“the study of the brains of human races would lose most of its interest and utility” if variation in size counted for nothing ([Broca] 1861 , p. 141). Quoted in Gould, 1996: 115)
The law is: small brain, little achievement; great brain, great achievement (Ridpath, 1891: 571)
I can’t hope to give as good a review as Gould’s review in Mismeasure of Man on the history of skull measuring, but I will try to show that hereditarians are mistaken in their brain size-IQ correlations and racial differences in brain size as a whole.
The claim that brain size is causal for differences in intelligence is not new. Although over the last few hundred years there has been back and forth arguments on this issue, it is generally believed that there are racial differences in brain size and that this racial difference in brain size accounted for civilizational accomplishments, among other things. Notions from Samuel Morton which seem to have been revived by Rushton in the 80s while formulating his r/K selection theory show that the racism that was incipient in the time period never left us, even after 1964. Rushton and others merely revived the racist thought of those from the 1800s.
Using MRI scans (Rushton and Ankney, 2009) and measuring the physical skull, Rushton asserted that the differences in brain size and quality between races accounted for differences in IQ. Although Rushton was not alone in this belief, this belief on the relationship between brain weight/structure and intelligence goes back centuries. In this article, I will review studies on racial differences in brain size and see if Rushton et al’s conclusions hold on not only brain size being causally efficacious for IQ but there being racial and differences in brain size and the brain size and IQ correlation.
The Morton debate
Morton’s skull collection has received much attention over the years. Gould (1978) first questioned Morton’s results on the ranking of skulls. He argued that when the data was properly reinterpreted, “all races have approximately equal capacities.” The skulls in Morton’s collection were collected from all over. Morton’s men even robbed graves to procure skulls for Morton, even going as far to take “bodies in front of grieving relatives and boiled flesh off fresh corpses” (Fabian, 2010: 178). One man even told Morton that grave robbing gave him a “rascally pleasure” (Fabian, 2010: 15). Indeed, grave robbing seems to have been a way to procure many skulls which were used in these kinds of analyses (Monarrez et al, 2022). Nevertheless, since skulls house brains, the thought is that by measuring skulls then we can ascertain the brain of the individual that the skull belonged to. A larger skull would imply a larger brain. And larger brains, it was said, belong to more “intelligent” people. This assumption was one that was held by the neurologist Broca, and this then justified using brain weight as a measure of intelligence. Though in 1836, an anti-racist Tiedemann (1836) argued that there were no differences in brain size between whites and blacks. (Also see Gould, 1999 for a reanalysis of Tiedemann where he shows C > M > N in brain size, but concludes that the “differencesare tiny and probably of no significancein the judgment of intelligence” (p 10).) It is interesting to note that Tiedemann and Morton worked with pretty much the same data, but they came to different conclusions (Gould, 1999; Mitchell, 2018).
In 1981 Gould published his landmark book The Mismeasure of Man (Gould, 1981/1996). In the book, he argued that bias—sometimes unconscious—pervaded science and that Morton’s work on his skull collection was a great example of this type of bias. Gould (1996: 140) listed many reasons why group (race) differences in brain size have never been demonstrated, citing Tobias (1970):
After all, what can be simpler than weighing a brain?—take it out, and put it on the scale. One set of difficulties refers to problems of measurement itself: at what level is the brain severed from the spinal cord; are the meninges removed or not (meninges are the brain’s covering membranes, and the dura mater, or thick outer covering, weighs 50 to 60 grams); how much time elapsed after death; was the brain preserved in any fluid before weighing and, if so, for how long; at what temperature was the brain preserved after death. Most literature does not specify these factors adequately, and studies made by different scientists usually cannot be compared. Even when we can be sure that the same object has been measured in the same way under the same conditions, a second set of biases intervenes—influences upon brain size with no direct tie to the desired properties of intelligence or racial affiliation: sex, body size, age, nutrition, nonnutritional environment, occupation, and cause of death.
Nevertheless, in Mismeasure, Gould argued that Morton had unconscious bias where he packed the skulls of smaller African skulls more loosely while he would pack the skulls of a smaller Caucasian skull tighter (Gould made this inference due to the disconnect between Morton’s lead shot and seed measurements).
Plausible scenarios are easy to construct. Morton, measuring by seed, picks up a threateningly large black skull, fills it lightly and gives it a few desultory shakes. Next, he takes a distressingly small Caucasian skull, shakes hard, and pushes mightily at the foramen magnum with his thumb. It is easily done, without conscious motivation; expectation is a powerful guide to action. (1996: 97)
…
Yet through all this juggling, I detect no sign of fraud or conscious manipulation. Morton mad e no attempt to cove r his tracks and I must presume that he was unaware he had left them. He explained all his procedure s and published all his raw data. All I can discern is an a priori conviction about racial ranking so powerful that it directed his tabulations along preestablished lines. Yet Morton was widely hailed as the objectivist of his age, the man who would rescue American science from the mire of unsupported speculation. (1996: 101)
But in 2011, a team of researchers tried to argue that Morton did not manipulate data to fit his a priori biases (Lewis et al, 2011). They claimed that “most of Gould’s criticisms are poorly supported or falsified.” They argued that Morton’s measurements were reliable and that Morton really was the scientific objectivist many claimed him to be. Of course, since Gould died in 2002 shortly after publishing his magnum opus The Stuecure of Evolutionary Theory, Gould could not defend his arguments against Morton.
Weisberg (2014) was the first to argue against Lewis et al’s conclusions on Gould. Weisberg argued that while Gould sometimes overstated his case, most of his arguments were sound. Weisberg argued that, contra what Lewis et al claimed, they did not falsify Gould’s claim, which was that the difference between shot and seed measurements showed Morton’s unconscious racial bias. While Weisberg rightly states that Lewis et al uncovered some errors that Gould made, they did not successfully refute two of Gould’s main claims: “that there is evidence that Morton’s seed‐based measurements exhibit racial bias and that there are no significant differences in mean cranial capacities across races in Morton’s collection.”
There is prima facie evidence of racial bias in Morton’s (or his assistant’s) seed‐basedmeasurements. This argument is based on Gould’s accurate analysis of the difference between the seed‐ and shot‐based measurements of the same crania.
Gould is also correct about two other major issues. First, sexual dimorphism is a very suspicious source of bias in Morton’s reported averages. Since Morton identified most of his sample by sex, this is something that he could have investigated and corrected for. Second, when one takes appropriately weighted grand means of Morton’s data, and excludes obvious sources of bias including sexual dimorphism, then the average cranial capacity of the five racial groups in Morton’s collection is very similar. This was probably the point that Gould cared most about. It has been reinforced by my analysis.
[This is Weisberg’s reanalysis]
So Weisberg successfully defended Gould’s claim that there are no general differences in the races as ascribed by Morton and his contemporaries.
In 2015, another defense of Gould was mounted (Kaplan, Pigliucci and Banta, 2015). Like Weisberg before them, they also state that Gould got some things right and some things wrong, but his main arguments weren’t touched by Lewis et al. Kaplan et al stated that while Gould was right to reject Morton’s data, he was wrong to believe that “a more appropriate analysis was available.” They also argue due to the “poor datasetno legitimateinferences to“natural” populations can be drawn.” (See Luchetti, 2022 for a great discussion of Kaplan, Pigliucci and Banta.)
