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It has come to my attention that near the end of 2007, Nike boasted about releasing a running shoe that specifically targeted Native American communities. Nike developed the shoe to “to address the specific fit and width requirements for the Native American foot.” Since Native Americans have a high rate of obesity and diabetes (“diabesity”), then it seems that it would be a good thing to promote a shoe specifically for and to the population in question. But do such gestures translate to racist ideas or do they translate to a corporation wanting to be seen as promoting health (while their ultimate goal is profit)? Nike, specializing in athletic clothing, surely would be a good organization to spearhead such a movement, right? On what research is this initiative based on and does it hold water?
Through such outreach programs, Nike hopes to be seen to make social and community impacts when it comes to health. As Welch (2019: 12) notes, the N7 imitative hopes “to further promote sport and physical activity in Native American communities.” Such programs and specific items that would catch the eye of the consumers in question to heighten their physical activity and, subsequently, lessen their rates of fatal diseases, should be seen as a good thing, which would be irrespective of the feelings of the groups in question who see such outreach as racist.
The shoe was developed by a podiatrist named Rodney Stapp who served the Native community for his whole life (b. 1961, d. 2016). This was the first—and since then, only—time that Nike developed a shoe for a specific racial group. Was it a good idea? Was it racist? Even if it could be construed as racist, wouldn’t it be negated by targeting a group that has some of the highest rates of diabesity in America, therefore leading to a more active population and mitigation of the diseases in question? (See Broussard et al, 1991; Narayan, 1996; Acton et al, 2002). Since exercise seems to be necessary in managing diabetes and its symptoms (Colberg et al, 2010; Kirwan, Sacks, and Nieuwoudt, 2018; Borhade and Singh, 2020), then it seems that, irrespective of whether or not such gestures are racist, that such outreach and initiatives are a net good for the population in question.
Stapp was a big-name figure in the outreach to Native groups in Texas, and was the podiatrist that Nike consulted with in the development of their Nike Native American N7 shoe. Stapp was the one that contacted Nike to make such a shoe, since the patients that he serviced did not like the black and bulky shoes that were specially developed for diabetics—the efficacy of such shoes, though, have been debated in the literature (e.g., Brunner, 2015), while others have noted that diabetics have stated that the style and appearance of such diabetic shoes are the reasons why there is such low compliance in wearing them (Macfarlane and Jensen, 2003). In any case, wouldn’t marketing shoes toward specific demographics be a net-good, irrespective of the ultimate goals of the company if they would then promote healthier behaviors in the population in question?
Nike, though, has been criticized for the initiative, with Native right’s groups claiming that Nike is using Native plight for profit (Cole, 2008; Sanders, Phillips, and Alexander, 2018). It has been criticized by such groups since they have embroidered the shoe with feathers and sunsets, arrows, and different kinds of symbolism prevalent in Native cultures in the Americas. Here, I would not say that such things are racist on its face, it’s just a marketing ploy to sell more of their shoes. While it can be construed that such marketing is racist in a way, I think that the good such a program and shoe would do to reach at-risk populations outweighs any racist connotations that the shoes and the outreach program makes.
But most would have a problem with the claim that the shoe was developed specifically for “Native American feet”. Stapp claimed that “Indians tend to have a wider foot, but their heels are about average“, which would indicate slippage while running in a normal running shoe. Nike’s press release on the shoe says that “A strong emphasis was placed on providing a performance product that would cater to the specific needs of Native American foot shapes and help provide motivation to Native Americans predisposed to, or suffering from, health issues that can be improved by leading physically active lifestyles“, while also stating that “Research has engaged individuals from over 70 tribes as well as consulting podiatrists and members of Indian Health Services and the National Indian Health Board.“
(I am unable to find the research in question; hopefully someone can point me in the right direction so that I can find it.)
There is a history of such differences in the appendages between North and South Native Americans—where North Americans have longer and more slender feet than South Americans (e.g., Kate, 1918). Nike stated that the reason they developed the shoes were so that they could accommodate Native American’s wider feet, along with combating the diabesity epidemic that affects them. In 2015, though, Stapp stated that he believed the introduction of the shoe dropped amputations from 5-6 per year to 0-1 per year. If it is indeed true that the shoes were related in lowering the incidences of foot amputations in Native communities, then it would seem that the cause of that would be that they are moving more and getting more blood to their lower extremities which would then lead to lowered rates of amputation in these diabetic populations.
The claim that such shoes “racially profile” Natives is ridiculous. Stapp said that Nike asked him if there were differences in the feet of Native groups compared to others to which he answered “Yes.” Apparently, around the time of the marketing for the shoes, Nike was told that Native Americans had problems fitting into Nike’s ‘normal’ running shoes due to the width of their feet (being wider than average). Along with Natives supposedly having wider feet, since diabetes causes inflammation of tissue, which is concentrated in the feet—for instance, with diabetic foot ulcers (Pendsey, 2010; Schoen and Norman, 2014; Tuttolomondo, Maida, and Pinto, 2015; Amin and Doupis, 2016)—would seem that the call for such shoes to be develop would be a net-good for the population.
Though I can see how the claims that the shoe targeted at a specific racial group could be construed as racist, the net-good that a shoe does in getting to certain populations would outweigh the negative connotations that the racist accusation brings on Nike. Indeed, some of the developers of the shoe were Native, worked with Natives, and developed it to specifically target and help Natives manage a debilitating disease that leads to many negative health outcomes—like foot amputation and eventually death. So if exercise is conducive to managing diabetes and diabetic foot and the N7’s would then target certain populations with different average foot morphology, then it seems that the shoe has been a net-good for the population since, according to Stapp, seven years after the introduction of the shoe diabetic foot amputations went from 5-7 to 0-1 per year. While he may have had financial incentives to say that, I don’t think that it underscores the fact that Nike’s N7 program did not have positive benefits—even if they could be construed in a negative way (i.e., claims of racism).
The answer to the question “Should we market shoes to specific demographics” is “Yes.” It would be a good idea to, for example, make more demographic-specific shoes with specific embroideries in order to attempt to target certain at-risk populations that are more likely to acquire certain diseases on the basis of physical inactivity—like the Nike N7 program and Nike Native American N7 shoe attempt to do. It is for these reasons, then (irrespective of whether or not such morphologic claims of the feet of Natives are true) that the initiative in question is a good thing. The moral “should” question on whether or not we “should” market things—in this example, shoes—to certain demographics seems to rest on whether or not the marketing would have a positive effect on the lifestyles of the groups in question. If it does have positive effects, then we should market such programs toward at-risk populations, irrespective of claims that such marketing is racist toward certain groups.
Read the original article here. The titular person here is a blogger of population genetics and fossils concern Southeast Asia. Here represents among his latest synthesis of modern human origins. I believe it is mostly well done, in particular in regards to alluding to an Asian origin for the LCA of Sapiens, Neanderthals, and Denisovans which he expanded upon here.
The focus for today, however, concerns issues in representing the geographical positioning of Sapiens, which he alludes to a Asian origin, thought eh fossils he uses are not supportive as firmly as he suggests.
For the not-too-long time, fossil evidence did support this narrative, although fossils from the past 150000 years were very rare and even absent in Africa, there were some older human skulls forced to support this narrative. It is different with East Asia, we can find fossils with modern morphology that lived between 190-130 Kya (Zhirendong, Luijiang). Even the signals of dental modernity have appeared since 296 000 years ago (Panxian Dadong), about 100 000 years preceding the modern teeth of Misliya Cave in the Levant (194-177 Kya). And the morphology and modern face shapes have appeared since 900,000 years ago (Yunxian, Nanjing, Zhoukoudian). Includes Dali’s human face (550-260 Kya).
