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The Oppression of the High IQs

1250 words

I’m sure most people remember their days in high school. Popular kids, goths, preppies, the losers, jocks, and the geeks are some of the groups you may find in the typical American high school. Each group, most likely, had another group that they didn’t like and became their rival. For the geeks, their rivals are most likely the jocks. They get beat on, made fun of, and most likely sit alone at lunch.

Should there be legal protection for such individuals? One psychologist argues there should be. Sonja Falck from the University of London specializes in high “ability” individuals and states that terms like “geek”, and “nerd” should be hate crimes and categorized under the same laws like homophobic, religious and racial slurs. She even published a book on the subject, Extreme Intelligence: Development, Predicaments, Implications (Falck, 2019). (Also see The Curse of the High IQ, see here for a review.)

She wants anti-IQ slurs to be classified as hate crimes. Sure, being two percent of the population (on a constructed normal curve) does mean they are a “minority group”, just like those at the bottom two percent of the distribution. Some IQ-ists may say “If the bottom two percent are afforded special protections then so should the top two percent.”

While hostile or inciteful language about race, religion, sexuality, disability or gender identity is classed as a hate crime, “divisive and humiliating” jibes such as ‘smart-arse’, ‘smart alec’, and ‘know-it-all’ are dismissed as “banter” and used with impunity against the country’s high-IQ community, she said.
According to Dr Falck, being labelled a ‘nerd’ in the course of being bullied, especially as a child, can cause psychological damage that may last a lifetime.
Extending legislation to include so-called ‘anti-IQ’ slurs would, she claims, help stamp out the “archaic” victimisation of more than one million Britons with a ‘gifted’ IQ score of 132 or over.
Her views are based on eight years of research and after speaking to dozens of high-ability children, parents and adults about their own experiences.
Non-discrimination against those with very high IQ is also supported by Mensa, the international high IQ society and by Potential Plus UK, the national association for young people with high-learning potential. (UEL ACADEMIC: ANTI-IQ TERMS ARE HATE CRIME’S ‘LAST TABOO’)

I’m not going to lie—if I ever came across a job application and the individual had on their resume that they were a “Mensa member” or a member of some other high IQ club, it would go into the “No” pile. I would assume that is discrimination against high IQ individuals, no?

It seems like Dr. Falck is implying that terms such as “smart arse”, “geek”, and “nerd” are similar to “moron” (a term with historical significance coined by Henry Goddard, see Dolmage, 2018), idiot, dumbass and stupid should be afforded the same types of hate crime legislation? Because people deemed to be “morons” or “idiots” were sterilized in America as the eugenics movement came to a head in the 1900s.

Low IQ individuals were sterilized in America in the 1900s, and the translated Binet-Simon test (and other, newer tests) were used for those ends. The Eugenics Board of North Carolina sterilized thousands of low IQ individuals in the 1900s—around 60,000 people were sterilized in total in America before the 1960s, and IQ was one way to determine who to sterilize. Sterilization in America (which is not common knowledge) continued up until the 80s in some U.S. states (e.g., California).

There was true, real discrimination against low IQ people during the 20th century, and so, laws were enacted to protect them. They, like the ‘gifted’ individuals, comprise 2 percent of the population (on a constructed curve by the test’s constructors), low IQ individuals are afforded protection by the law. Therefore, states the IQ-ist, high IQ individuals should be afforded protection by the law.

But is being called a ‘nerd’, ‘geek’, ‘smarty pants’, ‘dweeb’, ‘smart arse’ (Falck calls these ‘anti-IQ words‘) etc is not the same as being called terms that originated during the eugenic era of the U.S.. Falck wants the term ‘nerd’ to be a ‘hate-term.’ The British Government should ‘force societal change’ and give special protections to those with high IQs. People freely use terms like ‘moron’ and ‘idiot’ in everyday speech—along with the aforementioned terms cited by Falck.

Falck wants ‘intelligence’ to be afforded the same protections under the Equality Act of 2010 (even though ‘intelligence’ means just scoring high on an IQ test and qualifying for Mensa; note that Mensans have a higher chance for psychological and physiological overexcitability; Karpinski et al, 2018). Now, Britain isn’t America (where we, thankfully, have free speech laws), but Falck wants there to be penalities for me if I call someone a ‘geek.’ How, exactly, is this supposed to work? Like with my example above on putting a resume with ‘Mensa member’ in the “No” pile? Would that be discrimination? Or is it my choice as an employer who I want to work for me? Where do we draw the line?

By way of contrast, intelligence does not neatly fit within the definition of any of the existing protected characteristics. However, if a person is treated differently because of a protected characteristic, such as a disability, it is possible that derogatory comments regarding their intelligence might form part of the factual matrix in respect of proving less favourable treatment.

[…]

If the individual is suffering from work-related stress as a result of facing repeated “anti-IQ slurs” and related behaviour, they might also fall into the definition of disabled under the Equality Act and be able to bring claims for disability discrimination. (‘Anti-IQ’ slurs: Why HR should be mindful of intelligence-related bullying

How would one know if the individual in question is ‘gifted’? Acting weird? They tell you? (How do you know if someone is a Mensan? Don’t worry, they’ll tell you.) Calling people names because they do X? That is ALL a part of workplace banter—better call up OSHA! What does it even mean for one to be mistreated in the workplace due to their ‘high intelligence’? If there is someone that I work with and they seem to be doing things right, not messing up and are good to work with, there will be no problem. On the other hand, if they start messing up and are bad to work with (like they make things harder for the team, not being a team player) there will be a problem—and if their little quirks means they have a ‘high IQ’ and I’m being an IQ bigot, then Falck would want there to be penalties for me.

I have yet to read the book (I will get to it after I read and review Murray’s Human Diversity and Warne’s Debunking 35 Myths About Human Intelligence—going to be a busy winter for me!), but the premise of the book seems strange—where do we draw the line on ‘minority group’ that gets afforced special protections? The proposal is insane; name-calling (such as the cited examples in the articles) is normal workplace banter (you, of course, need thick skin to not be able to run to HR and rat your co-workers out). It seems like Mensa has their own out there, attempting to afford them protections that they do not need. High IQ people are clearly oppressed and discriminated against in society and so need to be afforded special protection by the law. (sarcasm)

This, though, just speaks to the insanity on special group protection and the law. I thought that this was a joke when I read these articles—then I came across the book.

Goddard Undefended

A recent YouTube video from the user “Modern Heresy” purports to critique Ken Richardson’s works in his 2017 book “Genes, Brains and Human Potential: The Science and Ideology of Intelligence” as well as some of his older works. I have addressed the claims most specifically about social class here, and RaceRealist has addressed the video as a whole here, but today I want to go more in detail on the issue of Goddard, since it took up basically a third of the video. I thought the section was fairly pedantic, as it’s barely two paragraphs of his book, but since the video creator thinks it to be so important [1], it must be addressed.

The issue of Goddard’s testing of immigrants on Ellis Island has long been the subject of academic controversy, being debated in the journal American Psychologist by Herrnstein, Kamin, Albee and others (Albee 1980; Dorfman 1982; Kamin 1982; Samelson 1985; Synderman & Herrnstein 1983). The most comprehensive rebuttal to Syndermann and Herrnstein’s erroneous paper can be found in Gelb et. al (1986), as noted by RaceRealist.

Basically, the issue that the video maker alleges is based around several small issues. The first relates to the proportion of the individuals tested that were found to be feeble-minded and the meaning of this result, and the other has to do with how Goddard tested immigrants on Ellis Island.

Richardson claims in his 2017 book that:

That was after long and trying journeys, using the tests in English through interpreters. By these means, the country came to be told that 83 percent of Jews, 80 percent of Hungarians, 79 percent of Italians, and 87 percent of Russians were feebleminded. Almost as bad were the Irish, Italians, and Poles and, bottom of the list, the blacks. Only the Scandinavians and Anglo- Saxons escaped such extremes of labeling.

Richardson (2017)

The video creator correctly notes that Goddard’s study was:

makes no determination of the actual percentage, even of these groups, who are feeble-minded.

Goddard (1917)

“Modern Heresy” then claims that this statement from the beginning of the Goddard paper demonstrates that Richardson was misrepresenting the paper. I agree that it is misrepresentation insofar as Richardson did not clarify that the primary purpose of the paper was not to determine the percentage of ‘feeble-minded’ individuals, but this is different than the primary claims that Richardson was making. Richardson’s broader point here is about the use of IQ tests to cause social harm, e.g. by the passage of the Immigration Act of 1924. Clearly, as Gelb et. al (1986) has shown, he is correct on this point. But the minutiae are what are interesting here, so let’s get into them

When Richardson states that:

83 percent of Jews, 80 percent of Hungarians, 79 percent of Italians, and 87 percent of Russians were feebleminded

Richardson (2017)

he is indeed accurately quoting a real statistic from one of Goddard’s paper (contra Herrnstein 1981), which occurs in Goddard’s Table II (Dorfman 1982). And again contra Herrnstein (and Cochran et. al 2006), this sample is not (entirely) a group of immigrants specifically chosen because of their feeblemindness, but includes a fairly representative sample. As noted by Goddard:

For the purpose of the first question an investigator selected 39 cases—20 were Italians and 19 were Russians—who appeared to her to be feeble-minded. These were then tested by the other investigator, the results being recorded for later study.

Goddard (1917)

Note that contra Cochran et. al (2006), there are no Jews in the sample that Goddard specifically selected of feebleminded individuals. But Goddard’s second selection is what is most relevant here, about which he states:

For the second question cases were picked who appeared to be representative of their respective groups. In this list we had 35 Jews, 22 Hungarians, 50 Italians and 45 Russians. (5 Jews, 2 Italians and 1 Russian were children under 12 years of age.