In 2016, Weisberg and Paul (2016) argued that Gould assumed that Morton’s lead shot method was an objective way to ascertain the cranial capacities of skulls. Gould’s argument rested on the differences between lead shot and seed. Then in 2018, Mitchell (2018) published a paper where he discovered lost notes of Morton’s and he argued that Gould was wrong. He, however, admitted that Gould’s strongest argument was untouched—the “measurement issue” (Weisberg and Paul, 2016) was Gould’s strongest argument, deemed “perceptive” by Mitchell. In any case, Mitchell showed that the case of Morton isn’t one of an objective scientist looking to explain the world sans subjective bias—Morton’s a priori biases were strong and strongly influenced his thinking.
Lastly, ironically Rushton used Morton’s data from Gould’s (1978) critique, but didn’t seem to understand why Gould wrote the paper, nor why Morton’s methodology was highly suspect. Rushton basically took the unweighted average for “Ancient Caucasian” skulls, and the sex/age of the skulls weren’t known. He also—coincidentally I’m sure—increased the “Mongoloid skull” size from 85 to 85.5cc (Gould’s table had it as 85cc). Amazingly—and totally coincidentally, I’m sure—Rushton miscited Gould’s table and basically combined Morton’s and Gould’s data, increased the skull size slightly of “Mongoloids” and used the unweighted average of “Ancient Caucasian” skulls (Cain and Vanderwolf, 1990). How honest of Rushton. It’s ironic how people say that Gould lied about Morton’s data and that Gould was a fraud, when in all actuality, Rushton was the real fraud, never recanting on his r/K theory, and now we can see that Rushton actually miscited and combined Gould’s and Morton’s results and made assumptions without valid justification.
The discussion of bias in science is an interesting one. Since science is a social endeavor, there necessarily will be bias inherent in it, especially when studying humans and discussing the causes of certain peculiarities. I would say that Gould was right about Morton and while Gould did make a few mistakes, his main argument against Morton was untouched.
Skull measuring after Morton
The inferiority of blacks and other non-white races has been asserted ever since the European age of discovery. While there were of course 2 camps at the time—one which argued that blacks were not inferior in intelligence and another that argued they were—the claim that blacks are inferior in intelligence was, and still is, ubiquitous. They argued that smaller heads meant that one was less intelligent, and if groups had smaller heads then they too were less intelligent than groups that had smaller heads. This then was used to argue that blacks hadn’t achieved any kind of civilizational accomplishments since they were intellectually inferior due to their smaller brains (Davis, 1869; Campbell, 1891; Hoffman, 1896; Ridpath, 1897; Christison, 1899).
Robert Bean (1906) stated, using cadavers, that his white cadavers had larger frontal lobes than his black cadavers. He concluded that blacks were more objective than whites who were more subjective, and that white cadavers has larger frontal and anterior lobes than black cadavers. However, it seems that Bean did not state one conclusion—that the brain’s of his cadavers seemed to show no difference. Gould (1996: 112) discusses this issue (see Mall, 1909: 8-10, 13; Reuter, 1927). Mall (1909: 32) concluded, “In this study of several anatomical characters said to vary according to race and sex, the evidence advanced has been tested and found wanting.”
Franz Boas also didn’t agree with Bean’s analysis:
Furthermore, in “The Anthropological Position of the Negro,” which appeared in Van Norden)- Magazine a few months later, Boas attempted to refute Bean by arguing that “the anatomical differences” between blacks and whites “are minute,” and “no scientific proof that will stand honest proof … would prove the inferiority of the negro race.”39 (Williams, 1996: 20)
In 1912, Boas argued that the skull was plastic, so plastic that changes in skull shape between immigrants and their progeny were seen. His results were disputed (Sparks and Jantz, 2002), though Gravlee, Bernard, and Leonard (2002) argued that Boas was right—the shape of the skull indeed was influenced by environmental factors.
When it comes to sex, brain size, and intelligence, this was discredited by Alice Lee in her thesis in 1900. Lee created a way to measure the brain of living subjects and she used her method on the Anthropological Society and showed a wife variation, with of course overlapping sizes between men and women.
Lee, though, was a staunch eugenicist and did not apply the same thinking to race:
After dismantling the connection between gender and intellect, a logical route would have been to apply the same analysis to race. And race was indeed the next realm that Lee turned to—but her conclusions were not the same. Instead, she affirmed that through systematic measurement of skull size, scientists could indeed define distinct and separate racial groups, as craniometry contended. (The Statistician Who Debunked Sexist Myths About Skull Size and Intelligence)
Contemporary research on race, brain size, and intelligence
Starting from the mid-1980s when Rushton first tried to apply r/K to human races, there was a lively debate in the literature, with people responding to Rushton and Rushton responding back (Cain and Vanderwolf, 1990; Lynn, 1990; Rushton, 1990; Mouat, 1992). Why did Rushton seemingly revive this area of “research” into racial differences in brain size between human races?
Centring Rushton’s views on racial differences needs to start in his teenage years. Rushton stated that being surrounded by anti-white and anti-western views led to him seeking out right-wing ideas:
JPR recalls how the works of Hans Eysenck were significantly influential to the teenage Rushton, particularly his personality questionnaires mapping political affiliation to personality. During those turbulent years JPR describes bundled as growing his hair long becoming outgoing but utterly selfish. Finding himself surrounded by what he described as anti-white and anti-western views, JPR became interested in right-wing groups. He went about sourcing old, forbidden copies of eugenics articles that argued that evolutionary differences existed between blacks and whites. (Forsythe, 2019) (See alsoDutton, 2018.)
Knowing this, it makes sense how Rushton was so well-versed in old 18 and 1900s literature on racial differences.
For decades, J. P. Rushton argued that skulls and brains of blacks were smaller than whites. Since intelligence was related to brain size in Rushtonian r/K selection theory, this meant that what would account for some of the intelligence differences based on IQ scores between blacks and whites could be accounted for by differences in brain size between them. Since the brain size differences between races accounted for millions of brain cells, this could then explain race differences in IQ (Rushton and Rushton, 2003). Rushton (2010) went as far to argue that brain size was an explanation for national IQ differences and longevity.
Rushton’s thing in the 90s was to use MRI to measure endocranial volumes (eg Rushton and Ankney, 1996). Of course they attempt to show how smaller brain sizes are found in lower classes, women, and non-white races. Quite obviously, this is scientific racism, sexism, and classism (which Murray 2020 also wrote a book on). In any case, Rushton and Ankney (2009) tried arguing for “general mental ability” and whole brain size, trying to argue that the older studies “got it right” in regard to not only intelligence and brain size but also race and brain size. (Rushton and Ankney, just like Rushton and Jensen 2005, cited Mall, 1909 in the same sentence as Bean, 1906 trying to argue that the differences in brain size between whites and blacks were noted then, when Mall was a response specifically to Bean! See Gould 1996 for a solid review of Bean and Mall.) Kamin and Omari (1998) show that whites had greater head height than blacks while blacks had greater head length and circumference. They described many errors that Lynn, Rushton and Jensen made in their analyses of race and head size. Not only did Rushton ignore Tobias’ conclusions when it comes to measuring brains, he also ignored the fact that American Blacks, in comparison to American, French and English whites, had larger brains in Tobias’ (1970) study (Weizmann et al, 1990).