Regarding the evidence of “modern” tendencies, here is what the record shows
Among these sites, Fuyan (Daoxian) Cave, Luna Cave, Zhirendong Cave, and Huanglong Cave are currently considered as the best evidence in support of the early presence of H. sapiens in China, based on a clearer chronostratigraphic context and a more diagnostic morphology. There are other sites such as Ganqian (Tubo; Shen et al. 2001), Tongtianyan (Liujiang; Shen et al. 2002; Yuan, Chen, and Gao 1986), Dingcun (Chen,
Yuan, and Gao 1984; Pei 1985), and Jimuyan (Wei et al. 2011) that we consider of interest to assess the evolution of modern humans in China. However, because of the more ambiguous morphology of the fossils and/or uncertainties about their antiquity they are considered less unequivocal than those from Fuyan Cave, Luna Cave, Zhirendong Cave, and Huanglong Cave.
Liujiang, which the author of the blog post associates with the same interval as Zhirendong from a cave study, Liujiang was not of the sane site, nor was the context firmly grounded. See here for references. As for the interval 130-190k for the Zhiren cave, that exceeded the direct date of 106-110k for the fossils themselves. The date he uses here is from a study on the cave itself.
For Panxian, I commented on this from another post(now deleted).
The Panxian specimens were mainly archaic, while PH3 was found derived but in no specific fashion.
The facial features he speaks off from 900k from China speaks mainly of the mid-face, and fully modern faces didn’t appear until Antecessor.
Dali, since the 2017 study, was concluded to represent geneflow due to the lack of conformity to local erectus fossils relative to African and European ones.
One of the easily distinguishable features of modern humans is the shape and morphology of the skull. When compared to its predecessors, the modern human skull is more gruff, the face is flatter vertically, the chin protrudes, and the braincase) which is more globular. If a skull has most of these features, then it is classified under our species, modern humans. The older skulls that have been suggested as part of our modern human ancestry are the Omo I and Omo II skulls from Omo Kibish, in southern Ethiopia (Leaky et al. 1967). The two Omo skulls are around 195,000 years old (initially only 130000 years old), have a mixture of archaic and modern features, something that is not surprising if we view them as African archaic humans who probably met their modern human ancestors from elsewhere, before evolving into modern humans. . Because of this, they were both named Homo sapiens idaltu . Idaltu in the Afar language means ‘older’.
The mixture of archaic features would also be expected if early and transitional. somehow this is lost.
Several skulls from East and South Africa also tell about the same thing. Things are thought to have improved when three Herto skulls were found in 1997 around Afar, Ethiopia, aged 154,000-160000 years, which also have mixed archaic and modern craniofacial features . Herto’s skull was found in the same layer containing Middle Stone Age (MSA) and Later Stone Age (LSA) aftefacts. The location and artifacts and age of the Herto man closely match the Out of Africa model , and convince many scientists that the Herto man could be the closest anatomical ancestor of modern humans ( Out of Ethiopia ).
Same as explain before, meanwhile in terms of cranial features China is lacking as far as skulls are concerned.
Some fossils are classified as part of Homo sapiens , such as Omo I and Herto (although they are substantially different, and both still have primitive morphology, and some scientists consider Herto to be a subspecies of Homo sapiens ). Jebel Irhoud’s human status is being debated, some paleoanthropologists openly accept him as a close relative of Homo sapiens , some do not accept it because he considers Jebel Irhoud to be part of archaic Africa , and may even be part of a different evolutionary line from the evolutionary line of Homo sapiens . Florisbad man, previously classified as Homo helmei, it is not sufficient to represent the evolutionary line of Homo sapiens due to its primitive character and absence of a braincase .
He doesn’t provide citation or quotes to demonstrate who thinks thinks way or explain how China solves this with it’s specimens on comparable levels. Outside of teeth that generally don’t go beyond the interval of 120k, China is lacking. While he mentions in the article that the Broken Hill Skull fails as an ancestor, the mixed skulls he mention however are morphologically expected as the study mentions.
Meanwhile, the 130k Braincase of Singa shows modern morphology.
Overall, his latest article does a better job but still presents issues. I’ll summarize them here in this deleted comment.
“Let’s look at Africa. One of the oldest candidates for Homo ergaster , KNM-ER 3733, turns out to be 1.63 million years old, and all specimens from the Turkana Basin have their estimate between 1.6-1.43 million years. Nariokotome Boy or Turkana Boy (KNM-WT 15000; 1.5 million years), which has always been predicted as a representative of Homo erectus , turns out to be in the Homo ergaster evolution line , because it does not have a canine fossa .”Yet we know that Erectus is oldest in South Africa currently, I evenseen you post this research.https://www.smithsonianmag.com/science-nature/homo-erectus-australopithecus-saranthropus-south-africa-180974571/“The Konso skull from Southern Ethiopia is about 1.4 million years old. Buia and Daka (about 1 million years old) best fit the transition between Homo ergaster to Homo rhodesiensis , as well as Gombore II (~ 780 Kya). Daka which is hypothesized asHomo erectus has more morphological similarities to KNM ER3733, so sharing one morphology with Homo antecessor or Homo erectus East Asia does not necessarily make it part of Homo erectus . The youngest Homo ergaster, OH 12, is 780 Kya, has a skull capacity and facial shape similar to that of KNM ER3733. With an age difference of about 8,50000 years, the morphological continuity is still very clear. Imagine if they were still classified as Homo erectus ? Yet it is clear that their evolutionary path does not lead to the Homo sapiens line of evolution. In addition, some of the morphologies of OH 12 are also similar to KNM ER3883, D2282 and D2700.”Some references for the affinities?“The Homo habilis specimens from Koobi Fora range from 1.75 to 1.65 million years old. If KNM-ER 1802 is classified as Homo habilis (we must first verify it based on the presence of canine fossa , or it could be Homo rudolfensis , represented by KNM ER 62000), then the origin of its appearance is about 2 million years ago. So far, specimens representing Homo habilis claim the shallow canine fossaincluding OH 24, OH 62, OH 65, KNM-ER 1813, and KNM-ER 42703 with a time span of 1.86-1.44 million years (but still needs to be investigated further due to limited references). Of course this is younger when compared to Longgudong human teeth, more than 2.14 million years old. In fact, in several locations in Ciscaucasus there are many traces of artifacts that are more than 2 million years old.”The problem here is that Koobi Floora isn’t the oldest Habilis, the oldest is 2.3 mya years old in Afar. In fact the oldest Homo (that is broken away from Australopithecus morphologically) is 2.5 mya.Also, as far as artifacts goes, unless you have evidence proving otherwise, both the Oldowan and Achuelean are oldest in Africa at 2.6 and 1.7 mya ago respectively.“Meanwhile, KNM ER 2598, which was assumed to be a candidate for the Out of Africa I population (with an estimated initial age of 1.88-1.9 million years ago), was found on the surface which may have originated from a younger stratigraphic deposit. KNM-ER 1813 is also estimated to be 1.86 million years old, or to be in the Olduvai Subchron boundary (1.95-1.78 million years ago).”See above mention of the South Africa find. Also, proof to support this suggestion?“Alternatively, KNM-ER 1813 and other hominins in Area 123 could be younger than 1.65 million years ago.”Again, evidence?“After 1.65 million years ago, Turkana Basin humans were dominated by Homo ergaster , who was contemporary with Sangiran early humans (Sangiran 4 and S27), but younger than early humans Bumiayu. So, the best candidates for the ancient Javanese ancestors could be between the early humans Dmanisi, or the ancient humans Longgudong (> 2.14 million years) and Yuanmou (1.7-1.72 million years).”The most recent evidence rules out longgudong, seeing how it is defined best as habilis and distinct from Erectus in regards to the teeth and.Likewise, studies in 2001 and 2002 place the latter specimen to below1 mya, therefore no consensus.Btw, Naledi does have a Canine Fossa.Otherwise, I agree with the rest of the article.