Goddard (1917)

Despite Goddard’s caution at the beginning of the article that “the study makes no determination of the actual percentage, even of these groups, who are feebleminded” (Goddard 1917, p. 243), he later notes that the sample is “representative”(Goddard 1917, p. 244) and that despite the selection involved in the sample due to the exclusion of “superior individuals”, the small number of them ” did not noticeably affect the character of the group” (Goddard 1917, p. 244). As such, he stated that to estimate the character of these national groups, one would only have to be “revised … by a relatively small amount” (Goddard 1917, p. 244). He finally concluded that “one can hardly escape the conviction that the intelligence of the average ‘third class’ immigrant is low, perhaps of moron grade”.

But the broader point that “the country came to be told that ….” that Richardson makes is equally both slightly misrepresentative but also broadly correct. A news article published in 1917 about Goddard’s paper noted that “the most favorable interpretation of their results is that two out of every five of the immigrants studied were feebleminded” (The Survey 1917). It also describes that 83 percent of Russians were found to be feebleminded using the typical criterion, meaning that Richardson’s note that the Amerikan was exposed to the claims of immigrant feeblemindedness is accurate, even if Goddard’s article itself can’t be used to make those conclusions. Indeed, it was Pioneer Fund president Harry Laughlin who cited Goddard’s figures in his testimony to Congress during the debate over the Immigration Act of 1924 (Swanson 1995). It is well known that science is commonly misrepresented by the public, and this example may be one of many (Dumas-Mallet et. al 2017). The video creator alleges that because Goddard attributed this low intelligence level to environment rather than heredity, Richardon’s discussion of Goddard is yet again incorrect. But Richardson does not name Goddard as an anti-immigrant xenophobe, he merely points out that these figures later became the basis for anti-immigration xenophobia, which is a historical fact as noted above. Again, the video creator confuses Richardon’s discussion of Goddard and the discussion of xenophobia and then conflate Richardson’s claims with the ones made by Kamin and Gould in the past.

There is one more issue brought up in the video as to Richardon’s portrayal of Goddard’s testing of immigrants, and it is Richardson’s claim that:

Amid distressing scenes at the infamous reception center on Ellis Island, he managed to ensure that all immigrants— men, women, and children of all ages— were given the IQ test as soon as they landed

Richardson (2017)

While it is unclear as to Goddard’s specific role in the development of the use of testing during immigration proceedings on Ellis Island, it is uncontested that there was widespread use of mental tests upon entry to the island (Mullan 1917; Zenderland 1998, p. 419 note 17), and that Goddard was the person who was sent out to inspect the mental testing procedures the immigration enforcement officers were engaging in in the first place (Goddard 1917; Sussman 2014, p. 84) following the US ban on “moronic immigrants” and subsequent fear that moronic immigrants were still getting through (Davis 1925, p. 218-219; Wilkes-Barre Record 1907). Again, while Richardson’s treatment of the issue is curt and may seem a bit reductive, it is not wholly inaccurate. He’s not writing a history textbook or publishing a paper in The American Historical Review, he’s writing a book that covers numerous topics about IQ.

[1] The author again brings up the Goddard issue in the comment reply to RR’s recent article.

Social Class, Ken Richardson and “Modern Heresy”

Note: I am new to this blog. I blog at https://developmentalsystem.wordpress.com and https://www.sillyolyou.com

As RaceRealist has already noted, a recent YouTube video purports to critique Ken Richardson’s work on IQ tests and their relationship with social class. Since he already covered a number of the relevant parts about Goddard, construct validity and a number of other topics, I wanted to focus more on the question of social class. This is one of the claims that RaceRealist brings up from Richardson’s work quite frequently, so it’s probably the most pertinent at this point in time.

Note: I watched the video about a week ago, so if I get any of the details mixed up, please let me know.

One of the claims that the author of the YouTube video makes is that because a large proportion of the variation in IQ is within-family, rather than between-families, it cannot be that IQ is a metric of social class. The logic here is quite simple: behavioral genetic studies tell us that the average difference between two siblings in the same family is about 12 IQ points, while the average difference between two randomly selected individuals in the population is 15 points. That means that, according to the creator of the video, “about 70% of the IQ variation in society is due to within-family differences”. We should note two things. The first is that the figure cited here is incorrect, even if we accept the values for the standard deviations within the family. The video creator seems to have calculated the percent of variation as a proportion of the standard deviations (\sigma), rather than the actual variances (\sigma^2). The proper proportion would be \frac{12^2}{17^2}=0.498, which is 49.8%. That still leaves 50.2% of the variation between families. The other issue is that I very much doubt the figure of a typical difference of 12 IQ points between siblings. The formula for the expected absolute difference between two siblings in the same family is \frac{2\cdot\sqrt{\frac{V_a}{2}+V_e}}{\sqrt{\pi}} (here V_e=1-V_a. If we assume that the phenotypic standard deviation is 15 (as defined for IQ tests), we can compute the expected difference for different values of heritability. We can quickly note that the issue with this is that if the heritability of the trait is zero, then the expected phenotypic difference for siblings is \frac{2\cdot\sqrt{\frac{0\cdot15^2}{2}+(1-0)\cdot15^2}}{\sqrt{\pi}}=16.9, whereas two random strangers would have a difference of \int_{-\infty}^{\infty} \int_{-\infty}^{\infty}\text{PDF}(\mathcal{N}(0,1),\text{x})\cdot\text{PDF}(\mathcal{N}(0,1),y)|y-x|\cdot 15 dx dy=16.9 [1]. If we were to take the author’s proposal for how much of the variation is within-family vis a vis between-family, we would have to conclude that \frac{16.9}{16.9}=1 or 100% of the variance is within-family, while just 0% of the variance is between-families. Does it make sense that that even if heritability were zero that only 0% could represent social class? No, it doesn’t, because there are issues here. The first is that variation in IQ is not the relevant metric here. If we take the notion that there is a factor of the matter about the IQ score of someone (i.e. there exists a ‘true score’), then IQ would have measurement error (Whitaker 2010). The consequence of this alleged measurement error would be to inflate the proportion of variation that is within-family. First, denote variances as such: V_a for additive genetic variance, V_e for environmental variance, and V_m for measurement error variance. The within-family calculation would be \frac{2\sqrt{\frac{V_a}{2}+V_e+V_m}}{\sqrt{\pi}} (per the formula above) while the between-family calculation would be \frac{2\sqrt{2\cdot(V_a+V_e+V_m)}}{\sqrt{\pi}} for observed IQ scores, while the true relevant quantities would be \frac{2\sqrt{\frac{V_a}{2}+V_e}}{\sqrt{\pi}} and \frac{2\sqrt{2\cdot(V_a+V_e)}}{\sqrt{\pi}}. Note that our fractions (percent of variation within families) \frac{\frac{2\sqrt{\frac{V_a}{2}+V_e+V_m}}{\sqrt{\pi}}}{\frac{2\sqrt{2\cdot(V_a+V_e+V_m)}}{\sqrt{\pi}}} and \frac{\frac{2\sqrt{\frac{V_a}{2}+V_e}}{\sqrt{\pi}}}{\frac{2\sqrt{2\cdot(V_a+V_e)}}{\sqrt{\pi}}}. Some simple algebra can show that \frac{\frac{2\sqrt{\frac{V_a}{2}+V_e+V_m}}{\sqrt{\pi}}}{\frac{2\sqrt{2\cdot(V_a+V_e+V_m)}}{\sqrt{\pi}}} > \frac{\frac{2\sqrt{\frac{V_a}{2}+V_e}}{\sqrt{\pi}}}{\frac{2\sqrt{2\cdot(V_a+V_e)}}{\sqrt{\pi}}} [2], which means that so long as V_a (additive genetic variance) and V_m (measurement error variance) are both positive (e.g. there is both measurement error and heritability), then the fraction of variation that is between-families calculated from observed IQs will be an overestimate because of measurement error.

The other issue with the creators claims is the “assumption that social class varies between families but not within families”. While it may seem obvious at first, there are a number of issues. The first is that an individual’s attained social class during adulthood (and thus the social class in which they inhabit) is not identical within families. Two kids may have started off with very similar IQs due to their family environments, but due to various reasons (random chance, developed interests, etc), they moved into different social classes in adulthood, following which their IQs diverged due to the different social classes they now inhabit. The reason why this is relevant is because the statistic that the creator is using to (erroneously) claim that 70% of the variation is within families does not specify the age at which these measurements were taken – it is likely that they were taken in later life, meaning that the social class of the individuals has already diverged.

Moreover, even when children are within the same family at earlier ages, there is reason to argue that their social class is also not identical. Sociologists now understand that social class is a dynamic structure that is not only reproduced by aspects of economic access, resources and opportunity that individuals have access to, but that sociocultural signifiers, subjective experiences, interests and other aspects also contribute to ones social class. As noted by Richardson himself, one’s subjective SES may better reflect the sociocognitive environment that one develops in (Richardson & Jones 2019):

It is self-conscious social status in relation to others in a class structure – i.e. what has been called subjective as opposed to objective social class – that seems to influence a wide range of educational and cognitive outcomes. There is only moderate correlation between that and current SES

And this subjective SES can quite evidently differ between siblings and differentially impact their IQs. Moreover, there are numerous other aspects of social class that can vary within-family such as: school quality (e.g. school resources; Leon & Valdiva 2015), peer effects (Hoxby 2000), teacher and classroom effects (Boyd-Zaharias 1999; Chetty et. al 2015), and societal expectations (Jensen & McHale 2016). Small initial differences in these environmental variables can be magnified through phenotype-environment processes (Beam & Turkheimer 2013) that can create a seemingly large within-family variation that cannot be attributed to social class, but could in fact be the result of it.