Rushton and Ankney (2009) review much of the same material they did in their 1996 review. They state:
The sex differences in brain size present a paradox. Women have proportionately smaller average brains than men but apparently have the same intelligence test scores.
This isn’t a paradox at all, it’s very simple to explain. Terman assumed that men and women should be equal in IQ and so constructed his test to fit that assumption. Since Terman’s Stanford-Binet test is still in use today, and since newer versions are “validated” on older versions that held the same assumption, then it follows that the assumption is still alive today. This isn’t some “paradox” that needs to be explained away by brain size, we just need to look back into history and see why this is a thing. The SAT has been changed many times to strengthen or weaken sex differences (Rosser, 1989). It’s funny how this completely astounds hereditarians. “There are large differences in brain size between men and women but hardly if any differences in IQ, but a 1 SD difference in IQ between whites and blacks which is accounted for in part by brain size.” I wonder why that never struck them as absurd? If Rushton accepted brain weight as an indicator that IQ test scores reflected differences in brain size between the races, then he would also need to accept that this should be true for men and women (Cernovsky, 1990), but Rushton never proposed anything like that. Indeed he couldn’t, since sex differences in IQ are small or nonexistent.
In their review papers, Rushton and Ankney, as did Rushton and Jensen (I should assume that this was Rushton’s contribution to the paper since he also has the same citations and arguments in his book and other papers) consistently return to a few references: Mall, Bean, Vint and Gordon, Ho et al and Beals et al. Cernovsky (1995) has a masterful response to Rushton where he dismantles his inferences and conclusions based on other studies. Cernovsky showed that Rushton’s claim that his claim that there are consistent differences between races in brain size is false; Rushton misrepresented other studies which showed blacks having heavier brains and larger cranial capacities than whites. He misrepresented Beals et al by claiming that the differences in the skulls they studied are due to race when race was spurious, climate explained the differences regardless of race. And Rushton even misrepresented Herskovits’ data which showed no difference in regarding statute or crania. So Rushton even misrepresented the brain-body size literature.
Now I need to discuss one citation line that Rushton went back to again and again throughout his career writing about racial differences. In articles like Rushton (2002)Rushton and Jensen (2005), Rushton and Ankney (2007, 2009) Rushton went back to a similar citation line: Citing 1900s studies which show racial differences. Knowing what we know about Rushton looking for old eugenics articles that showed that evolutionary differences existed between blacks and whites, this can now be placed into context.
Weighing brains at autopsy, Broca (1873) found that Whites averaged heavier brains than Blacks and had more complex convolutions and larger frontal lobes. Subsequent studies have found an average Black–White difference of about 100 g (Bean, 1906; Mall, 1909; Pearl, 1934; Vint, 1934). Some studies have found that the more White admixture (judged independently from skin color), the greater the average brain weight in Blacks (Bean, 1906; Pearl, 1934). In a study of 1,261 American adults, Ho et al. (1980) found that 811 White Americans averaged 1,323 g and 450 Black Americans averaged 1,223 g (Figure 1).
There are however, some problems with this citation line. For instance, Mall (1909) was actually a response to Bean (1906). Mall was race-blind to where the brains came from after reanalysis and found no differences in the brain between blacks and whites. Regarding the Ho et al citation, Rushton completely misrepresented their conclusions. Further, brains that are autopsied aren’t representative of the population at large (Cain and Vanderwolf, 1990; see also Lynn, 1989; Fairchild, 1991). Rushton also misrepresented the conclusions in Beals et al (1984) over the years (eg, Rushton and Ankney, 2009). Rushton reported that they found his same racial hierarchy in brain size. Cernovsky and Littman (2019) stated that Beals et al’s conclusion was that cranial size varied with climatic zone and not race, and that the correlation between race and brain size was spurious, with smaller heads found in warmer climates, regardless of race. This is yet more evidence that Rushton ignored data that fid not fit his a priori conclusions (see Cernovsky, 1997; Lerner, 2019: 694-700). Nevertheless, it seems that Rushton’s categorization of races by brain size cannot be valid (Peters, 1995).
It would seem to me that Rushton was well-aware of these older papers due to what he read in his teenage years. Although at the beginning of his career, Rushton was a social learning theorist (Rushton, 1980), quite obviously Rushton shifted to differential psychology and became a follower—and collaborator—of Jensenism.
But what is interesting here in the renewed ideas of race and brain size are the different conclusions that different investigators came to after they measured skulls. Lieberman (2001) produced a table which shies different rankings of different races over the past few hundred years.
Table 1 from Lieberman, 2001 showing different racial hierarchies in the 19th and 20th century
As can be seen, there is a stark contrast in who was on top of the hierarchy based on the time period the measurements were taken. Why may this be? Obviously, this is due to what the investigator wanted to find—if you’re looking for something, you’re going to find it.
Rushton (2004) sought to revive the scala naturae, proposing that g—the general factor of intelligence—sits a top a matrix of correlated traits and he tried to argue that the concept of progress should return to evolutionary biology. Rushton’s r/K theory has been addressed in depth, and his claim that evolution is progressive is false. Nevertheless, even Rushton’s claim that brain size was selected for over evolutionary history also seems to be incorrect—it was body size that was, and since larger bodies have larger brains this explains the relationship. (See Deacon, 1990a, 1990b.)
Salami et al (2017) used brains from fresh cadavers, severing them from the spinal cord at the forum magnum and they completely removed the dura mater. This then allowed them to measure the whole brain without any confounds due to parts of the spinal cord which aren’t actually parts of the brain. They found that the mean brain weight for blacks was 1280g with a ranging between 1015g to 1590g while the mean weight of male brains was 1334g. Govender et al (2018) showed a 1404g mean brain weight for the brains of black males.
Rushton aggregated data from myriad different sources and time periods, claiming that by aggregating even data which may have been questionable in quality, the true differences in brain size would appear when averaged out. Rushton, Brainerd, and Pressley, 1983 defended the use of aggregation stating “By combining numerous exemplars, such errors of measurement are averaged out, leaving a clearer view of underlying relationships.” However, this method that Rushton used throughout his career has been widely criticized (eg, Cernovsky, 1993; Lieberman, 2001).
Rushton was quoted as saying “Even if you take something like athletic ability or sexuality—not to reinforce stereotypes or some such thing—but, you know, it’s a trade-off: more brain or more penis. You can’t have both.” How strange—because for 30 years Rushton pushed stereotypes as truth and built a whole (invalid) research program around them. The fact of the matter is, for Rushton’s hierarchy when it comes to Asians, they are a selected population in America. Thus, even there, Rushton’s claim rests on values taken from a selected population into the country.
While Asians had larger brains and higher IQ scores, they had lower sexual drive and smaller genitals; blacks had smaller brains and lower IQ scores with higher sexual drive and larger genitals; whites were just right, having brains slightly smaller than Asians with slightly lower IQs and lower sexual drive than blacks but higher than Asians along with smaller genitals than blacks but larger than Asians. This is Rushton’s legacy—keeping up racial stereotypes (even then, his claims on racial differences in penis size do not hold.)