Hereditarianism is the theory that differences in psychology between individuals and groups have a ‘genetic’ or ‘innate’ (to capture the thought before the ‘gene’ was conceptualized) cause to them—which therefore would explain the hows and whys of, for example, the current social hierarchy. The term ‘racism’ has many referents—and using one of the many definitions of ‘racism’, one could say that the hereditarian theory is racist since it attempts to justify and naturalize the current social hierarchy.
In what I hope is my last word on the IQ/hereditarian debate, I will provide three conceptual arguments against hereditarianism: (1) psychologists don’t ‘measure’ any’thing’ with their psychological tests since there is no object of measurement, no specified measured object, and measurement unit for any specific trait; only physical things can be measured and psychological ‘traits’ are not physical so they cannot be measured (Berka, 1983; Nash, 1990; Garrison, 2009); (2) there is no theory or definition of “intelligence” (Lanz, 2000; Richardson, 2002; Richardson and Norgate, 2015; Richardson, 2017) so there can be no ‘measure’ of it, the example of temperature and thermometers will be briefly mentioned; (3) the logical impossibility of psychophysical reduction entails that mental abilities/psychological traits cannot be genetically inherited/transmitted; and (4) psychological theories are influenced by the current problems/going-on in society as well as society influencing psychological theories. These four objections are lethal to hereditarianism, the final showing that psychology is not an ‘objective science.’
(i) The Berka/Nash measurement objection
The Berka/Nash measurement objection is simply: if there is no specified measured object, object of measurement or measuring unit for the ‘trait’, then no ‘thing’ is truly being ‘measured’ as only physical things can be measured. Nash gives the example of a stick—the stick is the measured object, the length of the stick is the object of measurement (the property being measured) and inches, centimeters etc are the measuring units. Being that the stick is in physical space, its property can be measured—its length. Since psychological traits are not physical (this will also come into play for (ii) as well) nor do they have a physical basis, there can be no ‘measuring’ of psychological traits. Indeed, since scaling is accepted by fiat to be a ‘measure’ of something. This, though, leads to confusion, especially to psychologists.
The most obvious problem with the theory of IQ measurement is that although a scale of items held to test ‘intelligence’ can be constructed, there are no fixed points of reference. If the ice point of water at one atmosphere fixes 276.16 K, what fixes 140 points of IQ? Fellows of the Royal Society? Ordinal scales are perfectly adequate for certain measurements. Moh’s scale of scratch hardness consists of ten fixed points from talc to diamond, and is good enough for certain practical purposes. IQ scales (like attainment test scales) are ordinal scales, but this is not really to the point, for whatever the nature of the scale it could not provide evidence for the property IQ or, therefore, that IQ has been measured. (Nash, 1990: 131)
In first constructing its scales and only then preceding to induce what they ‘measure’ from correlational studies, psychometry has got into the habit of trying to do what cannot be done and doing it the wrong way round anyway. (Nash, 1990: 133)
The fact of the matter is, IQ tests don’t even meet the minimal theory of measurement since there is no—non-circular—definition of what this ‘general cognitive ability’ even is.
(ii) No theory or definition of intelligence
This also goes back to Nash’s critique of IQ (since there can be no non-circular definition of what “IQ tests” purport to measure): There is no theory or definition of intelligence therefore there CAN BE no ‘measure’ of it. Imagine saying that you have measured temperature without a theory behind it. Indeed, I have explained in another article that although IQ-ists like Jensen and Eysenck emphatically state that the ‘measuring’ of ‘intelligence’ with “IQ tests” is “just like” the measuring of temperature with thermometers, this claim fails as there is no physical basis to psychological traits/mental abilities so they, therefore, cannot be measured. If “intelligence” is not like height or weight, then “intelligence”‘ cannot be measured. “Intelligence” is not like height or weight. Therefore, “intelligence” cannot be measured.
We had a theory and definition of temperature and then the measuring tool was constructed to measure our new construct. The construct of temperature was then verified independently of the instrument used to originally measure it, with the thermoscope which then was verified with human sensation. Thus, temperature was verified in a non-circular way. On the other hand, “intelligence tests” are “validated” circularly, if the tests correlate highly with other older tests (like Terman’s Stanford-Binet), it is held that the new test ‘measures’ the construct of ‘intelligence’—even if none of the previous tests have themselves been validated!
Therefore, this too is a problem for IQ-ists—their scale was first constructed (to agree with the social hierarchy, no less; Mensh and Mensh, 1991) and then they set about trying to see what their scales ‘measure’ with correlational studies. But we know that since two things are correlated that doesn’t mean that one causes the other—there could be some unknown third variable causing the relationship or the relationship could be spurious. In any case, this conceptual problem, too, is a problem for the IQ-ist. IQ is nothing like temperature since temperature is an actual physical measure that was verified independently of the instrument constructed to measure the construct in the first place.
Claims of individuals as ‘intelligent’ (whatever that means) or not are descriptive, not explanatory—it is the reflection of one’s current “ability” (used loosely) in relation to their current age norms (Anastasi; Howe, 1997).
(iii) The logical impossibility of psychophysical reduction
I will start this section off with two (a priori) arguments:
Anything that cannot be described in material terms using words that only refer to material properties is immaterial.
The mind cannot be described in material terms using words that only refer to material properties.
Therefore the mind is immaterial; materialism is false.
If physicalism is true then all facts can be stated using a physical vocabulary.
But facts about the mind cannot be stated using a physical vocabulary.
So physicalism is false.
(Note that the arguments provided are valid, and I hold them to be sound thus an objector would need to reject then refute a premise.)
Therefore, if all facts cannot be stated using a physical vocabulary and if the mind cannot be described in material terms using words that only refer to material properties, then there can, logically, be no such thing as ‘mental measurement’—no matter what IQ-ists try to tell you.
Different physical systems can give rise to different mental phenomena—what is known as the argument from multiple realizability. Thus, since psychological traits/mental states are multiply realizable, then it is impossible for psychology to reduce to mental kinds to reduce to physical kinds—the mental kind can be realized by multiple physical states. Psychological states are either multiply realizable or they are type identical to the physio-chemical states of the brain. That is a kind of mind-brain identity thesis—that the mind is identical to the states of the brain. Although they are correlated, this does not mean that the mind is the brain or that the mind can be reduced to physio-chemical states, as Putnam’s argument from multiple realizability concludes. If type-physicalism is true, then it must be true that every and all mental properties can be realized in the same exact way. But, empirically, it is highly plausible that mental properties can be realized in multiple ways. Therefore, type-identity theory is false.
Psychophysical laws are laws connnecting mental abilities/psychological traits with physical states. But, as Davidson famously argued in his defense of Anomalous Monism, there can be no such laws linking mental and physical events. There are no mental laws therefore there can be no scientific theory of mental states. Science studies the physical. The mental is not physical. Thus, science cannot study the mental. Indeed, since there are no bridge laws that link the mental and physical and the mental is irreducible to and underdetermined by the physical, it then follows that science cannot study the mental. Therefore, a science of the mind is impossible.
Further note that the claim “IQ is heritable” reduces to “thinking is heritable”, since the main aspect of test-taking is thinking. Thinking is a mental activity which results in a thought. If thinking is a mental activity which results in a thought, then what is a thought? A thought is a mental state of considering a particular idea or answer to a question or committing oneself to an idea or an answer. These mental states are, or are related to, beliefs. When one considers a particular answer to a question, they are paving the way to holding a certain belief. So when they have committed themselves to an answer, they have committed themselves to a new belief. Since beliefs are propositional attitudes, believing p means adopting the belief attitude that p. So, since cognition is thinking, then thinking is a mental process that results in the formation of a propositional belief. Thus, since thinking is related to beliefs and desires (without beliefs and desires we would not be able to think), then thinking (cognition) is irreducible to physical/functional states, meaning that the main aspect of test-taking (thinking) is irreducible to the physical thus physical states don’t explain thinking which means the main aspect of (IQ) test-taking is irreducible to the physical.