Another vitally important thing to note is that even if we accept the concept of social class as measured by socioeconomic status as a simple standardized combination of income, parental education and occupational status, that doesn’t mean that this variable can’t differ in important ways within the family. First note that siblings are not always the same age (the exception is with twins). As a result, the developmental environment in which each child grows up with is not identical. As Richardson noted over a decade ago, children within the family do not experience the same environment (Richardson & Norgate 2005). This is not only because of perceptual experiences, phenotype→environment feedback loops, but because the importance of the timing of developmental experiences means that changes in parental socioeconomic status over the time means that children are exposed to different socioeconomic environments during these critical periods (Sylva 1997). For instance, parental socioeconomic status and as a result maternal stress can differ during the mother’s pregnancies (Richardson 2019), causing differences between the two children’s development.

Social Class or Sociocognitive Preparedness?

We should note that this critique is premised entirely on the idea that Richardson is positing that social class is a gigantic determinant of IQ, to the neglect of other environmental factors. This is an erroneous assumption, as the paper in which Richardson lays out his theory of what IQ tests are a proxy for (Richardson 2002; “What IQ Tests Test”), he argues that ” population variance in IQ scores can be described in terms of a nexus of sociocognitive-affective factors that differentially prepares individuals for the cognitive, affective and performance demands of the test”, that in effect, makes the test a measure of social class. Note that he does not quantify the specific amount of variation that is explained by social class, and that over 50% of the variation (as a minimum using the assumptions questioned above) explainable by social class (meaning a correlation of 0.7) could definitely qualify under his meaning. Regardless, Richardson’s primary explication is in terms of the “nexus of sociocognitive-affective factors” is perfectly compatible with the within vs between population variance described in the video.

There are numerous factors that influence intelligence that Richardson describes that can differ within families, such as “individuals’ psychological proximity to that set” of cultural tools, parental interactions with children (Hart & Risley 1995; Jensen & McHale 2016), affective preparedness, etc. All of these factors can additionally explain the IQ variance, meaning that the critique of Richardson’s explanation of IQ variance does not go through.

Predictive (In)Validity?

The creator of the video also claims that the Bell Curve demonstrated that IQ remains predictive once SES is controlled for and that IQ is a much better predictor that SES. Despite this common claim by Bell Curve fanatics, it has been demonstrated to be incorrect more times than one can count (Fischer et. al 1996; Ragin & Fiss 2016). In fact, a closer analysis of the model Murray and Herrnstein fit shows that they predicted NOT ONE of their poverty cases correctly (Krenz n.d.; see also Dickens et. al 1995, Goldberger & Manski 1995). A more thorough examination of the claims related to the alleged predictive validity of IQ can be found here.

[1] A simpler way to get the result is to calculate the variance from simple distribution addition/difference rules and then multiply that by the expected difference for normal distributions \frac{2}{\sqrt{\pi}}

[2] \frac{\frac{2\sqrt{\frac{V_a}{2}+V_e+V_m}}{\sqrt{\pi}}}{\frac{2\sqrt{2\cdot(V_a+V_e+V_m)}}{\sqrt{\pi}}}\geq \frac{\frac{2\sqrt{\frac{V_a}{2}+V_e}}{\sqrt{\pi}}}{\frac{2\sqrt{2\cdot(V_a+V_e)}}{\sqrt{\pi}}}\implies\frac{\sqrt{\frac{V_a}{2}+V_e+V_m}}{\sqrt{2\cdot(V_a+V_e+V_m)}}\geq\frac{\sqrt{\frac{V_a}{2}+V_e}}{\sqrt{2\cdot(V_a+V_e)}}\implies\frac{\frac{V_a}{2}+V_e+V_m}{2\cdot(V_a+V_e+V_m)}\geq\frac{\frac{V_a}{2}+V_e}{2\cdot(V_a+V_e)}\implies \frac{\frac{V_a}{2}+V_e+V_m}{V_a+V_e+V_m}\geq\frac{\frac{V_a}{2}+V_e}{V_a+V_e}\implies (\frac{V_a}{2}+V_e+V_m)(V_a+V_e)\geq(\frac{V_a}{2}+V_e)(V_a+V_e+V_m)\implies \frac{V_a^2}{2}+\frac{V_aV_e}{2}+V_eV_a+V_e^2+V_aV_m+V_eV_m\geq\frac{V_a^2}{2}+\frac{V_aV_e}{2}+\frac{V_aV_m}{2}+V_eV_a+V_e^2+V_eV_m\implies(\frac{V_a^2}{2}-\frac{V_a^2}{2})+(\frac{V_aV_e}{2}-\frac{V_aV_e}{2})+(V_eV_a-V_eV_a)+(V_e^2-V_e^2)+(V_aV_m-\frac{V_aV_m}{2})+(V_eV_m-V_eV_m)\geq0\implies \frac{V_aV_m}{2}\geq0

Correlation and Causation Regarding the Etiology of Lung Cancer in Regard to Smoking

1550 words

The etiology of the increase in lung cancer over the course of the 20th century has been a large area of debate. Was it smoking that caused cancer? Or was some other, unknown, factor the cause? Causation is multifactorial and multi-level—that is, causes of anything are numerous and these causes all interact with each other. But when it comes to smoking, it was erroneously argued that genotypic differences between individuals were the cause of both smoking and cancer. We know now that smoking is directly related to the incidence of lung cancer, but in the 20th century, there were researchers who were influenced and bribed to bring about favorable conclusions for the tobacco companies.

Psychologist Hans Eysenck (1916-1997) was a controversial psychologist researching many things, perhaps most controversially, racial differences in intelligence. It came out recently, though, that he published fraudulent papers with bad data (Smith, 2019). He, among other weird things, believed that smoking was not causal in regard to cancer. Now, why might Eysenck think that? Well, he was funded by many tobacco companies (Rose, 2010; Smith, 2019). He accepted money from tobacco companies to attempt to disprove the strong correlation between smoking and cancer. Between the 1977-1989, Eysenck accepted about 800,000 pounds from tobacco companies. He is not alone in holding erroneous beliefs such as this, however.

Biostatistician Ronald Fisher (1890-1962) (a pipe smoker himself), the inventor of many statistical techniques still used today, also held the erroneous belief that smoking was not causal in regard to cancer (Parascandola, 2004). Fisher (1957) argued in a letter to the British Medical Journal that while there was a correlation between smoking and the acquisition of lung cancer, “both [are] influenced by a common cause, in this case the individual genotype.” He went on to add that “Differentiation of genotype is not in itself an unreasonable possibility“, since it has been shown that genotypic differences in mice precede differences “in the frequency, age-incidence and type of the various kinds of cancer.

So, if we look at the chain it goes like this: people smoke; people smoking is related to incidences in cancer; but it does not follow that since people smoke that the smoking is the cause of cancer, since an unknown third factor could cause both the smoking and cancer. So now we have four hypotheses: (1) Smoking causes lung cancer; (2) Lung cancer causes smoking; (3) Both smoking and lung cancer are caused by an unknown third factor. In the case of (3), this “unknown third factor” would be the individual genotype; and (4) the relationship is spurious . Fisher was of the belief that “although lung cancer occurred in cigarette smokers it did not necessarily follow that the cancer was caused by cigarettes because there might have been something in the genetic make up of people destined to have lung cancer that made them addicted to cigarettes” (Cowen, 1999). Arguments of this type were popular in the 19th and 20th century—what I would term ‘genetic determinists’ arguments, in that genes dispose people to certain behaviors. In this case, genes disposed people to lung cancer which made them addicted to cigarettes.

Now, the argument is as follows: Smoking, while correlated to cancer is not causal in regard to cancer. Those who choose to smoke would have acquired cancer anyway, as they were predisposed to both smoke and acquire cancer at X age. We now know, of course, that such claims are ridiculous—no matter which “scientific authorities” they come from. Fisher’s idea was that differences in genotype caused differences in cancer acquisition and so along with it, caused people to either acquire the behavior of smoking or not. While at the time such an argument could have been seen as plausible, the mounting evidence against the argument did nothing to sway Fisher’s belief that smoking did not outright cause lung cancer.

The fact that smoking caused lung cancer was initially resisted by the mainstream press in America (Cowen, 1999). Cowen (1999) notes that Eysenck stated that, just because smoking and lung cancer were statistically associated, it did not follow that smoking caused lung cancer. Of course, when thinking about what causes, for example, an observed disease, we must look at similar habits they have. And if they have similar habits and it is likely that those with similar habits have the hypothesized outcome (smokers having a higher incidence of lung cancer, in this case), then it would not be erroneous to conclude that the habit in question was a driving factor behind the hypothesized disease.

It just so happens that we now have good sociological research on the foundations of smoking. Cockerham (2013: 13) cites Hughes’ (2003) Learning to Smoke: Tobacco Use in the West where he describes the five stages that smokers go through: “(1) becoming a smoker, (2) continued smoking, (3) regular smoking, (4) addicted smoking, and, for some, (5) stopping smoking.” Most people report their first few times smoking cigarettes as unpleasant, but power through it to become a part of the group. Smoking becomes somewhat of a social ritual for kids in high-school—with kids being taught how to light a cigarette and how to inhale properly. For many, starting smoking is a social thing that they do with their friends—it can be said to be similar to being social drinkers, they were social smokers. There is good evidence that, for many, their journey as smokers starts and is fully dependent on their social environment than actual physical addiction (Johnson et al, 2003; Haines, et al, 2009).