The misleading arguments on brain size lend further evidence against Rushton’s overarching program. Thus, this discussion is yet more evidence that Rushton was anything but a “serious scholar” who trolled shopping malls asking people their sexual exploits. He was clearly an ideologue with a point to prove about race differences which probably manifested in his younger, teenage years. Rushton got a ton wrong, and we can now add brain size to that list, too, due to his fudging of data, misrepresenting data, and not including data that didn’t fit his a priori biases.
Quite clearly, whites and Asians have all the “good” while blacks and other non-white races have all the “bad.” And thus, what explains social positions not only in America but throughout the world (based on Lynn’s fraudulent national IQs; Sear, 2020) is IQ which is mediated by brain size. Brain size was but a part of Rushton’s racial rank ordering, known as r-K selection theory or differential K theory. However, his theory didn’t replicate and it was found that any differences noticed by Rushton could be environmentally-driven (Gorey and Cryns, 1995; Peregrine, Ember and Ember, 2003).
The fact of the matter is, Rushton has been summarily refuted on many of his incendiary claims about racial differences, so much so that a couple of years ago quite a few of his papers were retracted (three in one swipe). While a theoretical article arguing about the possibility that melanocortin and skin color may mediate aggression and sexuality in humans (Rushton and Templer, 2012). (This appears to be the last paper that Rushton published before his death in October, 2012. How poetic that it was retracted.) This was due mainly to the outstanding and in depth look into the arguments and citations made by Rushton and Templer. (See my critique here.)
Conclusion
Quite clearly, Gould got it right about Morton—Gould’s reanalysis showed the unconscious bias that was inherent in Morton’s thoughts on his skull collection. Gould’s—and Weisberg’s—reanalysis show that there are small differences in skulls of Morton’s collection. Even then, Gould’s landmark book showed that the study of racial differences—in this case, in brain and skull size—came from a place of racist thought. Writings from Rushton and others carry on this flame, although Rushton’s work was shown to have considerable flaws, along with the fact that he outright ignored data that didn’t fit his a priori convictions.
Although comparative studies of brain size have been widely criticized (Healy and Rowe, 2007), they quite obviously survive today due to the assumptions that hereditarians have between “IQ” and brain size along with the assumption that there are racial differences in brain size and that these differences are causal for socially-important things. However, as can be seen, the comparative study of racial brain sizes and the assumption that IQ is causally mediated by it are hugely mistaken. Morton’s studies were clouded by his racial bias, as Gould and Weisberg and Kaplan et al showed. When Rushton, Jensen, and Lynn arose, they they tried to carry on that flame, correlating head size and IQ while claiming that smaller head sizes and—by identity—smaller brains are related to a suite of negative traits.
The brain is of course an experience-dependent organ and people are exposed to different types of knowledge based on their race and social class. This difference in knowledge exposure based on group membership, then, explains IQ scores. Not any so-called differences in brain size, brain physiology or genes. And while Cairo (2011) concludes that “Everything indicates that experience makes the great difference, and therefore, we contend that the gene-environment interplay is what defines the IQ of an individual“, genes are merely necessary for that, not sufficient. Of course, since IQ is an outcome of experience, this is what explains IQ differences between groups.
Table 1 from Lieberman (2001) is very telling about Gould’s overarching claim about bias in science. As the table shows, the hierarchy in brain size was constantly shifting throughout the years based on a priori biases. Even different authors coming to different conclusions in the same time period on whether or not there are differences in brain size between races pop up. Quite obviously, the race scientists would show that race is the significant variable in whatever they were studying and so the average differences in brain size then reflect differences in genes and then intelligence which would then be reflected in civilizational accomplishments. That’s the line of reasoning that hereditarians like Rushton use when operating under these assumptions.
Science itself isn’t racist, but racist individuals can attempt to use science to import their biases and thoughts on certain groups to the masses and use a scientific veneer to achieve that aim. Rushton, Jensen and others have particular reasons to believe what they do about the structure of society and how and why certain racial groups are in the societal spot they are in. However, these a priori conceptions they had then guided their research programs for the rest of their lives. Thus, Gould’s main claim in Mismeasure about the bias that was inherent in science is well-represented: one only needs to look at contemporary hereditarian writings to see how their biases shape their research and interpretations of data.
In the end, we don’t need just-so stories to explain how and why races differ in IQ scores. We most definitely don’t need any kinds of false claims about how brain size is causal for intelligence. Nor do we need to revive racist thought on the causes and consequences of racial differences in brain size. Quite obviously, Rushton was a dodgy character in his attempt to prove his tri-archic racial theory using r/K selection theory. But it seems that when one surveys the history of accounts of racial differences in brain size and how these values were ascertained, upon critical examination, such differences claimed by the hereditarian all but dissappear.
Reducing “intelligence” to the brain is nothing new. This has been the path hereditarians have taken in the new millennium to try to show that the hereditarian hypothesis is true. This is basically mind-brain identity as I have argued before. Why are African countries so different from other more developed countries? The hereditarian assumes that biology must be a factor, and it is there where they try to find the answer. This was what British Eugenicists in Kenya tried to show—that the brain of the Kenyan explained how and why East Africa is so different in comparison to Europe regarding civilizational accomplishments.
In this article, I will discuss eugenic attitudes on Kenyans and their attempted reduction of intelligence to the brain, how these attitudes and beliefs went with them which grew out of Galtonian beliefs, and how such beliefs never died out.
Eugenics in Kenya
Eugenic ideas on race and intelligence appeared in Kenya in the 1930s since it promised biological solutions to social problems (Campbell, 2007, 2012). Of course these ideas grew from the heartland of eugenics where it began, from Francis Galton. So it’s no surprise that Britons who went to Kenya held those ideals. Moreover, the attitudes that the Britons settlers had in Kenya on the law in regard to Africans seems reminiscent of Jim Crow America:
The law must be a tool used on behalf of whites to bend Africans to their will. It must be personal and racially biased, the punishment swift and sharp. (Shadle, 2010)
This story begins with F. Vint (1934) and and Henry Gordon (1934) (who was in Kenya beginning in 1925). (See Mahone, 2007.) Gordon met Vint while he was a visiting doctor at the Mathari Mental Hospital in Nairobi (Tilley, 2005: 235). Both of these men attempted to show that Africans were inferior to Europeans in intelligence, and used physical brain measures to attempt to show this.
Vint used two measures—brain weight and brain structure. He also argued that the pyramidal cell layer of the Kenyan brain was only 84 percent of the European brain. Vint used others’ comparisons of European’s brains for these studies, never studying them on his own. So he concluded that the average Kenyan reached only the development of a 7 or 8 year old European. While Vint (1934) argued that the brain of the Kenyan was 152 grams less than the average brain of the European, he didn’t explicitly claim in this paper that this would then lead to differences in intelligence. We can infer that this was an implication of the argument based on his other papers. Campbell (2007: 75) quotes Vint in his article A PreliminaryNote on the Cell Content of the Prefrontal Cortex of the East African Native on the subject of brain weight and intelligence:
Thus from the both the average weight of the African brain and measurements of its prefrontal cortex I have arrived, in this preliminary investigation, at the conclusion that the stage of mental development reached by the average native is that of the average European boy of between 7 and 8 years of age.