(iv) Reflexivity in psychology
In this last section, I will discuss the reflexivity—circularity—problem for psychology. This is important for psychological theorizing since, to its practitioners, psychology is seen to be an ‘objective science.’ If you think about psychology (and science) and how it is practiced, it (they) investigates third-personal, not first-personal, states. Thus, there can be no science of the mind (what psychology purports to be) and psychology can, therefore, not be an ‘objective science’ as the hard sciences are. The ‘knowledge’ that we attain from psychology comes from, obviously, the study of people. As Wade (2010: 5) notes, the knowledge that people and society are the object of study “creates a reflexivity, or circular process of cause and effect, whereby the ‘objects’ of study can and do change their behavior and ideas according to the conclusions that their observers draw about their behavior and ideas.”
It is quite clear that such academic concepts do not arise independently—in the history of psychology, it has been used in an attempt to justify the current social hierarchy of the time (as seen in 1900s America, Germany, and Britain). Psychological theories are influenced by current social goings-on. Thus, it is influenced by the bias of the psychologists in question. “The views, attitudes, and values of psychologists influence the claims they make” (Jones, Elcock, and Tyson, 2011: 29).
… scientific ideas did not develop in a vacuum but rather reflected underlying political or economic trends. 15
The current social context influences the psychological discourse and the psychological discourse influences the current social context. The a priori beliefs that one holds will influence what they choose to study. An obvious example being, hereditarian psychologists who believe there are innate differences in ‘IQ’ (they use ‘IQ’ and ‘intelligence’ interchangeably as if there is an identity relation) will undertake certain studies in order to ‘prove’ that the relationship they believe to be true holds and that there is indeed a biological cause to mental abilities within and between groups and individuals. Do note, however, that we have the data (blacks score lower on IQ tests) and one must then make an interpretation. So we have three possible scenarios: (1) differences in biology cause differences in IQ; (2) differences in experience cause differences in IQ; or (3) the tests are constructed to get the results the IQ-ists want in order to justify the current social hierarchy. Mensh and Mensh (1991) have succinctly argued for (3) while hereditarians argue for (1) and environmentalists argue for (2). While it is indeed true that one’s life experiences can influence their IQ scores, we have seen that it is logically impossible for genes to influence/cause mental abilities/psychological traits.
The only tenable answer is (3). Such relationships, as noted by Mensh and Mensh (1991), Gould (1996), and Garrison (2009), between test scores and the social hierarchy are interpreted by the hereditarian psychologist thusly: (1) our tests measure an innate mental ability; (2) if our tests measure an innate mental ability, then differences in the social hierarchy are due to biology, not environment; (3) thus, environmental differences cannot account for what is innate between individuals so our tests measure innate biological potential for intelligence.
The [IQ] tests do what their construction dictates; they correlate a group’s mental worth with its place in the social hierarchy. (Mensh and Mensh, 1991)
Richards (1997) in his book on racism in the history of psychology, identified 331 psychology articles published between 1909 (the first conceptualization of the ‘gene’, no less) and 1940 which argued for biology as a difference-maker for psychological traits while noting that 176 articles for the ‘environment’ side were published in that same time period.
Note that the racist views of the psychologists in question more than likely influenced their research interests—they set out to ‘prove’ their a priori biases. Indeed, they even modeled their tests after such biases. Tests that were constructed that agreed with their a priori pre-suppositions on who was or was not intelligence was kept whereas those that did not agree with those notions were thrown out (as noted by Hilliard, 2012). This is just as Jones, Elcock, and Tyson (2011: 67) note with the ‘positive manifold’ (‘general intelligence’):
Subtests within a battery of intelligence tests are included n the basis of them showing a substantial correlation with the test as a whole, and tests which do not show such correlations are excluded.
From this, it directly follows that psychometry (and psychology) are not sciences and do not ‘measure’ anything (returning to (i) above). What psychometrics (and psychology) do is attempt to use their biased tests in order to sort individuals into where they ‘belong’ on the social hierarchy. Standardized testing (IQ tests were one of the first standardized tests, along with the SAT)—and by proxy psychometrics—is NOT a form of measurement. The hierarchy that the tests ‘find’ is presupposed to exist and then constructed into existence using the test to ‘prove’ their biases ‘right.’
Indeed, Hilliard (2012) noted that in South Africa in the 1950s that there was a 15-point difference in IQ between two white cultural groups. Rather than fan flames of political tension between the groups, the test was changed in order to eliminate the difference between the two groups. The same, she notes, was the case regarding IQ differences between men and women—Terman eliminated such differences by picking and choosing certain items that favored one group and balanced them out so that they scored near-equally. These are two great examples from the 20th century that demonstrate the reflexivity in psychology—how one’s a priori biases influence what they study and the types of conclusions they draw from data.
Psychology, at least when it comes to racial differences in ‘IQ’, is being used to confirm pre-existing prejudices and not find any ‘new objective facts.’ “… psychology [puts] a scientific gloss on the accepted social wisdom of the day” (Christian, 2008: 5). This can be seen with a reading into the history of “IQ tests” themselves. The point is, that psychology and society influence each other in a reflexive—circular—manner. Thus, psychology is not and cannot be an ‘objective science’ and when it comes to ‘IQ’ the biases that led to the bringing of the tests to America and concurrently social policy are still—albeit implicitly—believed today.
Psychology originally developed in the US in the 19th century in order to attempt to fix societal problems—there needed to be a science of the mind and psychology purported to be just that. They, thusly, needed a science of ‘human nature’, and it was for this reason that psychology developed in the US. The first US psychologists were trained in Germany and then returned to the US and developed an American psychology. Though, do note that in Germany psychology was seen as the science of the mind while in America it would then turn out to be the science of behavior (Jones, Elcock, and Tyson, 2011). This also does speak to the eugenic views held by certain IQ-ists in the 20th and into the 21st century.
In Nazi Germany, Jewish psychologists were purged since their views did not line-up with the Nazi regime.
Psychology appealed to the Nazi Party for two reasons: because psychological theory could be used to support Nazi ideology, and because psychology could be applied in service to the state apparatus. Those psychologists who remained adapted their theories to suit Nazi ideology, and developed theories that demonstrated the necessary inferiority of non-Aryan groups (Jones and Elcock, 2001). These helped to justify actions by the state in discriminating against, and ultimately attempting to eradicate, thse other groups. (Jones, Elcock, and Tyson (2011: 38-39)
These examples show that psychology is influenced by society but also that society influences psychological theorizing. Clearly, what psychologists choose to study, since society influences psychology, is a reflection of a society’s social concerns. In the case of IQ, crime, etc, the psychologist attempts to naturalize and biologicize such differences in order to explain them as ‘innate’ or ‘genetic’. The rise of IQ tests in America, too, also coincided with the worry that ‘national intelligence’ was declining and so, the IQ test would need to be used to ‘screen’ prospective immigrants. (See Richardson, 2011 for an in-depth consideration on the tests and conditions that the testees were exposed to on Ellis Island; also see Gould, 1996.)