One individual interviewed in Johnson et al (2003: 1484) stated that “the social setting
of it all [smoking] is something that is somewhat addictive itself.” So, not only is the nicotine the addictive substance on the mind of the youth, so too is the social situation for the youth in which the smoking occurs. The need to fit in with their peers is one important driver for the beginning—and continuance—of the behavior of smoking. So we now have a causal chain in regard to smoking, the social, and disease: youths are influenced/pressured to smoke by their social group which then leads to addiction and then, eventually, health problems such as lung cancer.

The fact that the etiology of smoking is social leads us to a necessary conclusion: change the social network, change the behavior. Just as people begin smoking in social groups, so too, do people quit smoking in social groups (Christakis and Fowler, 2008). We can then state that, on the basis of the cited research, that the social is ultimately causal in the etiology of lung cancer—the vehicle of cancer-causation being the cigarettes pushed bu the social group.

Eysenck and Fisher, two pioneers of statistics and different methods in psychology, were blinded by self-interest. It is very clear with both Eysenck and Fisher, that their beliefs were driven by Big Tobacco and the money they acquired from them. Philosopher Donald Davidson famously stated that reasons are causes for actions (Davidson, 1963). Eysenck’s and Fisher’s “pro-belief” (in this case, the non-causation of smoking to lung cancer) would be their “pro-attitude” and their beliefs lead to their actions (taking money from Big Tobacco in an attempt to show that cigarettes do not cause cancer).

The etiology of lung cancer as brought on by smoking is multifactorial, multilevel, and complex. We do have ample research showing that the beginnings of smoking for a large majority of smokers are social in nature. They begin smoking in social groups, and their identity as a smoker is then refined by others in their social group who see them as “a smoker.” Since individuals both begin smoking in groups and quitting in groups, it then follows that the acquisition of lung cancer can be looked at as a social phenomenon as well, since most people start smoking in a peer group.

The lung cancer-smoking debate is one of the best examples of the dictum post hoc, ergo propter hoc—or, correlation does not equal causation (indeed, this is where the dictum first originated). While Fisher and Eysenck did hold to that view in regard to the etiology of lung cancer (they did not believe that since smokers were more likely to acquire lung cancer that smoking caused lung cancer), it does speak to the biases the two men had in their personal and professional lives. These beliefs were disproven by showing a dose-dependent relationship in regard to smoking and lung cancer: heavier smokers had more serious cancer incidences, which tapered down the less an individual smoked. Fisher’s belief, though, that differences in genotype caused both behavior that led to smoking and the lung cancer itself, while plausible at the time, was nothing more than a usual genetic determinist argument. We now know that genes are not causes on their own; they do not cause traits irrespective of their uses for the physiological system (Noble, 2012).

Everyone is biased—everyone. Now, this does not mean that objective science cannot be done. But what it does show is that “… scientific ideas did not develop in a vacuum but rather reflected underlying political or economic trends” (Hilliard, 2012: 85). This, and many more examples, speak to the biases of scientists. For reasons like this, though, is why science is about the reproduction of evidence. And, for that, the ideas of Eysenck and Fisher will be left in the dustbin of history.

African Neolithic Part 2: Misunderstandings Continue

Last time I’ve posted on this subject, it was dissecting the association between magical thinking and technological progress among Africans proposed by Rinderman. In general, I found it wanting of an up-to-date understanding of African anthropology, either in material culture or belief systems. This time, however, the central subject can’t be dismissed on the matter of ignorance. In fact, in a rather awkward way, his dismissal in on the grounds of how much he knows in bot his field and his own writings.

Henry Harpending, deceased, has been listed by the SPLC as a “white nationalist”, though it is the specific content of his quotes in regards to Africans, in light of his admittedly impressive contributions to SW African anthropology, is the major focus than classifying the nature of his bias. The claims in question are

  1. He has never meet an African who has a hobby, that is, one with the inclination to work.
  2.  Hunter Gatherers are impulsive, lazy, and violent.
  3. Africans are more interested in breeding than raising children.
  4. Africans, Baltimore Aframs, and PNG natives all share the same behavior in regard to points 2 and 3.
  5. Superstitions are pan-african and the only Herero he’s met that was an atheist had a ethnic German Father.

So Harpending seemingly has the edge given his background in Anthropology with specific experiences with Africans…this only makes the only more painful to articulate.

  1.  This will set the theme for the nature of my responses…his own work contradicts these assertions. The Herero refugee descent from Botswana, the main strain of Bantu-Speaking Africans he had studied,  were described and calculated as prosperous in regards to cattle per capita and ownership of rural homesteads that stand apart from typical Botswana farming infrastructure.

    Today, they are perceived as one of the wealthiest ethnic groups inBotswana and Namibia. They are known for their large herds, for theirs kill at managing cattle, and for their endogamy and staunch ethnicity even while participating fully in the developing economy and educational system of Botswana.

    His research even noted how age five is when Herero begin herding. A similar phenomenon is noted among the Dinka which prompted Dutton to review the literature of their intelligence scores.

  2.  Violence among the Khoi-San groups I’ll admit has been undermined. However, the Hadza, known for their discourage mean of conflict, express this through much lower rates of violent deaths compared to most others. The general consensus is that there is a mix, with the general trend towards higher rates but with cautious interpretation into the causes. On the charge of Laziness, however, is once again unfounded by his work on the lesser resources faced by mobile bands of foragers compared to sedentary ones on labor camps. The same link on the Hadza also pinpoints the hours spent in HG life working and accounts for the difficulty of those hours.
  3.  Harpending actually made a model of cads versus dads that he actually attributed to non-genetic factors. Otherwise, we are left with his work on the oddity of “Herero Households”.

    If women cannot provision themselves and their offspring without
    assistance, then the “cad/breeder” corner of Fig. 2 is not feasible, and we are left with “dad/feeder.” Draper and Harpending argue that this is true of the Ju/’hoansi, and other mobile foragers in marginal habitats. Among swidden agriculturalists, on the other hand, female labor is more productive, and men can afford to do less work. The theory thus predicts that such populations will be more likely to fall into the “cad/breeder” equilibrium, as in fact they seem to do. Although this theory is couched in Darwinian terms, Harpending and Draper do not see genetic evolution as the engine that accounts for variation within and among societies. Instead, they suggest a facultative adaptation: humans have “evolved the ability to sense household structure in infancy” and to alter their developmental trajectories in response to what is learned during this early critical period (1980, p. 63).

    There does not seem to be any durable group of associated individuals that we could usefully characterize as a household among the Herero. If forced we would say that the Herero have two parallel types of households. The “male household” is the homestead, consisting of an adult male, his wives, sisters, and other relatives, and it is defined by the herd and the kraals that he maintains for the herd. The “female household” is a woman and the children for whom she has responsibility, localized in a hut or hut cluster within a larger homestead. These aregynofocal households, rather than matrifocal households, since matrifocal implies mother and offspring while the Herero unit is a woman and children under the care of that woman. These children may be her own, her grandchildren, children of relatives, or even children leased from other tribes to work on the cattle. Men do not appear prominently in daily domestic life. They are gone at first light pursuing their own interests and careers with cattle, with hunting parties, or with other stereotyped male activities. Similarly, women are not prominently present at male areas like the wells where the cattle are watered. There is, then, not a Herero household, but rather there is a Herero male household that includes cattle and female households, and these females may be wives, or sisters, or other female relatives. The female households are the loci of domestic production and consumption. 

    However, it does not follow that the lack of interpersonal interaction means the lack of acknowledgement in parenthood within households. One is by association.


    We interviewed 161 adult Herero (112 females, 49 males) intensively about the residence of themselves, their siblings with whom they share a mother or a father and about their legal children (children born in marriage or children in whom they had purchased parental rights). None of the men we interviewed whose fathers were still alive (n = 10) considered his residence to be in a homestead different from his father’s. Only two of the men had sons with residences elsewhere –one was a child who had been purchased but was living with the mother and the other was a child borne by a wife from whom he was now divorced. We also heard of very few men ascertained in several hundred shorter demographic interviews that were residing in a homestead other than their fathers’. Most of the men(24/39) with deceased fathers had their own homesteads. Brothers who had both the same mother and father were more likely to stay together, however, than brothers who had different mothers. 

    The other comes from Harpending’s own blog post regarding his Herero friend who claims the children of his new wife as being of his household despite not actually conceiving them. Note, he also describes the man as “prosperous”.

  4. I sadly lack data on Bantu rates of violence, swearing I once found data showing it to be low compared to that of the Khoi-san. If anybody has quantified data like in the link regarding the Hadza then that would be appreciated. In regards to parenting however it doesn’t reflect that by comparing non-resident fathers. Regarding Africans, here’s a perspective from a female perspective.
  5. This point once again warrants the mention of superstitions still being quite common in non Western societies like China in regards to evil spirits and luck. Likewise, traditions are known to be modified or dropped among Herero in major urban centers. The Herero Harpending encountered that he labeled “employees” nonetheless grew up near the study areas.

Before I end this, I want to cover some further discrepancies by another author who refers to his work, Steve Sailer.

The small, yellow-brown Bushmen, hunters who mated more or less for life and put much effort into feeding their nuclear families, reminded Henry of his upstate New York neighbors. If fathers didn”€™t work, their children would go hungry.

In contrast, the Bantu Herero (distant relatives of American blacks) were full of surprises. In general, black African men seemed less concerned with bringing home the bacon to provision their children than did Bushmen dads.