Note the similarity between this and Lynn’s claim that Bushman IQ is 54 which corresponds to that of European 8 year olds. (See this article for a refutation of that claim.) So Vint believed that he had found the reason for racial backwardness, and this is of course through reduction to biology. Campbell (2007: 60) also tells us how the eugenic movement in Kenya grew out of British eugenic ideas along with the brain reductionism they espoused:
Eugenics in Kenya grew out of the theories disseminated from Britain; the application of current ideas about the transmission of innate characteristics, in particular intelligence, shaped a new and extreme eugenic interpretation of racial difference. The Kenyan eugenicists did not, however, use the most obvious methods, such as pedigrees, statistics and intelligence testing, which were applied by British eugenicists when assessing the intelligence of large social groups. When examining race, an area in which British eugenics had not prescribed a methodology, the Kenyan doctors most radically made histological counts of brain cells and physical measurements of brain capacity. This led to the adoption of a particularly pathologising theory about biological inferiority in the East African brain.
Gordon (1934) found an average cranial capacity of 1,316 cc in comparison to an average cranial capacity of 1,481 cc in European. This led to the conclusion that the Kenyan brain was both quantitatively and qualitatively inferior in comparison to the European brain. This of course meant that the brain was what we need to look at as this would show differences in intelligence between groups of people that we could actually measure. Gordon (1934: 231-232) describes some of Vint’s research on the brain, stating that physical and environmental causes must not be discounted:
Dr. Vint’s report on bis naked-eye and microscopic examintion of one hundred brains of normal male adults is to be published shortly in the Journal of Anatomy; but in order that we may have a little more light on the question of whether the East African cerebrum is, on the average, on a lower biological level than the European cerebrum, I may mention these facts:
In the areas of the cortex examined, Dr. Vint found a total inferinrity in quantity, as compared with the European, of 14-8 percent. His naked-eye examination revealed a significant simplicity of convolutional pattern and many features generally called primitive; e.g. the lunate sulcus, described by Professor Elliot Smith, was present in seventy of the one hundred brains. The microscopic examination showed the important supragranular layer of the cortex to be deficient in all the six areas that Von Economo examined, and the cells of these areas to be deficient very markedly in size, arrangement and in differentiation.
These, I think, are enough of Dr. Vint’s new facts to make us feel that the deficiencies found in examination of the living are indeed associated with suggestive deficiency in the native cerebrum; that we are in fact confronted in the East African with a brain on a lower biological level. This, I submit, is a matter requiring investigation by the highest expert skill into the question of heredity or environment or both.
However, going back above to what Campbell stated about Kenyan eugenicists not using tests, Gordon (1934) states that the Binet was “quite unsuitable“, while the Porteus maze test was “both suitable and to native liking.” Gordon stated that although the sample was too small to draw a definitive conclusion, the results trended inline with Vint’s measures of the brain at puberty as described by Gordon. Gordon, it seemed, had a negative view on cross-cultural comparisons between whites and blacks:
I find, on coming out of the darkness and confusion of Africa into the clear and tranquil air of European psychological thought and practice, that mental tests and mental ages by themselves are largely depended upon for the diagnosis of amentia. I venture to say only this: In my experience of many thousands of natives, intelligence in its ordinary connotation is present amongst them often to an enviable degree; nevertheiess, I believe we may do the native injustice and even injury if we are content to estimate his “intelligence” only in terms of his apparent ability to cope with the exactions of European scholastic education. Moreover, in the present state of psychological knowledge it seems to me that any use of mental tests as a means of comparison between European and African—races of widely different physical and social heritage and environment—carries the risk of misleading African education and legislative policy. The field for research by the trained psychologist of broad outlook is enormous in East Africa; his presence would be welcome. (Gordon, 1934)
Nevertheless, despite Gordon’s surprisingly negative view on the cross-cultural validity of tests, he did still believe that to ameliorate amentia in the native population that eugenic measures must be undertaken.
We can see now how Vint and Gordon attempted to infer mentality from the brain—and of course inferior mentality in the brain of the East African, in this case Kenyans (of course, the tribes that were studied). So due to Vint’s studies, it was proclaimed in this 1933 commentary in Nature titled European Civilisation and African Brains that due to brain differences, “Europeanisation” for the Kenyan just wasn’t possible. It was Gordon’s intention to use the study of racial differences to enact eugenic policies in Kenya. For if Kenyan “backwardness” is due to their intelligence which is due to their deficient brain, then this would have implications for their education and health. Regarding “backwardness”, Gordon (1945: 140) had this to say:
A few of the important questions ancillary to this leading qualitative question are: (I) Mental deficiency, ignored by the laws of Kenya including the immigration law; (2) Unprevented preventable diseases; (3) Miscegenation, present and future; (4) The introduction of contraceptives to Asiatics and Africans and no appearance of organized family planning.
The second momentous qualitative issue is the accepted “backwardness” of our African group and the question: what is backwardness? This condition, long discussed, has never been investigated; its causes and nature are wholly unknown; the correct treatment for it is wholly unknown. There are some who think they know these things and have unwittingly intensified a situation containing a deep appeal for truth. This situation must inevitably be encountered by a population inquiry.
I have often pointed out that scientific light upon “backwardness ” is required for commonsense thought and action in regard to difficult questions in trusteeship for our Africans, of which I name only the following: (I) Scholastic education and vocational training; (2) Mental deficiency and mental disorder; (3) Alcoholism and drug addiction; (4) Adult and juvenile crime; (5) The ayah question; (6) The urbanization of a backward rural people; (7) The capacity of the East African Native to acquire British culture.
Such questions cannot be lightly brushed aside or lightly answered by a nation anxious to help up a weaker people; nor is the responsibility of taking charge of that people and its future without scientific answers to such questions one to be lightly continued. It should be more widely known that the differences between the white and the black man are far from being confined to colour, and that to proceed as if the resemblances were all that matters may be a grievous error.
Gordon stated that the most important “resource” for study was the population, which other scientists ignored. Gordon dubbed this the “population problem.” Due to these kinds of eugenic ideas, there were blood banks in Kenya that were racially segregated (Dantzler, 2017). What Gordon, Vint and other Kenyan eugenicists were worried about was amentia, which is intellectual disability or severe mental illness. Although Gordon (1934) did discuss some environmental influences on the brain development of the East African in his talk to the African Circle, Gordon argued for eugenic proposals due to what he claimed to be a high level of amentia in the population which led to decreased intelligence. In this same talk, he discusses the previous research of Vint’s, showing data that the brain growth of the East African was about half as much as that of the European. He also stated that they were inferior to Europeans not only in brain measures, but also in “certain physical and psychophysical attributes, but also inreaction to the mental tests used by the enquiry, although itis not pretended that mental tests suitable to the East Africanhave yet been arrived at (Gordon, 1934: 235). He then stated that only eugenic proposals could fix the inborn attributes of the so-called “aments.” Thus, if there are differences in the brain between Europeans and East Africans, then “efforts to educate the African to the standard of the European could prove to be either futile or disastrous” (Mahone, 2007).