(i) The Berka/Nash measurement objection is one of the most lethal arguments for IQ-ists. If they cannot state the specified measured object, the object of measurement, and the measuring unit for IQ then they cannot say that any’thing’ is being ‘measured’ by ‘IQ tests.’ This then brings us to (ii). Since there is no theory or definition of what is being ‘measured’, and if the tests were constructed first before the theory, then there will necessarily be a built-in bias to what is being ‘measured’ (namely, so-called ‘innnate mental potential’). (iii) Since it is logically impossible for psychology to reduce to physical structure, and since all facts cannot be stated using a physical vocabulary nor can the mind be described using material terms that only refer to material properties, then this is another blow to the claim that psychology is an ‘objective science’ and that some’thing’ is being ‘measured’ by their tests (constructed to agree with their a priori biases). And (iv) The bias that is inherent in psychology (for both the right and the left) influences the practitioners’ theorizing and how they interpret data. Society has influenced psychology (and psychology has influenced the society) and we only need to look at America and Nazi Germany in the 20th century to see that this holds.
The relationship between psychology and society is inseparable—it is a truism that what psychologists choose to study and how and why they formulate their conclusions will be influenced by the biases they already hold about society and how and why it is the way it is. For these reasons, psychology/psychometry are not ‘sciences’ and hereditarianism is not a logically sound position. Hereditarianism, then, stays what it was when it was formulated—a racist theory that attempts to bilogicize and justify the current social hierarchy. Thus, one should not accept that psychologists ‘measure’ any’thing’ with their tests; one should not accept the claim that mental abilities can be genetically transmitted/inherited; one should not accept the claim that psychology is an objective ‘science’ due to the reflexive relationship between psychology and society.
The arguments given show why hereditarianism should be abandoned—it is not a scientific theory, it just attempts to naturalize biological inequalities between individuals and groups (Mensh and Mensh, 1991; Gould, 1996; Garrison, 2009). Psychometrics (what hereditarians use to attempt to justify their claims) is, then, nothing more than a political ring.
The term ‘racism’ has many definitions. What does it mean for a person to be a ‘racist’? What does it mean for a person to have ‘racist beliefs’? What does the term ‘racism’ refer to? The answers to these questions then will inform the next part—what does racism have to do with stress and physiology?
What is ‘racism’?
Racism has many definitions, so many—and so many for uses in different contexts—that it has been argued, for example by those in the far-right, that it is, therefore, a meaningless term. However, just because there are many definitions of the term, it does not then mean that there is no referent for the term we use. A referent is a thing that is signified. In this instance, what is the referent for racism? I will provide a few on-hand definitions and then discuss them.
In Part VI of The Oxford Handbook of Race and Philosophy (edited by Naomi Zack, 2016) titled Racisms and Neo-Racisms, Zack writes (pg 469; my emphasis):
Logically, it would seem as though ideas about race would have to precede racism. But the subject of racism is more broad and complicated than the subject of race, for at least these two historical reasons. First, the kind of prejudice (prejudged cognitions and negative emotions) and discrimination (treating people differently on the grounds of group identities) that constitute racism have a longer history than the modern idea of race, for instance in European anti-Semitism. And second, insofar as modern ideas of race have been in the service of the dominant interests in international and internal interactions, these ideas of race are ideologies that have devalued non-white groups. That is, ideas of race are themselves already inherently racist.
In philosophy, racism has been treated as attitudes and actions of individuals that affect nonwhites unjustly and social structures and institutions that advantage whites and disadvantage nonwhites. The first is hearts-and-minds or classic racism, for instance the use of stereotypes and harmful actions by whites against people of color, as well as negative feelings about them. The second is structural racism, for instance the use of stereotypes or institutional racism, for instance, the facts of how American blacks and Hispanics are, compared to whites, worse off on major measures of human well-being, such as education, income, family wealth, health, family stability, longevity, and rates of incarceration.
John Lovchik in his book Racism: Reality Built on a Myth (2018: 12) notes that “racism is a system of ranking human beings for the purpose of gaining and justifying an unequal distribution of political and economic power.” Note that using this definition, “hereditarianism” (the theory that individual differences between groups and individuals can be reduced to genes; I will give conceptual reasons why hereditarianism is false as what I hope is my final word on the debate) is a racist theory as it attempts to justify the current social hierarchy. (The reason why IQ tests were first brought to America and created by Binet and Simon; see The History and Construction of IQ Tests and The Frivolousness of the Hereditarian-Environmentalist IQ Debate: Gould, Binet, and the Utility of IQ Testing.) This is why hereditarianism saw its resurgence with Jensen’s infamous 1969 paper. Indeed, many prominent hereditarians have held racist beliefs, and were even eugenicists espousing eugenic ideas.
Headley (2000) notes a few definitions of racism—motivational, behavioral, and cognitive racism. Motivational racism is “the infliction of unequal consideration, motivated by the desire to dominate, based on race alone“; behavioral racism is “failure to give equal consideration, based on the fact of race alone”; and cognitive racism is “unequal consideration, out of a belief in the inferiority of another race.”
I have presented six definitions of racism—though there are many more. Now, for the purposes of this article, I will present my own: the ‘inferiorization’ of a racialized group which is then used to explain disparities in things like IQ test scores, social class/SES, education differences, personality, etc. Now, knowing what we know about physiological systems and how they react to the environment around them—the immediate environment and the social environment—how does this then relate to stress and physiology?
Racism, stress, and physiology
Now that we know what racism is, having had a rundown of certain definitions of ‘racism’, I will now discuss the physiological effects such stances could have on groups racialized as ‘races’ (note that I am using socialraces in this article; recall that social constructivists about race need to be realists about race).
The term ‘weathering’ refers to the body’s breaking down due to stress over time. Such stressors can come from one’s immediate environment (i.e., pollution, foodstuffs, etc) or their social environment (a demanding job, how one perceives themselves and how people react to them). So as the body experiences more and more stress it becomes more and more ‘weathered’ which then leads to heightened risk for disease in stressed individuals/populations.
Allostatic states “refer to altered and sustained activity levels of the primary mediators (e.g., glucocorticosteroids) that integrate energetic and associated behaviours in response to changing environments and challenges such as social interactions, weather, disease, predators and pollution” (McEwen, 2005). Examples of allostatic overload such as acceleration of atherosclerosis, hypertension (HTN), stroke, and abdominal obesity (McEwen, 2005) are more likely to be found in the group we racialize as ‘black’ in America—particularly women (Gillum, 1987; Gillum and Hyattsville, 1996; Barnes, Alexander, and Staggers, 1997; Worral et al, 2002; Kataoka et al, 2013).
Geronimus et al (2006) set to find out whether or not the heightened rate of stressors (e.g., racism, environmental pollution, etc) can explain why black bodies are more ‘weathered’ than white bodies. They found that such differences were not explained by poverty, indicating that it even affects well-off blacks. Allostatic load refers to heightened hormonal production in response to stressors. We know that physiological is homeodynamic and therefore changes based on the immediate environment and social environment (for example, when you feel like you’re about to get into a fight, your heart rate increases and you get ready to ‘fight or flight’).
Experiencing racism (environmental stimuli; real or imagined, the outcome is the same) is associated with increased blood pressure (HTN). So if one experiences racism they will them experience an increase in blood pressure, as BP is a physiological variable (Armstead et al, 1987; McNeilly et al, 1995; see Doleszar et al, 2018 for a review). The concept of weathering, then, shows that racial health disparities are, in fact, racist health disparities (Sullivan, 2015: 106). Racism, then, contributes to higher levels of allostasis and, along with it, higher levels of certain hormones associated with higher allostasis.
One way to measure biological age is by measuring the length of telomeres. Telomeres are found at the ends of chromosomes. Since telomere lengths shorten with age (Shammas, 2012), those with shorter telomeres are ‘biologically older’ than those of the same age with longer telomeres. Geronimus et al (2011) showed that black women had shorter telomeres than white women, which was due to subjective and objective stressors (i.e., racism). Black women in the age group 49-55 were 7.5 years ‘older’ than white women. Thus, they had an older physiological age compared to their chronological age. It is known that direct contact with discriminatory events is associated with poor health outcomes. Harrell, Hall, and Taliaferro (2003) note that:
“…physiological set points and the mechanisms governing them are not fixed. External stressors can permanently alter physiological functioning. Racism increases the volume of stress one experiences and may contribute directly to the physiological arousal that is a marker of stress-related diseases.