This doesn’t deviate too far from what Harpending explains. That comes later.

In black African farming cultures, women do most of the work because agriculture involves light weeding with hoes rather than heavy plowing. Men are less expected to contribute functionally to their children’s upkeep, but are expected to be sexy.

So technically this is correct but only to a certain degree in regards to division of labor. It’s particular to farming schemes where root/tuber agriculture is done, and in those areas forest clearing is done by males.

One parallel is that Baumann views climatic and environmental factors as closely
associated with differences in the participation of the sexes in agriculture. He observes that the northern boundary of women’s predominance in agriculture is constrained by the limits of the tropical forest region, and that the boundary of female agriculture also tends to coincide with that between root crops and cereal grains. Baumann’s view of the economies of labor is also similar to our own. He emphasizes that land clearing is more difficult in the forest than in the savannah, and that males often perform clearing in the forest zones in spite of the predominance of female labor, whereas soil preparation is more difficult in the savannah than in the forest. He notes the higher male participation in agriculture in the savannah region of the Sudan than in the West African and Congo forest regions, and more generally, that women are much more likely to participate in root cultivation than in cereal cultivation.

Not mention other activities such as crafts and trading. Baumann’s old scheme as it is is still simplistic. More research shows that labor between sexes shift depending on circumstances. See this on Igbo yam farming or West African Cocoa farming. This trend of shifting continues into the modern day.

In many places in Africa, traditionally there has been a
strict division of labor by gender in agriculture. This
division of labor may be based on crop or task, and both
types of division of labor by gender may occur
simultaneously. Women may mobilize male labor for some
tasks involved in their crops and men frequently mobilize
women’s labor for crops that they control. These divisions
are not static and may change in response to new
economic opportunities.

Likewise, male development in connection to their father is represented in this early anthropological text through inheritance of property and apprenticeship. Collective Fatherhood through the extended family is also recognized, with actual absence being highly due to migrant labor in Southern African countries.

The “Sexy” part is rather presumptuous and absent from the text, where it is in fact the woman that is scrutinized uphold standards in the chapter of Ibo courtship, which seems to be widespread. The simple and lazy role reversal is obvious, as it assumes that female labor undermined the general trend of patriarchy since they weren’t always dependent on the male.

So with all this said, what is there to make of it?: As far as direct connections to the Herero go, Harpending didn’t show any particular malice. Any such was more towards western phenomenon that he draws parallels with. As far as his conference comments, obvious bias is just that. His blog posts don’t even read as such, clearly contradicting it comments of industry among Africans according to his experience for one matter.

It may sadly suggest the type of filter scene through experience in this “field”.

The “World’s Smartest Man” Christopher Langan on Koko the Gorilla’s IQ

1500 words

Christopher Langan is purported to have the highest IQ in the world, at 195—though comparisons to Wittgenstein (“estimated IQ” of 190), da Vinci, and Descartes on their “IQs” are unfounded. He and others are responsible for starting the high IQ society the Mega foundation for people with IQs of 164 or above. For a man with one of the highest IQs in the world, he lived on a poverty wage at less than $10,000 per year in 2001. He has also been a bouncer for the past twenty years.

Koko is one of the world’s most famous gorillas, most-known for crying when she was told her cat got hit by a car and being friends with Robin Williams, also apparently expressing sadness upon learning of his death. Koko’s IQ, as measured by an infant IQ test, was said to be on-par or higher than some of the (shoddy) national IQ scores from Richard Lynn (Richardson, 2004; Morse, 2008). This then prompted white nationalist/alt-right groups to compare Koko’s IQ scores with that of certain nationalities and proclaim that Koko was more ‘intelligent’ than those nationalities on the basis of her IQ score. But, unfortunately for them, the claims do not hold up.

The “World’s Smartest Man” Christopher Langan is one who falls prey to this kind of thinking. He was “banned from” Facebook for writing a post comparing Koko’s IQ scores to  that of Somalians, asking why we don’t admit gorillas into our civilization if we are letting Somalian refugees into the West:

“According to the “30 point rule” of psychometrics (as proposed by pioneering psychometrician Leta S. Holingsworth), Koko’s elevated level of thought would have been all but incomprehensible to nearly half the population of Somalia (average IQ 68). Yet the nation’s of Europe and North America are being flooded with millions of unvetted Somalian refugees who are not (initially) kept in cages despite what appears to be the world’s highest rate of violent crime.

Obviously, this raises the question: Why is Western Civilization not admitting gorillas? They too are from Africa, and probably have a group mean IQ at least equal to that of Somalia. In addition, they have peaceful and environmentally friendly cultures, commit far less violent crime than Somalians…”

I presume that Langan is working off the assumption that Koko’s IQ is 95. I also presume that he has seen memes such as this one floating around:

kokooiq

There are a few problems with Langan’s claims, however. (1) The notion of a “30-point IQ point communication” rule—that one’s own IQ, plus or minus 30 points, denotes where two people can understand each other; and (2) bringing up Koko’s IQ and the comparing it to “Somalians.”

It seems intuitive to the IQ-ist that a large, 2 SD gap in IQ between people will mean that more often than not there will be little understanding between them if they talk, as well as the kinds of interests they have. Neuroskeptic looked into the origins of the claim of the communication gap in IQ, found it to be attributed to Leta Hollingworth and elucidated by Grady Towers. Towers noted that “a leadership pattern will not form—or it will break up—when a discrepancy of more than about 30 points comes to exist between leader and lead.Neuroskeptic comments:

This seems to me a significant logical leap. Hollingworth was writing specifically about leadership, and in childen [sic], but Towers extrapolates the point to claim that any kind of ‘genuine’ communication is impossible across a 30 IQ point gap.

It is worth noting that although Hollingworth was an academic psychologist, her remark about leadership does not seem to have been stated as a scientific conclusion from research, but simply as an ‘observation’.

[…]

So as far as I can see the ‘communication range’ is just an idea someone came up with. It’s not based on data. The reference to specific numbers (“+/- 2 standard deviations, 30 points”) gives the illusion of scientific precision, but these numbers were plucked from the air.

The notion that Koko had an “elevated level of thought [that] would have been all but incomprehensible to nearly half the population of Somalia (average IQ 68)” (Langan) is therefore laughable, not only for the reason that a so-called communication gap is false, but for the simple fact that Koko’s IQ was tested using the Cattell Infant Intelligence Scales (CIIS) (Patterson and Linden,1981: 100). It seems to me that Langan has not read the book that Koko’s handlers wrote about her—The Education of Koko (Patterson and Linden, 1981)—since they describe why Koko’s score should not be compared with human infants, so it follows that her score cannot be compared with human adults.

The CIIS was developed “to a downward extension of the Stanford-Binet” (Hooper, Conner, and Umansky, 1986), and so, it must correlate highly with the Stanford-Binet in order to be “valid” (the psychometric benchmark for validity—correlating a new test with the most up-to-date test which had assumed validity; Richardson, 1991, 2000, 2017; Howe, 1997). Hooper, Conner, and Umansky (1986: 160) note in their review of the CIIS, “Given these few strengths and numerous shortcomings, salvaging the Cattell would be a major undertaking with questionable yield. . . . Nonetheless, without more research investigating this instrument, and with the advent of psychometrically superior measures of infant development, the Cattell may be relegated to the role of an historical antecedent.” Items selected for the CIIS—like all IQ tests—“followed a quasi-statistical approach with many items being accepted and rejected subjectively.” They state that many of the items on the CIIS need to be updated with “objective” item analysis—but, as Jensen notes, items emerge arbitrarily from the heads of the test’s constructors.

Patterson—the woman who raised Koko—notes that she “tried to gauge [Koko’s]
performance by every available yardstick, and this meant administering infant IQ tests
” (Patterson and Linden, 1981: 96). Patterson and Linden (1981: 100) note that Koko did better than human counterparts of her age in certain tasks over others, for example “her ability to complete logical progressions like the Ravens Progressive Matrices test” since she pointed to the answer with no hesitation.

Koko generally performed worse than children when a verbal rather than a pointing response was required. When tasks involved detailed drawings, such as penciling a path through a maze, or precise coordination, such as fitting puzzle pieces together. Koko’s performance was distinctly inferior to that of children.

[…]

It is hard to draw any firm conclusions about the gorilla’s intelligence as compared to that of the human child. Because infant intelligence tests have so much to do with motor control, results tend to get skewed. Gorillas and chimps seem to gain general control over their bodies earlier than humans, although ultimately children far outpace both in the fine coordination required in drawing or writing. In problems involving more abstract reasoning, Koko, when she is willing to play the game, is capable of solving relatively complex problems. If nothing else, the increase in Koko’s mental age shows that she is capable of understanding a number of the principles that are the foundation of what we call abstract thought. (Patterson and Linden, 1981: 100-101)

They conclude that “it is specious to compare her IQ directly with that of a human infant” since gorillas develop motor skills earlier than human infants. So if it is “specious” to compare Koko’s IQ with an infant, then it is “specious” to compare Koko’s IQ with the average Somalian—as Langan does.

There have been many critics of Koko, and similar apes, of course. One criticism was that Koko was coaxed into signing the word she signed by asking Koko certain questions, to Robert Sapolsky stating that Patterson corrected Koko’s signs. She, therefore, would not actually know what she was signing, she was just doing what she was told. Of course, caregivers of primates with the supposed extraordinary ability for complex (humanlike) cognition will defend their interpretations of their observations since they are emotionally invested in the interpretations. Patterson’s Ph.D. research was on Koko and her supposed capabilities for language, too.

