted to emulate what they saw. Nevertheless, this does seem to be a good case study into the Asian eyes, white eyes claim—they needed to attempt to ‘white-pass’ so they would not go to the concentration camps for the Japanese.

This is a good example of transracialism as stated by Overall; they attempted to ‘white-pass’ but it was for a reason—to live free. They would, presumably, then blend into society as their chosen race (or unchosen race), showing that one can, indeed, change their race by changing their outward appearance since race in America is partly (or fully depending on your view) based on one’s physical appearance—one’s phenotype, which they have some degree of control over.

Conclusion

Is Dolezal black? No, she is not. She can ‘black-pass’ all she wants, she can say that “We’re all African” all she wants, she can say that police mark her as black all she wants (and while she would be socially ‘black’, which is what she is going for, she is not ‘black’ in the OMB way), she can say that she ticks off the “black/African American’ box on applications, but this would only very weakly mean that she is ‘black.’ In virtue of having NO recent African ancestry, Dolezal is NOT black and is, therefore, running around in blackface. One cannot change their biological race, but it may be possible to change their socialrace—which race society says one is.

The many cases one can find on blacks that ‘white-pass’ and even those blacks that have NO IDEA that they ARE black speaks to the complex nature of ‘race’ in America. Yes, race is partially socially constructed and if we are going plainly off of how Americans in society state what ‘race’ is, just based on appearance, one would be hardpressed to say that Dolezal is not ‘black’—she ‘looks’ it, right? So Dolezal can be said to be ‘black-passing’ just as the woman mentioned above could be said to be ‘white-passing’—but this does not CHANGE THEIR RACE!

The case of blepharoplasties is interesting and further lends something to this discussion—certain Asian groups in America, and back home in their countries, attempted to have the double-eyelid surgery in order to change their appearance—some of them doing so to ‘white-pass’ so that they would not get sent to the concentration camps in America.

Lastly, there was a woman a few years back who had melanin injections in her skin and had botox and whatnot to change the appearance of her lips—her change is shocking, to say the least, and is an example of Overall’s definition of transracialism.

I did not discuss the Hypatia controversy (Tuvel, 2017) (I will do so in the future), but here is Tuvel’s argument:

(1) We accept the following premises about trans people and the rights and dignity to which they are entitled; (2) we also accept the following premises about identities and identity change in general; (3) therefore, the common arguments against transracialism fail, and we should accept that there’s little apparent logically coherent reason to deny the possibility of genuine transracialism.

Race, Gender, and the SAT

2200 words

IQ-ists like to talk about the correlation between “IQ” tests and scholastic achievement tests like the SAT (Scholastic Assessment Test) and how this is one piece of evidence for the ‘validity’ of IQ—the same kinds of score distributions noted on the SAT are also noted in the ‘standard IQ tests.’ However, a confusion rests with the IQ-ists. They, circularly, point to the fact that there is a high correlation between “IQ tests” and the SAT. But what they fail to realize—and what I rarely see discussed—is the process of item selection and removal has a strong impact on scores. Such score differences are, indeed, built-in to the SAT, just as they are for IQ.

The SAT was created in 1924 by eugenicist Carl Brigham—one of the psychologists who also worked on the Army Alpha tests. When he created the test, it was called the Scholastic Aptitude Test. Harvard then used the test as an admissions test and then other Ivy League schools used it as a scholarship test. The SAT was developed directly off of the first IQ tests—so they are intricately linked. First, I will talk about gender differences; second I will talk about race differences. Then I will discuss how and why these differences persist.

Gender differences in the SAT

Differences in IQ were built-out of the test (like with Terman’s Stanford-Binet test), but for the SAT, items and subtests were directly chosen BECAUSE they showed a gap in knowledge between the two groups. Men have always scored higher on the SAT than women since the test’s inception which was due to men’s higher math scores while this was partially off-set by women’s higher verbal scores. However, the ETS then changed the test in the late 80s, stating that there was then “a better balance for the scores between the sexes” (quoted in Rosser, 1989: 38)—which was an eleven-point score advantage for men. They had added more verbal items that favored men, but they did not add more math items which favored women. BUT, interestingly, girls have higher GPAs than boys.