Social factors can, indeed, influence physiology and there is a wealth of information on how the social becomes biological and how environmental (social) factors influence physiological systems. Forrester et al (2019) replicated Geronimus’ findings, showing that blacks have a higher ‘biological age’ than whites and that psychosocial factors affect blacks more than whites. Simons et al (2020) also replicated Geronimus’ findings, showing that persistent exposure to racism was associated with higher rates of inflammation in blacks which then predicted higher rates of disease in blacks compared to whites. Such discrimination can help to explain differences in birth outcomes (e.g., Jasienska, 2009), stress, inflammation, obesity, stroke rates, etc in blacks compared to whites (Molnar, 2015).
But what is the mechanism by which higher allostatic load scores contribute to negative outcomes and shorter telomeres indicating a higher biological age? When one feels that they are being discriminated against, the sympathetic nervous system activates due to chronic stress and along with it HPA dysfunction. What this means is that there is a loss of the anti-inflammatory effects of cortisol—it becomes blunted. This then increases oxidative stress and inflammation. Thus, the inflammatory processes result in cardiovascular disease and immune and metabolic dysfunction. The HPA axis monitors and responds to stress—allostatic load. When stress hormones are released, the adrenal gland is targeted. When it receives a signal from the pituitary gland, it pumps epinephrine and norepinephrine into the body, causing our hearts to beat faster, causing us to breathe more deeply—what is known as ‘fight or flight.’ Cortisol is also released and is known as a stress hormone, but when the stressful event is over, all three hormones return to baseline. Thus, the higher amount of stress hormones in circulation indicates higher levels of allostatic load—higher levels of stress in the individual in question. We know that blacks have higher levels of allostatic load (i.e., stress-related hormones) than whites (Duru et al, 2012). Barr (2014: 71-72) writes:
Imagine, though, that before the allostatic load has a chance to return to its baseline level, another stressor is sensed by the hypothalamus. The allostatic load will once again increase to the plateau level. Should the perception of stressors be ongoing, the allostatic load will not have the chance to ever fully recharge, and the adrenal gland will be producing an ongoing stream of stress response hormones. The body will experience chronic elevation in its allostatic load. […] A person experiencing repeated stressors, without the opportunity for intervals that are relatively stress-free, will experience a chronically elevated allostatic load, with higher than normal levels of circulating stress response hormones.
What these studies show, then, is that race is a cause of health inequalities, but it’s not inherent in biology but due to social factors that influence the physiology of the individual in question. The term ‘racism’ has many referents, and using one of them identifies ‘hereditarianism’ as a racist ideology (it is inherently ideological). These overviews of studies show that racial health inequalities are due, in part, to perceived discrimination (racism) thus they are racist health disparities. We know that physiology is a dynamic system that can respond to what occurs in the immediate environment—even the social environment (Williams, 1992). Thus, what explains part of the health inequalities between races is perceived discrimination—racism—and how it affects the body’s physiological systems (HPA axis, HTN, etc) and telomeres.
The physical interactions behind cognitive variation are arguably the most studied and elusive aspects of human diversity. Despite the HBD community’s enormous interest in the mind, I find that many of the modern theories they propagate are lacking conceptual rigor. Within this thesis I will attempt the following: 1) To persuade the audience that my conception of particular mental phenomena is more precise than or at least endorses the most epistemically accurate contemporary hypotheses. And 2) To lay out a simple yet reliable framework for future HBDers to base new ideas on by giving biological explanations of particular psychological phenomena. For this purpose alone you can treat this article as a short summarization of the extensive research into our concept of consciousness, as such I will not be covering any of this in extreme detail, neither will I be covering every single aspect of the mind, but it will of course be accompanied by studies and papers that will elucidate these concepts further for anyone who is interested.
Philosophy of mind
First, I think it’s appropriate to cover the philosophical grounds of my views. It should be no surprise that Physicalism/Naturalism is the most dominant position among philosophers within that domain (Bourget and Chalmers, 2013). The number is even greater if you consider scientists as philosophers (which they are). These figures are expected because Physicalism is the most parsimonious explanatory model for how our world works. So what is Physicalism? At the basic level, Physicalism is the belief that our world is a result of physical laws. I cannot highlight the entirety of this debate, the intricacy of the subjects within this article could span the length of multiple textbooks. I will delve more into this in future posts. Instead, I’m going to simply rebut what I believe are common fallacies that underlie dualistic thinking.
The arguments I have read tend to follow similar patterns in their reasoning. The one we will discuss first is the intensional fallacy. Dualist arguments that suffer from this flaw are presented in the following format:
P1: X (usually the mind) has property A
P2: Y (usually the brain/body or just physical entities in general) has property B
P3: Leibniz law which states: Necessarily, for anything, x, and anything, y, x is identical to y if and only if for any property x has, y has, and for any property y has, x has.
C1: X is not Y
From the onset this doesn’t seem that fallacious, and of course some would even argue the intensional fallacy cannot apply here, as leibniz law is not dependent on what someone knows but the properties a target may exhibit. This is incorrect, knowing the different properties the entity may possess by definition requires knowledge and subsequently a thinker. To see why this argument is ultimately fallacious, observe the following syllogism:
P1: Water is knowable with the unaided eye
P2: H2O is unknowable with the unaided eye
P3: leibniz law
C1: Water is not H2O
Descartes, Ross, and arguments on the unity of consciousness tend to all commit this fallacy. We could replace the subjects and their properties with that of neon and boron and the conclusion would be true, the problem is that discrepancies between the descriptions of physical and mental states (or any concept) does not necessarily entail that the two cannot be identical in reference. To make definitive statements on the mind’s characteristics requires an identification of the mechanisms that catalyze such functions. Physicalists have this luxury, Dualists do not. This idea is echoed (actually I’m the echo) by Kant (1781) in his 2nd paralogism of his Critique of Pure Reason (Kitcher, 1990) This brings me to the second fallacy: ad ignorantiam. We know a lot about the mind, Philosophy, Art, History, Literature, Psychology, Neuroscience, etc. What seems to be the crux of the issue is how subjectivity arises from objectivity. I am not charging any particular Dualist argument with this fallacy. Instead, I believe this fallacy pervades Dualism as a whole. It usually goes:
P1: Despite Physicalism’s explanatory power, it hasn’t explained the phenomenological character of experience.
P2: Since Physicalism cannot explain this particular aspect it cannot be a tenable model for our world
C1: Dualism is the only tenable position
What makes this a fallacious argument is that the proponent is essentially asking you to “prove him wrong”. Phenomenology is a difficult concept to ground in physical structures simply because of the sheer complexity behind it. Donald davidson even advocated Dual Aspect Monism as a solution to this perceived indeterminism (more on stochasticity later). Despite the debate on the aforementioned subject, if Dualists accept interactionism (which they have to), positing an “ectoplasmic” nature to mental states is pure ad hoc. This brings me to the final fallacy I will discuss: begging the question. If Physicalists can account for these qualities then any Dualist argument against Physicalism already presupposes the need for Dualism. If Physicalism cannot account for said phenomena then these criticisms could cut both ways. More on Dualism and its presumed fallacies.