Perhaps the strongest criticism of these kinds of interpretations of Koko comes from Terrace et al (1979). Terrace et al (1979: 899) write:

The Nova film, which also shows Ally (Nim’s full brother) and Koko, reveals a similar tendency for the teacher to sign before the ape signs. Ninety-two percent of Ally’s, and all of Koko’s, signs were signed by the teacher immediately before Ally and Koko signed.

It seems that Langan has never done any kind of reading on Koko, the tests she was administered, nor the problems in comparing them to humans (infants). The fact that Koko seemed to be influenced by her handlers to “sign” what they wanted her to sign, too, makes interpretations of her IQ scores problematic. For if Koko were influenced what to sign, then we, therefore, cannot trust her scores on the CIIS. The false claims of Langan are laughable knowing the truth about Koko’s IQ, what her handlers said about her IQ, and knowing what critics have said about Koko and her sign language. In any case, Langan did not show his “high IQ” with such idiotic statements.

China’s Project Coast?

1250 words

Project Coast was a secret biological/chemical weapons program developed by the apartheid government in South Africa started by a cardiologist named Wouter Basson. One of the many things they attempted was to develop a bio-chemical weapon that targets blacks and only blacks.

I used to listen to the Alex Jones show in the beginning of the decade and in one of his rants, he brought up Project Coast and how they attempted to develop a weapon to only target blacks. So I looked into it, and there is some truth to it.

For instance, The Washington Times writes in their article Biotoxins Fall Into Private Hands:

More sinister were the attempts — ordered by Basson — to use science against the country’s black majority population. Daan Goosen, former director of Project Coast’s biological research division, said he was ordered by Basson to develop ways to suppress population growth among blacks, perhaps by secretly applying contraceptives to drinking water. Basson also urged scientists to search for a “black bomb,” a biological weapon that would select targets based on skin color, he said.

“Basson was very interested. He said ‘If you can do this, it would be very good,'” Goosen recalled. “But nothing came of it.”

They created novel ways to disperse the toxins: using letters and cigarettes to transmit anthrax to black communities (something those old enough to be alive during 911 know of), lacing sugar cubes with salmonella, lacing beer and peppermint candy with poison.

Project Coast was, at its heart, a eugenics program (Singh, 2008). Singh (2008: 9) writes, for example that “Project Coast also speaks for the need for those involved in scientific research and practice to be sensitized to appreciate the social circumstances and particular factors that precipitate a loss of moral perspective on one’s actions.”

Jackson (2015) states that another objective of the Project was to develop anti-fertility drugs and attempt to distribute them into the black population in South Africa to decrease birth rates. They also attempted to create vaccines to make black women sterile to decrease the black population in South Africa in a few generations—along with attempting to create weapons to only target blacks.

The head of the weapons program, Wouter Basson, is even thought to have developed HIV with help from the CIA to cull the black population (Nattrass, 2012). There are many conspiracy theories that involve HIV and its creation to cull black populations, though they are pretty farfetched. In any case, though, since they were attempting to develop new kinds of bioweapons to target certain populations, it’s not out of the realm of possibility that there is a kernel of truth to the story.

So now we come to today. So Kyle Bass said that the Chinese already have access to all of our genomes, through companies like Steve Hsu’s BGI, stating thatthere’s a Chinese company called BGI that does the overwhelming majority of all the sequencing of U.S. genes. … China had the genomic sequence of every single person that’s been gene types in the U.S., and they’re developing bio weapons that only affect Caucasians.”

I have no way to verify these claims (they’re probably bullshit), but with what went on in the 80s and 90s in South Africa with Project Coast, I don’t believe it’s outside of the realm of plausibility. Though Caucasians are a broad grouping.

It’d be like if someone attempted to develop a bioweapon that only targets Ashkenazi Jews. They could let’s say, attempt to make a bioweapon to target those with Tay Sach’s disease. It’s, majorly, a Jewish disease, though it’s also prevalent in other populations, like French Canadians. It’d be like if someone attempted to develop a bioweapon that only targets those with the sickle cell trait (SCT). Certain African ethnies are more like to carry the trait, but it’s also prevalent in southern Europe and Northern Africa since the trait is prevalent in areas with many mosquitoes.

With Chinese scientists like He Jiankui CRISPR-ing two Chinese twins back in 2018 to attempt to edit their genome to make them less susceptible to HIV, I can see a scientist in China attempt to do something like this. In our increasingly technological world with all of these new tools we develop, I would be surprised if there was nothing strange like this going on.

Some claim that “China will always be bad at bioethics“:

Even when ethics boards exist, conflicts of interest are rife. While the Ministry of Health’s ethics guidelines state that ethical reviews are “based upon the principles of ethics accepted by the international community,” they lack enforcement mechanisms and provide few instructions for investigators. As a result, the ethics review process is often reduced to a formality, “a rubber stamp” in Hu’s words. The lax ethical environment has led many to consider China the “Wild East” in biomedical research. Widely criticized and rejected by Western institutions, the Italian surgeon Sergio Canavero found a home for his radical quest to perform the first human head transplant in the northern Chinese city of Harbin. Canavero’s Chinese partner, Ren Xiaoping, although specifying that human trials were a long way off, justified the controversial experiment on technological grounds, “I am a scientist, not an ethical expert.” As the Chinese government props up the pseudoscience of traditional Chinese medicine as a valid “Eastern” alternative to anatomy-based “Western” medicine, the utterly unscientific approach makes the establishment of biomedical regulations and their enforcement even more difficult.

Chinese ethicists, though, did respond to the charge of a ‘Wild East’, writing:

Some commentators consider Dr. He’s wrongdoings as evidence of a “Wild East” in scientific ethics or bioethics. This conclusion is not based on facts but on stereotypes and is not the whole story. In the era of globalization, rule-breaking is not limited to the East. Several cases of rule-breaking in research involved both the East and the West.

Henning (2006) notes that “bioethical issues in China are well covered by various national guidelines and regulations, which are clearly defined and adhere to internationally recognized standards. However, the implementation of these rules remains difficult, because they provide only limited detailed instructions for investigators.” With a large country like China, of course, it will be hard to implement guidelines on a wide-scale.

Gene-edited humans were going to come sooner or later, but the way that Jiankui went about it was all wrong. Jiankjui raised funds, dodged supervision and organized researchers in order to carry out the gene-editing on the Chinese twins. “Mad scientists” are, no doubt, in many places in many countries. “… the Chinese state is not fundamentally interested in fostering a culture of respect for human dignity. Thus, observing bioethical norms run second.

Countries attempting to develop bioweapons to target specific groups of people have already been attempted recently, so I wouldn’t doubt that someone, somewhere, is attempting something along these lines. Maybe it is happening in China, a ‘Wild East’ of low regulations and oversight. There is a bioethical divide when it comes to East and West, which I would chalk up to differences in collectivism vs individualism (which some have claimed to be ‘genetic’ in nature; Kiaris, 2012). Since the West is more individualistic, they would care about individual embryos which eventually become a person; since the East is more collectivist, whatever is better for the group (that is, whatever can eventually make the group ‘better’) will override the individual and so, tinkering with individual genomes would be seen as less of an ethical charge to them.

A Systems View of Kenyan Success in Distance Running

1550 words

The causes of sporting success are multi-factorial, with no cause being more important than the other since the whole system needs to work in concert to produce the athletic phenotype–call this “causal parity” of athletic success determinants. For a refresher, take what Shenk (2010: 107):

As the search for athletic genes continues, therefore, the overwhelming evidence suggests that researchers will instead locate genes prone to certain types of interactions: gene variant A in combination with gene variant B, provoked into expression by X amount of training + Y altitude + Z will to win + a hundred other life variables (coaching, injuries, etc.), will produce some specific result R. What this means, of course, What this means, of course, is that we need to dispense rhetorically with thick firewall between biology (nature) and training (nurture). The reality of GxE assures that each person’s genes interacts with his climate, altitude, culture, meals, language, customs and spirituality—everything—to produce unique lifestyle trajectories. Genes play a critical role, but as dynamic instruments, not a fixed blueprint. A seven- or fourteen- or twenty-eight-year-old is not that way merely because of genetic instruction. (Shenk, 2010: 107) [Also read my article Explaining African Running Success Through a Systems View.]

This is how athletic success needs to be looked at; not reducing it to genes or a group of genes that ’cause’ athletic success. Since to be successful in the sport of the athlete’s choice takes more than being born with “the right” genes.

Recently, a Kenyan woman—Joyciline Jepkosgei—won the NYC marathon in here debut (November 3rd, 2019), while Eliud Kipchoge—another Kenyan—became the first human ever to complete a marathon (26.2 miles) in under 2 hours. I recall in the spring reading that he said he would break the 2-hour mark in October. He also attempted to break it in 2017 in Italy but, of course, he failed. His official time in Italy was 2:00:25! While he set the world record in Berlin at 2:01:39. Kipchoge’s official time was 1:59:40—twenty seconds shy of 2 hours—that means his average mile pace was about 4 minutes and 34 seconds. That is insane. (But the IAAF does not accept the time as a new world record since it was not in an open competition—Kipchoge had a slew of Olympic pacesetters following him; an electric car drove just ahead of him and pointed lasers at the ground showing him where to run; so he shaved 2 minutes off his time—2 crucial minutes—according to sport scientist Ross Tucker; and . So he did not set a world record. His feat, though, is still impressive.)