So without a good understanding of eugenics and how it works, then it didn’t make sense to try to develop African civilizations since their inferior mentality due to their brains made it a forgone conclusion that they wouldn’t be able to upkeep what they would need to to be educated and in good health. Thus, to Kenyan eugenicists like Gordon and Vint, Kenyans were biologically inferior due to their brains.
It is worth noting that Gordon didn’t believe that human races were the same species and that the Kenya colony was in danger of degrading due to the emigration of “mentally unstable” Europeans from the upper classed. He did, though, believe that some of them could be cured and become useful in the colony, he did believe that such the “mental unstables” should not have been sent to the colony (Campbell, 2007). Gordon also claimed that high grade “aments” could flourish in a low level society undetected, only being detected once introduced to European civilization.
After Gordon and Vint, came J. C. Carothers who, despite lacking psychiatric training was sent to Kenya as a specialist psychologist (Prince, 1996: 235). He became the director of the Mathari mental hospital in Nairobi in 1938 and held the position until 1950 (Carson, 1997) while studying the “insane” at the Mathari mental hospital (Carothers, 1947). Although he seemed to be influenced by Gordon and Vint, and seemed to share the same brain reductionism as them, he looked at it from an environmental tilt although he did not discount heredity in being a factor in racial differences. Carothers claimed that mental illness and cognitive/mental deficiency are “normal physical state[s]” in the African:
In searching for a plausible theory of African psychology, Carothers attempted to explain a perceived difference between Africans and Europeans. He notes gross variation in physical characteristics, such as skin color, which he then correlates with supposed differences in cognitive capability. He quotes Sequeira, the renowned dermatologist, in support:
“both the cerebral cortex and the epidermis are derived from the same elementary embryonic layer–the epiblast….It should therefore not be surprising on embryological grounds to find differences in the characters of the cerebral cortex in different races (2).”
Carothers also investigated the general shape, fissuration and cortical histology of the African brain as compared to the European brain. While he notes that “no sweeping conclusions in regard to African mentality can be arrived at on the basis of these data,” his general conclusion was that Africans exhibit a “cortical sluggishness” due to under-use of the frontal lobes, which inhibited their ability to synthesize information (3).
With the frontal lobe hypothesis, Carothers claimed that cognitive or mental inferiority was an inherent state in the African. “With the Negro,” he writes, “emotional, momentary and explosive thinking predominates… dependence on excitement, on external influences and stimuli, is a characteristic sign of primitive mentality.” According to Carothers, the African’s “mental development is defined by the time he reaches adolescence, and little new remains to be said” (3). In this supposed child-like permanence, “above all, the importance of physical needs (nutrition, sexuality)” prevail (2). This belief was used as proof that Africans could not appreciate the Victorian moral values of hard work and education, the desire for which was said to have come in part through denial of the sexual drive. By extension, the African was denied the possibility of reaching a civilized state.
Carothers also claimed that the African exhibits an “impulsivity [that is] violent but unsustained, … an ‘immaturity’ which prevents complexity and integration in the emotional life” (2). Using this discourse of violence, he medicalized “mental illness” as a normal physical state in the African. When the British administration in Kenya called upon Carothers to assess the Mau Mau rebellion (1945-1952), ethnopsychiatry was “commandeered to clothe the political interests of the colonists in the pseudo-scientific language of psychiatry to legitimize European suzerainty” (4). After due investigation, Carothers reported to the British government that “the onus for the rebellion rests with the deficiencies characteristic of the native Kenyans and not with the policies of the British colonial desire” (3). (Carson, 1997)
In 1951, Carothers (1951: 47) argued for a cultural view to explain the “frontal idleness” of the African, while not discounting “the possibility of anatomical differences” in explaining it:
This frontal idleness in turn can be accounted for on cultural grounds alone, but the possibility of anatomical differences, is not thereby excluded.
Finally, a plea is voiced for expert anatomical study of the African brain and, in view of his resemblance to a certain type of European psychopath, of the brains of the latter also.
Carothers published a WHO report in 1953 where he stated that he would relate cultural factors and malnutrition and disease to mental development (Carothers, 1953). Carothers (1953: 106) stated that “The psychology of the African is essentially the psychology of the African child.” This claim, of course, seems to gel well with the Gordon-Vint claim that the brain growth of the East African seems to subside way earlier than that of the European brain. Carothers also reinterpreted Vint’s findings on the thinner cerebral cortex.
[Carothers] introduced an interpretation which permitted education to play a role in post-natal cerebral development. Noting the remarkable enhancement in interest and alertness “that comes to African boys and girls as a result of only a very little education… often comprising little more than some familiarity with written symbols in reading, writing and arithmetic;’ he raised the question whether,”it is not possible that the maturation of those cortical cells in Europe is also dependant on the acquisition of that skill” (Carothers, 1962, p. 134). (Prince, 1996: 237)
Though regarding the so-called thinner cortex of the African, Tobias (1979) stated:
Published interracial comparisons of thickness of the cerebral cortex and, particularly, of its supragranular layer, are technically invalid: there is no acceptable proof that the cortex of Negroes is thinner in whole, or in any layer, than that of Europeans. It is concluded that vast claims have been based on insubstantial evidence.
However, Cryns (1962: 237) stated that while there are differences in brain morphology between whites and blacks, there was no evidence that this accounted foe the alleged inferiority in intelligence in Africans:
With regard to brain fissuration and the histological structure of the cortex, both Carothers (14, p. 80) and Verhaegen (49, p. 54) state that there is no scientific evidence sufficient to assume that mental capacity is in some degree related to the surface or structure of the cerebral cortex.
The general conclusion, then, to be drawn from the above anatomical and physiological brain studies is that there is sufficient empirical evidence indicating the existence of morphological differences between White and Negro brains, but that there is no sufficient evidence to indicate that the morphological peculiarities found in the African brain are of functional significance, i.e., account for an alleged intellectual inferiority.
Gordon and Vint’s works and conclusions in the modern day
Reading the works of these two men, we can see that what they are saying is nothing new—since contemporary hereditarians argue for almost similar conclusions. Rushton was one of the main hereditarians who argued that biological reductionism was true and he authored many studies with Ankney on the correlation between general mental ability (GMA) and the brain (Rushton and Ankney, 2007; 2009).
Rushton, however, aggregated numerous different measurements from different time periods, even from authors who did not subscribe the racial hierarchies that Rushton proposed—in fact, this “hierarchy” changed numerous times throughout the ages (Lieberman, 2001). The current hierarchy came about due to East Asia’s economic uprise starting after WW2, and the “shrinking skulls” of Europeans began in the 1980s with Rushton (Lieberman, 2001). Although Lynn, (1977, 1982) did speak of higher Japanese IQs, it is of course in the context of “Japan’s dazzling commercial success.” (See here for a refutation of Lynn’s genetic hypothesis regarding Asians.)
It is quite obvious by looking at how contemporary hereditarian research is trending, that the biological reductionism of Gordon and Vint is still alive today in fMRI and MRI studies. Contemporary hereditarians have also implicated the frontal lobe as being part of the reason why blacks are “less intelligent” than whites, and as we have seen, this is a decades-old claim. These beliefs were held due to outdated and outright racist views on the “quality” of the greatest “resource”, according to Gordon: The population.