Nature of the system
These following sections won’t be new or helpful to anyone versed in current literature on neuroscience or similar fields. This is simply a reference point for those less knowledgeable on the subject. Usually, when you read on the Nervous system, authors will refer to its descriptions with computer and engineering metaphors (Furber and Temple, 2007). This article will do the same, but for conceptual clarity I will stress that the brain is not a computer. Yes, it’s true that computers are the closest thing to a brain that we’ve engineered, but it is a biological organ that has been crafted by millions of years of sloppy evolution. As obvious as that is, let it serve as a reminder to not to take the metaphors too seriously. Despite my previous views, the brain is not a parallel system. There aren’t actual physical boundaries that could represent independence. Subsequently, the brain and the mind cannot be modular as modularity also requires independence. The NS and its parts is in fact parallel if you consider each neuron as its own processor with each synaptic cleft as a physical boundary (though you could arguably still contest the independence). Unfortunately, this is not what Scientists of the mind refer to when they use these terms. Cognitive scientists and Psychologists refer to more complex interactions, and as a result many of their computational models could be labelled parallel. Their divisions are more abstract, the subject of this article is a more empirically grounded level of function.
If anything the brain is an integrated memory system. Which is to say that it is dependent upon neighboring receivers to produce certain behaviors and actions. An integrated system has the same potential as a parallel one, as it can run multiple operations simultaneously (Born 2001). I find integration a better description of our nervous system because it allows for the dependency we clearly witness. Compartmentalization of the cerebral hemispheres is arbitrary. As you can see from the previous video, simple observation indicates that there are no real anatomical boundaries except possibly sulci. However, this would still be against the interests of the consensus. Despite this, localization can still be realized through averaging the enormous variation in functionality (Sporns, Tononi, and Kotter, 2005). Localization is still tricky to realize, as the brain is a biological construct with a general purpose function. This implies that neuronal activity of the same tasks can vary in individuals day by day. There exists a tug and pull between minimization of cost and maximization of growth and adaptation. This is how the brain retains plasticity via a “winner takes all” scenario while simultaneously allowing arborization of localized functionality to solidify (Barbey, 2018). These functions are carried out by populations of neurons. This is because there is no specificity (except maybe some kind of spatial tendency) in regard to the connections between individual neurons. It should be noted that this is not in reference to variation over time. The plasticity of individual neuronal connections and the categorical selection of pathways that groups of neurons take is determined by a multitude of factors that can be coherently expressed, so a lack of specificity is not equivalent to indeterminism in this context. RaceRealist has an interesting article that could explain the stochasticity of low level connectivity. This link will also be helpful to those interested in how this connectivity is realized. As far as the connectivity on the population level goes, there is considerable determinism that shapes the probabilistic nature of cognition (Dold et al., 2018).
This is possibly the most important aspect of consciousness, as it is an accumulation of our memories that help formulate how we perceive and establish ourselves. Alzheimers is a type of dementia that affects memory which can slowly make its carrier lose themselves over time. Our memories are completely dependent on external stimuli. Sub-mechanisms of neural plasticity are responsible for this function and can be carried out in multiple ways. Synaptic plasticity is the most commonly discussed aspect of neuroplasticity. Nonsynaptic Plasticity is newer to the field of neuroscience but works synergistically with the former to carry out key mechanisms involving memory and learning (Tully, Hennig, and Lansner, 2014). Simply put, learning a new skill requires locally specific neurons and their glial modulators to strengthen or weaken their connections with each other. The more you carry out these tasks the stronger these connections become, and subsequently the easier it becomes to perform said tasks. Your eyes, ears and skin are sensory organs that transfer information to your brain where it is integrated, which then catalyzes a motor response (most of the time). The world we model around us completely relies on the information from these organs. Because of this, the brain can be said to be experience dependent. Hence, why the brain is a memory system above all else.
There is considerable debate how memories are stored or retrieved. These traces of memories are called engrams. The most prevalent theory is that the patterns of neurons that were initiated when a memory was solidified are what reactivate when a memory is retrieved. These patterns all happen to be a part of a redundant circuitry, just in case if an engram is wiped out it can still be reformed by using alternative pathways. This is important to note, because this means our brains do not perfectly recall information, they reconstruct it. One counter (though they may coincide with each other) to this theory is the possibility that memory is stored in DNA or RNA through epigenetic changes (Bedecarrats, Chen, Pearce, Cai, Glanzman, 2018). In this study, the researchers were able to transfer memories from a trained slug to an untrained one by injecting it with RNA of the former. Usually the criticism against this study has to do with the supposed “conflation” of memory with the response showcased by the untrained Aplysia (an example being Mattei, 2018). This is an obfuscation from a distinction without a difference. In reality, this effect probably explains how instincts become ingrained within organisms over evolutionary time. The difference is simply the complexity involved and it’s quite possible both mechanisms are responsible for the propagation of memories. Refer to Abraham, Jones, and Glanzman, 2019 for further information on the topic.
In my opinion, emotions are probably the hardest aspect for laymen to conceptualize properly. At the most basic level emotions are simply a type of interoception (Critchley, Garfinkel, 2018). Interoception is the brain’s ability to receive information on the internal state of its physiological systems which allows it to maintain homeostasis. These fluctuations in physiology can be triggered by exogenous stimuli and depending on cultural/social differences these stimuli will have varying responses from the individual (Barrett, 2017). Those specific factors are very important as some studies and experiments have showcased that different emotions can have incredibly similar physiological responses. A frequently cited example is Dutton and Aron, 1974. Not only can different emotions have nearly the same physiological effects there are also overlapping physiological effects for different emotions! However, there is enough consistency that localization is reliable (Nummenmaa, Glerean, Hari, Hietanen, 2013). To give an example that many HBDers would probably relate to. Let’s say the sight of interracial sex angers me. The external input (interracial sex) is recieved by sensory organs (my eyes) and then because of accompanying mental dispositions (like racism) it triggers physiological responses like increased heart beat, higher blood pressure, your brain becomes flooded with catecholamines giving you a burst of energy, your muscles tense, breathing becomes more rapid, etc. This holistic process is itself what we refer to as emotion.
Now emotions are an important part of our decision making processes. You literally cannot make decisions without emotions. As emotions not only dictate the type of decisions we make, they also influence which path we choose when confronted with choice. Cold logic is far more subjective than most people would even realize. This brings forth a new question: What is the relationship between intelligence and emotional intelligence?
Before discussing this we need to first make it clear what exactly it is we’re talking about. Pumpkinperson recognizes that EQ is a very vague concept that isn’t distinguished well from others in his 2016 article. He states that: “And Goleman ruined his whole construct by not distinguishing between people who are smart at emotions (i.e. a master manipulator), and those who just have good emotions (someone who doesn’t feel the need to overeat).” The latter definition is closer to what we will be using. I believe the former is more akin to what we know of as “social intelligence”. For the sake of this post we will be defining it specifically as the ability to regulate and recognize one’s emotions, as I believe attributing any more to the concept will render it indistinguishable from Theory of Mind. Instead it would be more accurate to say that SQ and EQ are subsidiary abilities to TOM.
Since we’ve more or less established that emotions are a type of interoception it seems the best way to answer the previous question is to find exactly what the relationship between interoception and IQ is. To find this out we need to understand how one goes about quantifying this construct. Garfinkel, Seth, Barrett, Suzuki, Critchley, 2015 do just this by making the distinction between subjective and objective measurements of interoception and how both are required to make accurate assessment of one’s EQ (see table one for detailed examples). Now of course the authors cited never mention EQ once in the paper, but I believe conceptually what they are measuring is incredibly similar if not identical to EQ. For example, Garfinkel et al, 2016 found that people with higher anxiety had poorer abilities to accurately gauge their respiratory functions. This connection is further corroborated by some studies indicating that IQ and EQ overlap heavily in the neural networks that create said properties (Barbey, Colom, Grafman, 2012). Our own Racerealist provided considerable evidence that the mediating factor behind racial differences in aggression was education, not testosterone: “However, as I’ve noted last year (and as Alvarado, 2013 did as well), young black males with low education have higher levels of testosterone which is not noticed in black males of the same age group but with more education (Mazur, 2016). Since blacks of a similar age group have lower levels of testosterone but are more highly educated then this is a clue that education drives aggression/testosterone/violent behavior and not that testosterone drives it.