Now, Kipchoge is Kenyan—but what’s his ethnicity? Surprise surprise! He is of the Nandi tribe, more specifically, of the Talai subgroup, born in Kapsisiywa in the Nandi county. Jepkosgei, too, is Nandi, from Cheptil in Nandi county. (Jepkosgei also set the record for the half marathon in 2017. Also, see her regular training regimen and what she does throughout the day. This, of course, is how she is able to be so elite—without hard training, even without “the right genetic makeup”, one will not become an elite athlete.) What a strange coincidence that these two individuals who won recent marathons—and one who set the best time ever in the 26.2 mile race—are both Kenyan, specifically Nandi?

Both of these runners are from the same county in Kenya. Nandi county is elevated about 6,716 ft above sea level. Being born and living at a high elevation means that they have different kinds of physiological adaptations due to being born at such a higher elevation. Living and training at such high elevations means that they have greater lung capacities since they are breathing in thinner air. Those born in highlands like Kipchoge and Jepkosgei have larger lungs and thorax volumes, while oxygen intake is enhanced by increases in lung compliance, pulmonary diffusion, and ventilation (Meer, Heymans, and Zijlstra, 1995).

Those exposed to such elevation develop what is known as “high-altitude hypoxia.” Humans born at high altitudes are able to cope with such a lack of oxygen, since our physiological systems are dynamic—not static—and can respond to environmental changes within seconds of them occurring. Babes born at higher elevations have increased ventilation, and a rise in the alveolar and the pressure of arterial oxygen (Meer, Heymans, and Zjilstra, 1995).

Kenyans have 5 percent longer legs and 12 percent lighter muscles than Scandinavians (Suchy and Waic, 2017). Mooses et al (2014) notes that “upper leg length, total leg length and total leg length to body height ratio were correlated with running performance.” Kong and de Heer (2008) note that:

The slim limbs of Kenyan distance runners may positively contribute to performance by having a low moment of inertia and thus requiring less muscular effort in leg swing. The short ground contact time observed may be related to good running economy since there is less time for the braking force to decelerate forward motion of the body.

An abundance of type I muscle fibers is conducive to success in distance running (Zierath and Hawley, 2004), though Kenyans and Caucasians have no difference in type I muscle fibers (Saltin et al, 1995Larsen and Sheel, 2015). That, then, throws a wrench in the claim that a whole slew of anatomic and physiologic variables conducive to running success is the cause for Kenyan running success—specifically the type I fibers—right? Wrong. Recall that the appearance of the athletic phenotype is due to nature and nurture—genes and environment—working together in concert. Kenyans are more likely to have slim, long limbs with lower body fat while they lived and trained over 6000 ft high. Their will to win to better themselves and their families’ socioeconomic status, too, plays a part. As I have argued in-depth for years—we cannot understand athletic success and elite athleticism without understanding individual histories, how they grew up, and what they did as a child.

For example, Wilbur and Pitsiladis (2012) espouse a systems view of Kenyan marathon success, writing:

In general, it appears that Kenyan and Ethiopian distance-running success is not based on a unique genetic or physiological characteristic. Rather, it appears to be the result of favorable somatotypical characteristics lending to exceptional biomechanical and metabolic economy/efficiency; chronic exposure to altitude in combination with moderate-volume, high-intensity training (live high + train high), and a strong psychological motivation to succeed athletically for the purpose of economic and social advancement.

Becoming a successful runner in Kenya can lead to economic opportunities not afforded to those who do not do well in running. This, too, is a factor in Kenyan running success. So, for the ignorant people who would—pushing a false dichotomy of genes and environment—state that Kenyan running success is due to “socioeconomic status”—they are right, to a point (even if they are mocking it and making their genetic determinism seem more palatable). See figure 6 for their hypothetical model:

fig6

This is one of the best models I have come across explaining the success of these people. One can see that it is not reductonist; note that there is no appeal to genes (just variables that genes are implicated IN! Which is not the same as reductionism). It’s not as if one can have an endomorphic somatotype with Kenyan training and their psychological reasons for becoming runners. The ecto-dominant somatotype is a necessary factor for success; but all four of these—biomechanical & physiological, training, and psychological—factors explain the success of the running Kenyans and, in turn, the success of Kipchoge and Jepkosgei. African dominance in distance running is, also, dominated by the Nandi subtribe (Tucker, Onywera, and Santos-Concejero, 2015). Knechtle et al (2016) also note that male and female Kenyan and Ethiopian runners are the youngest and fast at the half and full marathons.

The actual environment—climate—on the day of the race, too plays a factor. El Helou et al (2012) note that “Air temperature is the most important factor influencing marathon running performance for runners of all levels.Nikolaidis et al (2019) note that “race times in the Boston Marathon are influenced by temperature, pressure, precipitations, WBGT, wind coming from the West and wind speed.

The success of Kenyans—and other groups—shows how the dictum “Athleticism is irreducible to biology” (St. Louis, 2004) is true. How does it make any sense to attempt to reduce athletic success down to one variable and say that that explains the overrepresentation of, say, Kenyans in distance running? A whole slew of factors needs to occur to an individual, along with actually wanting to do something, in order for them to succeed at distance running.

So, what makes Kenyans like Kipchoge and Jepkosgei so good at distance running? It’s due to an interaction with genes and environment, since we take a systems and not a reductionist view of sport success. Even though Kipchoge’s time does not count as an official world record, what he did was still impressive (though not as impressive if he would have done so without all of the help he had). Looking at the system, and not trying to reduce the system to its parts, is how we will explain why some groups are better than others. Genes, of course, play a role in the ontogeny of the athletic phenotype, but they are not the be-all-end-all that genetic reductionists seem to make it out to be. The systems view for Kenyan running success shown here is how and why Kenyans—Kipchoge and Jepkosgei—dominate distance running.

Genetic and Epigenetic Determinism

1550 words

Genetic determinism is the belief that behavior/mental abilities are ‘controlled by’ genes. Gerick et al (2017) note that “Genetic determinism can be described as the attribution of the formation of traits to genes, where genes are ascribed more causal power than what scientific consensus suggests“, which is similar to Oyama (1985) who writes “Just as traditional though placed biological forms in the mind of God, so modern thought finds ways of endowing genes with ultimate formative power.” Moore (2014: 15) notes that genetic determinism is “the idea that genes can determine the nature of our characteristics” or “the old idea that biology controls the development of characteristics like intelligence, height, and personality” (pg 39). (See my article DNA is not a Blueprint for more information.)

On the other hand, epigenetic determinism is “the belief that epigenetic mechanisms determine the expression of human traits and behaviors” (Wagoner and Uller, 2016). Both views are, of course, espoused in the scientific literature as well as usual social discourse. Both views, as well, are false. Moore (2014: 245) notes that epigenetic determinism is “the idea that an organism’s epigenetic state invariably leads to a particular phenotype.

Genetic Determinism

The concept of genetic determinism was first proposed by Weismann in 1893 with a theory of germplasm. This, in contemporary times, is contrasted with “blank slatism” (Pinker, 2002), or the Standard Social Science Model (SSSM; Tooby and Cosmides, 1992; see Richardson, 2008 for a response). Genes, genetic determinists hold, determine the ontogeny of traits, being a sort of “director.” But this betrays modern thinking on genes, what they are, and what they “do.” Genes do nothing on their own without input from the physiological system—that is, from the environment (Noble, 2011). Thus, gene-environment interaction is the rule.

This lead to either-or thinking in regard to the origin of traits and their development—what we now call “the nature-nurture debate.” Nature (genes/biology) or nurture (experience, how one is raised), gene determinists hold, are the cause of certain traits, like, for example, IQ.

Plomin (2018) asserts that nature has won the battle over nurture—while also stating that they interact. So, which one is it? It’s obvious that they interact—if there were no genes there would still be an environment but if there were no environment there would be no genes. (See here and here for critiques of his book Blueprint.)

This belief that genes determine traits goes back to Galton—one of the first hereditarians. Indeed, Galton was the one to coin the phrase “nature vs nurture”, while being a proponent of ‘nature over nurture.’ Do genes or environment influence/cause human behavior? The obvious answer to the question is both do—and they are intertwined: they interact.

Griffiths (2002) notes that:

Genetic determinism is the idea that many significant human characteristics are rendered inevitable by the presence of certain genes; that it is futile to attempt to modify criminal behavior or obesity or alcoholism by any means other than genetic manipulation.

Griffiths then argues that genes are very unlikely to be deterministic causes of behavior. Genes are thought to have a kind of “information” in them which then determines how the organism will develop. This is what the “blueprint metaphor” for genes attempts to show. Genes contain this information for trait development. The implicit assumption here is that genes are context-independent—that the (environmental) context the organism is in does not matter. But genes are context-dependent—“the very concept of a gene requires the environment” (Schneider, 2007). This speaks to the context-dependency of genes. There is no “information”—genes are not like blueprints or recipes. So genetic determinism is false.

But even though genetic determinism is false, it still stays in the minds of our society/culture and scientists (Moore, 2008), while still being taught in schools (Jamieson and Radick, 2017).

The claim that genes determine phenotypes can be shown in the following figure from Kampourakis (2017: 187):

Figure 9.6 (a) The common representation of gene function: a single gene determines a single phenotype. It should be clear by what has been present in the book so far that is not accurate. (b) A more accurate representation of gene function that takes development and environment into account. In this case, a phenotype is produced in a particular environment by developmental processes in which genes are implicated. In a different environment the same genes might contribute to the development of a different phenotype. Note the “black box” of development.

Richardson (2017: 133) notes that “There is no direct command line between environments and genes or between genes and phenotypes.” The fact of the matter is, genes do not determine an organism’s characters, they are merely implicated in the development of the character—being passive, not active templates (Noble, 2011).