For example, of all of the SAT math questions, the one that produced the largest gender gap was a question in which the win-loss record of a basketball team needed to be computed, which is noted by Rosser (1989: 40-41) in tables 2 and 3:

satgender1

satgender2

Interestingly, Rosser (1989: 19) reports that in one county in Maryland, where boys and girls took the same advanced math courses, girls outscored boys academically, but they had SAT-M scores 37-47 points lower than boys. The kinds of items that go onto a test are tried-out on a sample of children, and then the kinds of distributions the constructors want is what they get. For example, by adding/subtracting certain questions and subtests, they can get what they want to see. Rosser (1989) notes that “if the 10 most “pro-boy” items were replaced with items similar to the 10 most “pro-girl” items, boys nationally would outscore girls by about 29 points thus eliminating more than a third of the existing gender gap” (pg 23). Further, for the 1986 SAT, if the ten items that favored boys the most were removed and were replaced by items that favored girls more, then girls would outscore boys by 4 points. In virtue of what was the current test the ‘right’ one, and what justifies the assumptions of the ETS? But in Rosser’s (1989) analysis, “Hispanic” women showed the largest gap while African-American women had the lowest gap when compared with men of their own ‘race.’ See some examples from the Appendixes on some of the items which showed the most extreme sex differences (pg 156-161):

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Looking at types of questions such as these—and understanding how the SAT has evolved regarding gender differences since its inception since the mid-1920s—will understand how and why boys and girls score differently. For, if different assumptions were had on the ‘nature’ of ‘cognitive’ differences between boys and girls, more questions favoring girls would be added and then, we would be having a whole different kind of conversation right now.

When it comes to math, though, Niederle and Vesterlund (2010: 140) conclude:

… that competitive pressure may cause gender differences in test scores that exaggerate the underlying gender differences in math skills.

Women are, furthermore, less likely to guess (that is, less likely to risk-take) compared to men. This then translates to the testing environment where a guess is penalized while leaving it blank is not.

The new SAT has disadvantaged female testers; the AEI has stated that such differences have persisted for 50 years. Yes, SAT-M score differences are there, but, as noted above, when children were taught in the same advanced maths classroom, girls outperformed boys but they ended up scoring lower on the SAT-M section than boys—and looking at the SAT-M questions points us to why this paradox occurs. And, to top it all off, the SAT “underpredicts first-year college performance for women and overpredicts for men — thus violating one of the testers’ own, specially designed standard of validity” (Mensh and Mensh, 1991: 71).

Race and the SAT

Now, we turn to race and the SAT. Kidder and Rosner (2002) studied 100000 SAT test-takers in 1989 and also included another database of over 200000 people in New York. They examined around 580 SAT questions between the years 1988-89 and noted the percentage of questions that white, black, and Mexican students answered correctly. If 60 percent of whites answered a question correctly and only 20 percent of blacks did, then the racial impact was 40 percent for that question. For 78 verbal items, whites answered 59.8 percent correctly while blacks answered 46.4 percent correctly, for a racial impact of 13.4 (Kidder and Rosner, 2002: 148).

How are such differences explained? Of the six sections on the SAT, the ETS uses one of the sections for experimental test items. By using whites as a reference, if blacks or another group answers more questions correctly than whites, the item is discarded as invalid. Kidder and Rosner (2002) note that for an item with medium difficulty, whites scored 62 percent correctly while blacks answered 38 percent correctly. But, comparing a question with similar difficulty showed that blacks outscored whites by 8 percent, and 9 percent of women outscored men on the same question. Au (2008: 66) explains:

Test designers determined that this question, where African Americans scored higher than hites (and women higher than men), was psychometrically invalid and was not included in future SATs. The reason for this was that ETS bases its test question selection on statistics established by performance averages on previous tests: The students who statistically on average score higher on the SAT did not answer this question correctly enough of the time, while those who statistically on average score lower on the SAT answered this question correctly too often. By psychometric standards this means that this question was an anomaly and therefore was not considered a “valid” or “reliable” test question for a standardized test such as the SAT. White students outperform black students on the SAT. Higher-scoring students, who tend to be white, correctly answer SAT experiemental test questions at higher rates than typically lower scoring students, who tend to be non-White, ensuring that the test question selection process itself has a relf-reinforcing, racial bias.

Rosner, in his article On White Preferences, explains this well:

I don’t believe that ETS–the Educational Testing Service, the developer of the SAT and the source of this October 1998 test data–intended for the SAT to be a white preference test. However, the “scientific” test construction methods the company uses inexorably lead to this result. Each individual SAT question ETS chooses is required to parallel the outcomes of the test overall. So, if high-scoring test-takers–who are more likely to be white–tend to answer the question correctly in pretesting, it’s a worthy SAT question; if not, it’s thrown out. Race and ethnicity are not considered explicitly, but racially disparate scores drive question selection, which in turn reproduces racially disparate test results in an internally reinforcing cycle.