Mazur (2016) also replicated Assari, Caldwell, and Zimmerman’s (2014) finding that “Our model in the male sample suggests that males with higher levels of education has lower aggressive behaviors. Among males, testosterone was not associated with aggressive behaviors.”” This all seems to imply that both EQ and IQ are heavily integrated with one another. In fact, intelligence may be required to regulate one’s emotions and that this creates a feedback loop where emotional issues cause intellectual issues and vice versa. This of course has effects on the racial level that I will delve into in another blog post.
What exactly is intelligence? Pumpkinperson and I usually define it as the mental ability to adapt and I imagine most people would agree, but there is no actual agreed upon definition and I tend to see great variation when reading upon the subject. Truthfully, most variations are semantic rather than conceptual. Macdonald & Woodley, 2016 refer to intelligence as novel problem solving. They state: “Intelligence is usually distinguished from learning which subsumes a variety of mechanisms that allow the organism to take advantage of temporary regularities in its environment – paradigmatically classical and operant conditioning….Intelligence, on the other hand, assumes no environmental regularities – even temporary ones – nor does it refer to learning how to achieve a goal by observing others who have already solved the problem. Rather, as stated in Jerison’s definition, there is the implication that the organism has a goal and is integrating its knowledge in order to solve problems.” I see this definition the most in regards to Evolutionary Biology, and while it is not that different from Pumpkin and I’s definition, notice that we already established earlier that no aspect of cognition can be independent of one’s previous experience. So “novel problem solving” is a nonsensical term. Subsequently one cannot define mental constructs as being separate from the cultural/environmental conditions they are situated in because said mental constructs cannot develop or exist without input from these exogenous factors. Intelligence is holistically catalyzed, so terms like innate, novel, or potential cannot be accurate descriptors for this concept.
Unfortunately, intelligence is almost always coextensive with these terms. These types of issues can cause all sorts of conceptual misunderstandings in discourse on the subject. For example a common criticism thrown at intelligence testing is the idea that they are culturally biased. Now these types of critiques are appropriate when in reference to more menial aspects of cultural differences like how the Japanese read right to left instead of left to right like Americans, or how the former tends to think more collectively than the latter. However, when you divorce the idea of “culture free potential” and “intelligence” from one another it becomes clear that intelligence is not really distinguishable from the application of cultural knowledge. Obviously it doesn’t take some sort of genius to see the fallacy in trying to give a Ugandan who only speaks his native tongue and has never ventured outside of his country the Weschler in english and then call him stupid when he inevitably fails, but that is not what’s happening. The truth of the matter is that East Asians consistently score higher on Intelligence and academic achievement tests than do westerners whom the tests are supposedly biased in favor of.
Ultimately, since human environments are their culture (Fuentes, 2018) and intelligence is the cognitive expression of your imprinted culture it may controversially imply that some cultures are just superior to others. Now of course you can’t impose any idea of “superiority” without first defining a reference point. So if intelligence is simply the mental ability to adapt then what is a good hallmark of intelligence? Innovation for one, and as most HBDers are aware, 1st world countries like South Korea and Germany have the highest levels of Innovation. Historically, western societies have also had the most instances of technological innovation. Even Physical Anthropologists use technological complexity( among other things) to deduce differences in intelligence between species of hominins (of course there are some exceptions). So some cultures are superior at producing innovation and concurrently are better at fostering the development of intelligence than others.
Originally I was planning on dedicating this section to the supposed construct validity of IQ tests which are currently the most accurate measures we have of intelligence. However, recently I came across what I believe is the single best critique(some may disagree) of IQ that I’ve read (Garrison, 2004). Garrison states in his section on validity: “In traditional psychometric theory, validity is defined as the degree to which a test measures what it claims to measure. I want to first point out the oddity of this formulation. For example, how does the reader respond to this: my ruler is valid to the degree to which it measures length? Is it normal practice to begin ruler validation by asking this seemingly circular question? Rulers by definition measure length. Note as well that by asking what a test measures the assumption that something is being measured goes unchallenged.” Notice, Garrison correctly points out the absurdity of construct validity as a sort of litmus test on whether a test supposedly measures what it purports to. Its circularity renders the use of construct validity in this way as fallacious and simultaneously charges of its supposed lack of construct validity (like Richardson, Norgate, 2015) are critically impotent.
In Garrison’s section on the “Scientific status of Psychometry” he states: “ The development of measurement has generally progressed from classification (qualities), to topology (comparisons) to metrication (measurements) (Berka, 1983). Classification concepts such as “cold” become topological when comparisons are used, such as colder than . . . . Thus they “enable us, not only to establish the sameness (or difference), but also to mutually compare at least two objects which possess a given property and, consequently, to arrange them into a sequence” (Berka, 1983, p. 6). he then goes on to claim that IQ tests only satisfy the first two criteria: “For example, norm-referenced achievement tests offer results in terms of percentile ranks, not delineations of what a student does or does not know about a given field of study, let alone diagnoses of the cause of difficulty. Put another way, scoring in the 70th percentile only indicates how well one did relative to the norm; it does not indicate 70 percent of required material was mastered. Thus the test remains at the topological level,” and because of this “The same problem exists with so-called measures of ability. Nash (1990) contends that norm-referenced ability tests only provide rank order information. “Students are ranked, in effect, by their ability to correctly answer test items, but it is inaccurate to argue that their ‘cognitive ability’ is therefore being measured” (Nash, 1990, p. 63).”. Of course this idea is false for reasons already iterated earlier in this post. Does answering test items correctly not require cognitive ability? However, Garrison believes that because “The validity discourse about test score meaning relative to testing purpose is based on value not residing in things or phenomenon themselves, but in their relation to subjects. Length, however, is a property of an object.” IQ tests are actually assessments of social value not measurements. First I need to clarify that there is a distinction between Criterion-referenced tests (CRT) and Norm-referenced tests (NRT), IQ is an example of the latter, and the former is indeed a measurement of a students knowledge in a particular field, not simply a comparison to the rankings of other students. Garrison may be correct in saying that because of this, IQ is just an assessment but scores on NRTs will highly predict those on CRTs and vice versa. So this distinction may matter little to the practical utility of IQ tests. But maybe I’m wrong, maybe its norm referencing isn’t the only reason it’s “just an assessment” and maybe the CRT’s don’t provide extra corroboration to these tests. Even If IQ is just an “assessment” instead of a “measurement” why does that matter? Moreover, even if it’s just an assessment of social value…so what? Do we not value the skills that are learned in school? Should we prioritize something else? Does he believe this subjectivity makes something less scientific? All definitions are inherently circular and thus are subjectively created. If we define this social value as intelligence is it not an ‘“assessment” of intelligence? What does this dichotomy really matter to the overall purpose of these tests?
In this article we’ve clarified what intelligence is, what emotions are, how both of these are catalyzed biologically. I’ve also cleared up logical misconceptions and criticisms on the subjects in the process: IQ is not something that is coextensive with innate potential and consciousness is not a biological mystery (at least in the sense of what it is). Furthermore, a lot of these ideas are not compatible with the consensus within HBD circles. If HBD wants to be taken seriously it needs to either address these issues and inconsistencies or get used to being treated like it’s astrology.
I’m going to go ahead and end this paper here. Simply because we’re already around 4,000 words and I’m sure I’ve bored half of you to death in the process. In the next part I’ll be going more into depth on the racial differences in EQ, what a culture neutral (not culture-free) IQ test may look like, our concept of personality, and the evolution of intelligence.
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.
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 al “lost 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.
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.
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.)