Moore (2014: 199) tells us how genetic determinism fails since genes do not work in a vaccuum:

There is just one problem with the neo-Darwinian assumption that “hard” inheritance is the only good explanation for the transgenerational transmission of phenotypes: It is hopelessly simplistic. Genetic determinism is a faulty idea, because genes do not operate in a vacuum; phenotypes develop when genes interact with nongenetic factors in their local environments, factors that are affected by the broader environment.

Epigenetic Determinism

On the other hand, epigenetic determinism, the belief that epigenetic mechanisms determine the behavior of the organism, is false but in the other direction. Epigenetic determinists decry genetic determinism, but I don’t think they realize that they are just as deterministic as they are.

Dupras et al (2018) note how “overly deterministic readings of epigenetic marks could promote discriminatory attitudes, discourses and practices based on the predictive nature of epigenetic information.” While epigenetics—specifically behavioral epigenetics—refutes notions of genetic determinism, we can then fall into a similar trap, but determinism all the same. This means, though, that since genes don’t determine, epigenetics does not either, so we cannot epigenetically manipulate pre- or perinatally since what we would attempt to manipulate—‘intelligence’, contentment, happiness—all  develop over the lifespan. Moore (2014: 248) continues:

Even in situations where we know that certain perinatal experiences can have very long-term effects, determinism is still an inappropriate framework for thinking about human development. For example, no one doubts that drinking alcohol during pregnancy is bad for the fetus, but in the hundreds of years before scientists established this relationship, innumerable fetuses exposed to some alcohol nonetheless grew up to be healthy, normal adults. This does not mean that pregnant women should drink alcohol freely, of course, but it does mean that developmental outcomes are not as easy to predict as we sometimes think. Therefore, it is probably always a bad idea to apply a deterministic worldview to a human being. Like DNA segments, epigenetic marks should not be considered destiny. How a given child will develop after trauma, for example, depends on a lot more than simply the experience of the trauma itself.

In an interview with The Psych Report Moore tells us that people not know enough about epigenetics for there to be epigenetic determinists (though many journalists and some scientists talk like they are :

I don’t think people know enough about epigenetics yet to be epigenetic determinists, but I foresee that as a problem. As soon as people start hearing about these kinds of data that suggest that your early experiences can have long-term effects, there’s a natural assumption we all make that those experiences are determinative. That is, we tend to assume that if you have this experience in poverty, you are going to be permanently scarred by it.

The data seem to suggest that it may work that way, but it also seems to be the case that the experiences we have later in life also have epigenetic effects. And there’s every reason to think that those later experiences can ameliorate some of the effects that happened early on. So, I don’t think we need to be overly concerned that the things that happen to us early in life necessarily fate us to certain kinds of outcomes.

While epigenetics refutes genetic determinism, we can run into the problem of epigenetic determinism, which Moore predicts. But journalists note how genes can be turned on or off by the environment, thereby dictating disease states, for example. Though, biological determinism—of any kind, epigenetic or genetic—is nonsensical as “the development of phenotypes depends on the contexts in which epigenetic marks (and other developmentally relevant factors, of course, are embedded” (Moore, 2014: 246).

What really happens?

What really happens regarding development if genetic and epigenetic determinism are false? It’s simple: causal parity (Oyama, 1985; Noble, 2012): the thesis that genes/DNA play an important role in development, but so do other variables, so there is no reason to privilege genes/DNA above other developmental variables. Genes are not special developmental resources and so, nor are they more important than other developmental resources. So the thesis is that genes and other developmental resources are developmentally ‘on par’. ALL traits develop through an interaction between genes and environment—nature and nurture. Contra ignorant pontifications (e.g., Plomin), neither has “won out”—they need each other to produce phenotypes.

So, genetic and epigenetic determinism are incoherent concepts: nature and nurture interact to produce the phenotypes we see around us today. Developmental systems theory, which integrates all factors of development, including epigenetics, is the superior framework to work with, but we should not, of course, be deterministic about organismal development.

A not uncommon reaction to DST is, ‘‘That’s completely crazy, and besides, I already knew it.” — Oyama, 2000, 195, Evolution’s Eye

Hereditarian “Reasoning” on Race

1100 words

The existence of race is important for the hereditarian paradigm. Since it is so important, there must be some theories of race that hereditarians use to ground their theories of race and IQ, right? Well, looking at the main hereditarians’ writings, they just assume the existence of race, and, along with the assumption, the existence of three races—Caucasoid, Negroid, and Mongoloid, to use Rushton’s (1997) terminology.

But just assuming race exists without a definition of what race is is troubling for the hereditarian position. Why just assume that race exists?

Fish (2002: 6) in Race and Intelligence: Separating Science from Myth critiques the usual hereditarians on what race is and their assumptions that it exists. He cites Jensen (1998: 425) who writes:

A race is one of a number of statistically distinguishable groups in which individual membership is not mutually exclusive by any single criterion, and individuals in a given group differ only statistically from one another and from the group’s central tendency on each of the many imperfectly correlated genetic characteristics that distinguish between groups as such.

Fish (2002: 6) continues:

This is an example of the kind of ethnocentric operational definition described earlier. A fair translation is, “As an American, I know that blacks and whites are races, so even though I can’t find any way of making sense of the biological facts, I’ll assign people to my cultural categories, do my statistical tests, and explain the differences in biological terms.” In essence, the process involves a kind of reasoning by converse. Instead of arguing, “If races exist there are genetic differences between them,” the argument is “Genetic differences between groups exist, therefore the groups are races.”

Fish goes on to write that if we take a group of bowlers and a group of golfers then, by chance, there may be genetic differences between them but we wouldn’t call them “golfer races” or “bowler races.” If there were differences in IQ, income and other variables, he continues, we wouldn’t argue that the differences are due to biology, we would attempt argue that the differences are social. (Though I can see behavioral geneticists try to argue that the differences are due to differences in genes between the groups.)

So the reasoning that Jensen uses is clearly fallacious. Though, it is better than Levin’s (1997) and Rushton’s (1997) assumptions that race exists, it still fails since Jensen (1998) is attempting argue that genetic differences between groups make them races. Lynn (2006: 11) uses a similar argument to the one Jensen provides above. (Nevermind Lynn conflating social and biological races in chapter 2 of Race Differences in Intelligence.)

Arguments exist for the existence of race that doesn’t, obviously, assume their existence. The two best ones I’m aware of are by Hardimon (2017) and Spencer (2014, 2019).

Hardimon has four concepts: the racialist race concept (what I take to be the hereditarian position), the minimalist/populationist race concept (they are two separate concepts, but the populationist race concept is the “scientization” of the minimalist race concept) and the socialrace concept. Specifically, Hardimon (2017: 99) defines ‘race’ as:

… a subdivision of Homo sapiens—a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographic ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population.

Spencer (2014, 2019), on the other hand, grounds his racial ontology in the Census and the OMB—what Spencer calls “the OMB race theory”—or “Blumenbachian partitions.” Take Spencer’s most recent (2019) formulation of his concept:

In this chapter, I have defended a nuanced biological racial realism as an account of how ‘race’ is used in one US race talk. I will call the theory OMB race theory, and the theory makes the following three claims:

(3.7) The set of races in OMB race talk is one meaning of ‘race’ in US race talk.

(3.8) The set of races in OMB race talk is the set of human continental populations.

(3.9) The set of human continental populations is biologically real.

I argued for (3.7) in sections 3.2 and 3.3. Here, I argued that OMB race talk is not only an ordinary race talk in the current United States, but a race talk where the meaning of ‘race’ in the race talk is just the set of races used in the race talk. I argued for (3.8) (a.k.a. ‘the identity thesis’) in sections 3.3 and 3.4. Here, I argued that the thing being referred to in OMB race talk (a.k.a. the meaning of ‘race’ in OMB race talk) is a set of biological populations in humans (Africans, East Asians, Eurasians, Native Americans, and Oceanians), which I’ve dubbed the human continental populations. Finally, I argued for (3.9) in section 3.4. Here, I argued that the set of human continental populations is biologically real because it currently occupies the K = 5 level of human population structure according to contemporary population genetics.

Whether or not one accepts Hardimon’s and Spencer’s arguments for the existence of race is not the point here, however. The point here is that these two philosophers have grounded their belief in the existence of race in a sound philosophical grounding—we cannot, though, say the same things for the hereditarians.

It should also be noted that both Spencer and Hardimon discount hereditarian theory—indeed, Spencer (2014: 1036) writes:

Nothing in Blumenbachian race theory entails that socially important differences exist among US races. This means that the theory does not entail that there are aesthetic, intellectual, or moral differences among US races. Nor does it entail that US races differ in drug metabolizing enzymes or genetic disorders. This is not political correctness either. Rather, the genetic evidence that supports the theory comes from noncoding DNA sequences. Thus, if individuals wish to make claims about one race being superior to another in some respect, they will have to look elsewhere for that evidence.

So, as can be seen, hereditarian ‘reasoning’ on race is not grounded in anything—they just assume that races exist. This stands in stark contrast to theories of race put forth by philosophers of race. Nonhereditarian theories of race exist—and, as I’ve shown, hereditarians don’t define race, nor do they have an argument for the existence of races, they just assume their existence. But, for the hereditarian paradigm to be valid, they must be biologically real. Hardimon and Spencer argue that they are, but hereditarian theories do not have any bearing on their theories of race.

There is the hereditarian ‘reasoning’ on race: either assume its existence sans argument or argue that genetic differences between groups exist so the groups are races. Hereditarians need to posit something like Hardimon or Spencer.