My considered hypothesis is that every question chosen to appear on every SAT in the past ten years has favored whites over blacks. The same pattern holds true on the LSAT and the other popular admissions tests, since they are developed similarly. The SAT question selection process has never, to my knowledge, been examined from this perspective. And the deeper one looks, the worse things get. For example, while all the questions on the October 1998 SAT favored whites over blacks, approximately one-fifth showed huge, 20 percent gaps favoring whites. Skewed question selection certainly contributes to the large test score disparities between blacks and whites.

So, in order to attempt to rectify this situation, the College Board wants to award out “adversity points”. Their SAT scores would be compared to their parental SES level and adjustments would then be made to their scores. Further, there was discussion on whether or not to give 230 “bonus points” to blacks, 130 to “Hispanics” and penalize Asians by 50 points.

But why do Asians score slightly higher than whites? Simple: they, too, would be in the group of higher-scoring students and, therefore, the test items would—indirectly—be shaped to them. The same holds for ‘Hispanics’ and blacks, as Kidder and Rosner note (regarding test questions), and so, the same would hold for Asians and whites. I think such discussions of “bonus points” and penalization on such tests, while a start, does not get to the assumptions so baked-in to these kinds of tests. Such tests are biased in virtue of the content on them—that is, the item content.

Kidder and Rosner (2002: 210) conclude:

… by reminding readers that, based on our empirical findings and review of the educational measurement literature, the process currently used to construct the SAT, LSAT, GRE, and similar tests unintentionally operates to select questions with larger racial and ethnic disparities (favoring Whites).

Conclusion

While, of course, test-prep can be identified as a factor that causes X group to score higher than Y group, other, more valid hypotheses can be—and have been—considered. Analyzing the items on these tests, we see that they are far from ‘objective’ ‘measures’ of ‘ability.’ The IQ-ist will cry that there is some’thing’ being measured in virtue of the correlation between the SAT and IQ—but, no ‘thing’ is being measured by any of these tests (Nash, 1990); they were created for the sole purpose of justifying and reproducing our current social hierarchies (Mensh and Mensh, 1991; Au, 2009; Garisson, 2009).

One needs only to know how such items are selected for inclusion on these tests. Andrew Strenio writes in his book The Testing Trap (1981: 95):

We look at individual questions and see how many people get them right, and which people get them right. We consciously and deliberately select questions so that the kind of people who scored low on the pretest will score low on subsequent tests. We do the same for the middle or high scorers. We are imposing our will on the outcome.

Only one way, though, exists for test constructors to do so—and this is to presuppose, a priori, who the high, middle and low scorers are and construct the test accordingly.

Take a thought experiment in a world in which our society was reversed. Blacks outscored whites and had better life prospects and the same holds for men and women. The hereditarians in this imagined world would then see that the scores on these tests correlated with smaller brain sizes, a lower amount of neurons, and whatnot. What, then, could the test constructors say justify how women and blacks scored higher than men and whites?

Though these are 35-year-old questions, I fail to see why there would be any changes in 2020—test construction has not changed. Such assumptions are, as argued at-length, built into the test. The outcome of these tests, of course, is determined by the nature of the content of the test—the test’s questions. IQ-ists, then, point to the score differentials between groups (men/women, blacks/whites, etc) and then say “See! There are differences so we are not all-the-same-blank-slates!” But statements like this fail to appreciate how tests are constructed—they believe that these tests are ‘objective “measures”‘ and that it, in a way, shows one’s ‘genetic potential’—and this claim is false.

If the nature of the test’s questions—which items are chosen for inclusion on the test—are determined by test constructors and the experimental questions on the SAT—of which whites are more likely to score higher—then it will indeed follow (and empirical evidence shows this) that what drives such large score disparities between whites and blacks on the SAT is, in fact, biased test questions. The same, too, holds for the differences between men and women. Change the assumptions, change the nature and the outcome of the test, then change what you study to ‘find’ the differences ‘causing’ such test score differences between groups. Hopefully, putting it in this way will show the absurdity of using biased tests to show that ‘biology’ is somehow responsible for score differences between groups.

Such inequalities in standardized test scores like the SAT—just like IQ—then, is structured into the test itself—so, tests like this only reproduce the differences between groups that they claim to ‘measure’—which is a circular claim. Studies like this show the folly of thinking that one group is ‘genetically smarter’ than another—which is what the hereditarians set out to prove. Too bad they have no meausuring unit, object of measurment or measured object.