Conclusion
Eugenics in Kenya—as it was in America—wasn’t a scientific movement; it was a social and political one. Eugenic ideas were practiced all over the world from the time of antiquity all the way to the modern day. The biological reductionism espoused by Kenyan eugenicists is still with us today, and instead of using post-mortem brains and crude skull measures, we are using more sophisticated technologies to try to show this reductionism is true. However, since mind doesn’t reduce to brain, this is bound to fail.
As we can see, the kind of gross biological reductionism hasn’t left us, it has only strengthened. The mental and physical reductionism inherent in these theories have never died—they just quieted down for a bit after WW2.
What is inherent in such claims is that there are not only racial brains, but racial minds. What Gordon, Vint and Carothers tried arguing was that it wasn’t due to the rule of the British and the society that they attempted to create in Kenya, the capacity for rebellion was inherent in the Kenya native. This seems to me to be like the “drapetomania” craze during slavery in America: pathologizing a normal response—like wanting to escape slavery—and create a new psychological diagnosis to explain why they act a certain way. The views espoused by the scientific racists in Kenya were not new, since earlier in the 19th century the inferiority of the “black brain” was well-noted and discussed. Although I have found one (1) view from Tiedemann (1836: 504) who claims that his studies led him to the belief that “by measuring the cavity of the skull of Negroes and men of the Caucasian, Mongolian, American, and Malayan races, that the brain of the Negro is as large as thsg of the European and other nations.”
Campbell (2007: 219-220) explains that although most probably still held their eugenic beliefs, the changing intellectual climate in Britain was a main reason why the eugenics movement in Kenya was not sustained.
By the late 1930s, although there had been no radical change in settler attitudes to race and no upheaval in the policy or personnel of the colonial administration the Kenyan eugenics movement petered out. We must assume that individuals retained their eugenic beliefs, but its potency in Kenya’s lore of human biology was lost. The causes of the demise of Kenyan racial eugenics lay in the financial retrenchment of the 1930s and responses in the metropole at a time when scientific racism was being increasingly undermined on both political and intellectual grounds. Without metropolitan support, Kenyan eugenics could not be sustained as a social movement. The size and composition of the Kenyan European community was such that there were not enough individuals with the intellectual and scientific interests and authority to establish an independent, self-sufficient organisation. Kenyan eugenics was forced to look to the metropole for financial, intellectual and institutional legitimacy. The demise of Kenyan eugenics is therefore intimately linked with a changing intellectual climate in Britain.
The views espoused by Gordon, Vint and Carothers have not left us. After Arthur Jensen revived the race and IQ debate in 1969, searches for the cause of why blacks are less intelligent than whites began coming back into the mainstream. Rushton and Jensen relied on such works to argue for their conclusion that the cause of lower intelligence and hence lower civilizational attainment and academic performance was due to genes and their brain structure. Such antiquated views, it seems, just will not die. Lieberman (2001) showed how the racial hierarchy in brain size has changed throughout the ages based on current social thought, and of course, this has affected hereditarian thinking in the modern day.
Although some authors in the 18 and 1900s proclaimed that brain weight had no bearing on one’s mental faculties, quite obviously the Kenyan eugenicists never got that memo. Nevertheless, there are a few studies that contradict Rushton’s racial hierarchy in brain size, showing that the brain’s of blacks are in range with those of whites.
Discussions on the “quality” of brains of different groups of course have not went away, they just changed their language. It seems to me that, like with most hereditarian claims, it’s just racists citing racists as “consensus” for their claims. Gordon (1934) asked why the brain of the Kenyan does not develop in the same way as the European’s. Since the reductionism they held to is false, such a question isn’t really relevant.
The concept of “intelligence” has enthralled many people who wish to understand human cognition, including cognitive scientists, philosophers and psychologists. The claimed identity between IQ and intelligence has even led to the sterilization of people in the 1900s around the world. One’s IQ is an outcome, not a cause, and in this article I will explore arguments showing that IQ is best viewed as an outcome not a cause and I will provide arguments for the claim.
What would it mean for IQ to be a cause? Put simply, it means that IQ is causally efficacious for X. For example, the hereditarian may say that “IQ predicts” certain things, and so IQ explains and causes those things. This claim, though, is false. The claim “IQ predicts” is another way of saying “IQ is correlated with.” We all know that correlation doesn’t equal causation. So the claim fails.
When it comes to IQ as a whole, IQ is forced to a bell curve; the bell curve is not a mere outcome of test design, it was deliberately forced by the test constructors by adding and subtracting certain items that certain groups do well on over others. This is seen for the SAT for men and women (Rosser, 1989) and for the SAT for blacks and whites (Kidder and Rosner, 2002)—the fact of the matter is, these two studies are the best evidence that by having different assumptions about people and groups, the test constructors can get the distribution of scores they want by manipulating the test items. Thus, due to the way IQ tests are constructed, I can rightly state that IQ is arbitrary.
As a matter of fact, the bell curve was not an empirical discovery, it was posited a priori by Adolphe Quetelet. He believed that a sign of moral perfection was mathematical regularity. Quetelet’s observations led him create the concept of l’homme moyen—the average man. The bell curve is a main point of contention in the debate about IQ. Though we know that it is a forced consequence of test construction, that is item design and analysis, and it is not real and does not exist in nature (Fendler, 2014) while Richardson (2017: 45-50) notes that few biological traits are distributed in that manner. For example, the brain is log-normal (log-dynamic), meaning it’s strongly skewed with a heavy tail (Buszaki and Mizuseki, 2014). Since the bell curve is a “necessary component of IQ testing” as Fendler rightly notes, then if it can be shown that the assumption of a normal distribution is just not tenable, then it can be rightly inferred that the assumptions of IQ-ists should be questionable since their assumptions are false.
More evidence that IQ is an outcome and not a cause can be seen from the fact that schooling is causally efficacious for IQ and that summer vacation decreases IQ. Why does this happen? It’s quite simple—due to the content on test and the structure of it, when one goes on summer vacation they are thrown out of the school rhythm. Class gaps grew in the summer, which is yet another reason that the claim IQ tests are mere class-specific knowledge tests is true. This evidence shows that IQ is an outcome of what one is exposed to and that the knowledge on the test is class-specific. This class-specific knowledge is what the tests show; cultural and social exposure to information explains IQ gaps, not genes. Cognition is thinking and thinking is the main aspect of IQ test-taking, and thinking is an action which is irreducible to anything physical, so genes can’t explain IQ. Clearly, due to the nature of the tests, what explains how one scores is the knowledge they are exposed to. That much is clear.
IQ is a mere proxy for social class, and it helps to legitimatize social hierarchies (Mensh and Mensh, 1990; Roberts, 2015). Of course, Richard Herrnstein attempted to argue that the social hierarchies seen were a natural consequence of inherited differences among people, that is inherited differences that cause IQ. However, Stephen Ceci (1996) showed that when IQ is equated and social class is not, social class is predictive of life success. So the IQ-income relationship is in all actuality due to schooling and family background, not IQ.
A psychological test score is no more than an indication of how well someone has performed at a number of questions that have been chosen for largely practical reasons. Nothing is genuinely being measured. (Howe 1997: 17)
It is in this context that we need to assess claims about social class and race differences in IQ. These could be exaggerated, reduced, or eliminated in exactly the same way. That they are allowed to persist is a matter of social prejudice, not scientific fact. In all these ways, then, we find that the IQ testing movement is not merely describing properties of people—it has largely created them. (Richardson, 2017: 82)
The distinction between causes and outcomes
If X is an outcome, then X can’t be a cause. So if IQ is an outcome, then it can’t be a cause. So IQ doesn’t cause anything.
The conceptual distinction between an outcome and a cause will show that IQ can’t be a cause. Causes are events, actions or factors which precede outcomes and serve as initiating factors which set into motion chains of events which lead to a particular outcome. So causes come before the outcome they produce which establishes directionality in the cause and effect relationship.
The fact of the matter is, the malleability of IQ shows that IQ is an outcome not a cause. IQ can be changed over time through various experiences and interventions. What this suggests is that rather than being something that shows one’s potential, IQ could then be seen as how prepared one is to take a test with class-specific items. So if a characteristic is malleable and subject to change, then it is an outcome. IQ is a characteristic that is malleable and subject to change. Thus, IQ is an outcome and not a cause.
Causes shape or determine outcomes. They exert their effects on the occurrence of an outcome. That is, causes provide the driving force of the eventual outcome. But outcomes are passive in nature. They are the direct result or consequence that emerge as a direct or indirect consequence of the cause. So causes shape, influence, or determine the outcome while outcomes reflect the consequences of causal factors. Causal factors are what give rise to outcomes.
P1: If X is an outcome, then it is a result or consequence of certain factors or events. P2: Y is a cause. P3: If Y is a cause, then it cannot be an outcome. P4: X is an outcome. C: Thus, X cannot be a cause.
Since IQ is subject to change development over time, this shows how it is malleable. Due to the differences in cultural and psychological tools between groups (Richardson, 2002), they will necessarily be exposed to different kinds of knowledge. Thus, if people are exposed or not exposed to certain things and they take a test which have a narrow set of class-specific knowledge and skills, then the group more familiar with the content—in virtue of being surrounded by it—would score higher.
P1: If IQ is an outcome, then it is influenced by various factors like education and environment. P2: IQ is influenced by various factors such as education and environment. C: Thus, IQ is an outcome.
I can see someone trying to say “IQ is an outcome, you’re right—an outcome of one’s genetic constitution.” However, this claim fails. It fails due to the fact that such a claim reduces to “The way one thinks is an outcome of one’s genetic constitution.” Different cultures and environments can lead one into thinking in different ways since they are exposed to different knowledge bases. Since anything mental is irreducible to the physical, then one’s IQ can’t be an outcome of one’s genetic constitution.
In On Intelligence, Ceci (1996: 118) describes how cultural context is an important part of cognition:
One’s cultural context is an integral part of cognition because the culture arranges the occurrence or nonoccurrence of events that are known to affect cognitive developments (e.g., literacy and orientation in hostile situations). Each culture and subculture presents a limited number of contexts in which children may interact during development, and many of these could have an impact on cognitive performance. Moreover, culture controls the frequency of occurrence of events, thus dictating the amount of time spent doing some tasks (e.g., weaving) over others (e.g., abstracting and interacting with others).
Similarly, cultures control the level of difficulty of tasks within various contexts. For example, in many cultures it is “uneconomical” to encourage each child’s maximal or potential cognitive growth. Rather, these societies endeavor to keep their children in a “zone of proximal development,” which is the difference between their level of independent problem solving and their level of problem solving under adult guidance or in collaboration with more capable peers (Vygotsky, 1978, p. 86). The advantage of the latter is that children are exposed to a complete task while only engaging in those aspects found at the limits of their own cognitive competence.
…
…large-scale cultural differences are likely to affect cognition in important ways. One’s way of thinking about things is determined in the course of interactions with others of the same culture; that is, the meaning of a cultural context is always negotiated between people of that culture. This, in turn, modifies both culture and thought. (119)
In order to establish cause and effect (say, the claim that genes cause or influence the etiology of IQ and differences between individuals), then it is necessary for there to be a theory or definition of the so-called cause. The absence of a well-established theory and definition of intelligence makes it difficult to establish that intelligence is a cause. So this lack of consensus establishes that it can’t be defined easily or measured. The lack of a consensus definition, the multi-determined nature of IQ, the presence of mediating factors, along with cultural variability establishes that IQ/intelligence isn’t a cause.
Since all tests are culture-bound, then a culture-free test is an impossibility (Cole, 2002). Since culture-free tests are an impossibility, then what explains differences between cultures (say, blacks and whites, Asians and whites), is the item content on them that are biased toward certain classes. Since items are biased toward certain classes, then one getting a low score is due to them not being prepared for the test’s content due to being exposed to different knowledge bases. So since all tests are culture-bound, then what explains differences between groups are methodological test construction differences, and we can state this since IQ test results have been changed in the past due to differing assumptions.
P1: If IQ is a cause, the specific outcomes can be solely attribute to IQ. P2: Specific outcomes cannot be attributed to IQ. C: Thus, IQ isn’t a cause.
P1: If changes in IQ are observed as a result of external interventions, then IQ is an outcome. P2: Changes in IQ are observed as a result of external interventions. C: Thus, IQ is an outcome, not a cause.
Conclusion
For these reasons and more, IQ is an outcome not a cause. And believing that IQ is a cause and not merely an outcome has had some troubling consequences for some people, as the eugenics movement in America in the early 1900s has shown.
Adoption studies (Skodak and Skeels, 1949; Dumaret and Stewart, 1985; van Izendoorn et al, 2005; Kendler et al, 2015; see also Nisbett et al, 2012 for a review of adoption studies and Brockwood, 2021 for review of Skeels and Skodak) along with the results of Headstart and natural experiments like summer vacation show that IQ isn’t a cause, but it’s merely an outcome of what one was exposed to in their lives. This is necessarily true, due to the kinds of items on the test which are specific to certain groups of people. The fact that IQ is an outcome not a cause shows that one can’t invoke IQ as an explanation for anything. One may try to say that IQ is an outcome of genetics, but I’ve argued that those claims fail.
At the end of the day, IQ-ists are trying to say that one’s IQ is causal for how they act in their life. They base this on flawed studies of IQ and job performance (Richardson and Norgate, 2015). In any case, the arguments given in this article show that IQ isn’t a cause and it is an outcome.
To claim that IQ is a cause means that’s it’s a causal factor for something. This means that a higher or lower IQ would have a causal impact on different aspects of one’s life. This is true regarding academic performance but this is due to there being similar items and structure between the tests so they are in effect different versions of the same test. Nevertheless,
To claim that IQ is an outcome means that IQ is the result or consequence of numerous factors rather than the primary cause or determinant of those factors. Thus, IQ is a mere reflection of the influences on an individual’s cognition, not a causal factor which directly affects other aspects of their lives.
The very fact that genetic and mental reductionism are false means that the outcome can’t be due to genes. If it can’t be due to genes, then it has to be due to one’s life experiences. If it’s due to one’s life experiences, then we must recognize IQ as being an outcome due to the environmental factors they are exposed to along with the experiences they have.
NotPoliticallyCorrect 