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Race Differences in Penis Size Revisited: Is Rushton’s r/K Theory of Race Differences in Penis Length Confirmed?
In 1985 JP Rushton, psychology professor at the University of Ontario, published a paper arguing that r/K selection theory (which he termed Differential K theory) explained and predicted outcomes of what he termed the three main races of humanity—Mongoloids, Negroids and Caucasoids (Rushton, 1985; 1997). Since Rushton’s three races differed on a whole suite of traits, he reasoned races that were more K-selected (Caucasoids and Mongoloids) had slower reproduction times, higher time preference, higher IQ etc in comparison to the more r-selected Negroids who had faster reproduction times, lower time preference, lower IQ etc (see Rushton, 1997 for a review; also see Van Lange, Rinderu, and Bushmen, 2017 for a replication of Rushton’s data not theory). Were Rushton’s assertions on race and penis size verified and do they lend credence to his Differential-K claims regarding human races?
Rushton’s so-called r/K continuum has a whole suite of traits on it. Ranging from brain size to speed of maturation to reaction time and IQ, these data points supposedly lend credence to Rushton’s Differential-K theory of human differences. Penis size is, of course, important for Rushton’s theory due to what he’s said about it in interviews.
Rushton’s main reasoning for penis size differences between race is “You can’t have both”, and that if you have a larger brain then you must have a smaller penis; if you have a smaller penis you must have a larger brain. He believed there was a “tradeoff” between brain size and penis size. In the book Darwin’s Athletes: How Sport Has Damaged Black America and Preserved the Myth of Race, Hoberman (1997: 312) quotes Rushton: “Even if you take something like athletic ability or sexuality—not to reinforce stereotypes or some such thing—but, you know, it’s a trade-off: more brain or more penis. You can’t have both.” This, though, is false. There is no type of evidence to imply that this so-called ‘trade-off’ exists. In my readings of Rushton’s work over the years, that’s always something I’ve wondered: was Rushton implying that large penises take more energy to have and therefore the trade-off exists due to this supposed relationship?
Andrew Joyce of the Occidental Observer published an article the other day in defense of Richard Lynn. Near the end of his article he writes:
Another tactic is to belittle an entire area of research by picking out a particularly counter-intuitive example that the public can be depended on to regard as ridiculous. A good example is J. Philippe Rushton’s claim, based on data he compiled for his classic Race, Evolution and Behavior, that average penis size varied between races in accord with the predictions of r/K theory. This claim was held up to ridicule by the likes of Richard Lewontin and other crusaders against race realism, and it is regularly presented in articles hostile to the race realist perspective. Richard Lynn’s response, as always, was to gather more data—from 113 populations. And unsurprisingly for those who keep up with this area of research, he found that indeed the data confirmedRushton’s original claim.
The claim was ridiculed because it was ridiculous. This paper by Lynn (2013) titled Rushton’s r-K life history theory of race differences in penis length and circumference examined in 113 populations is the paper that supposedly verifies Rushton’s theory regarding race differences in penis size, along with one of its correlates in Rushton’s theory (testosterone). Lynn (2013) proclaims that East Asians are the most K-evolved, then come Europeans, while Africans are the least K-evolved. This, then, is the cause of the supposed racial differences in penis size.
Lynn (2013) begins by briefly discussing Rushton’s ‘findings’ on racial differences in penis size while also giving an overview of Rushton’s debunked r/K selection theory. He then discusses some of Rushton’s studies (which I will describe briefly below) along with stories from antiquity of the supposed larger penis size of African males.
Our old friend testosterone also makes an appearance in this paper. Lynn (2013: 262) writes:
Testosterone is a determinant of aggression (Book, Starzyk, & Quinsey, 2001; Brooks & Reddon, 1996; Dabbs, 2000). Hence, a reduction of aggression and sexual competitiveness between men in the colder climates would have been achieved by a reduction of testosterone, entailing the race differences in testosterone (Negroids > Caucasoids > Mongoloids) that are given in Lynn (1990). The reduction of testosterone had the effect of reducing penis length, for which evidence is given by Widodsky and Greene (1940).
Phew, there’s a lot to unpack here. (I discuss Lynn 1990 in this article.) Testosterone does not determine aggression; see my most recent article on testosterone (aggression increases testosterone; testosterone does not increase aggression. Book, Starzyk and Quinsey, 2001 show a .14 correlation between testosterone and aggression, whereas Archer, Graham-Kevan, and Davies 2005 show the correlation is .08). This is just a correlation. Sapolsky (1997: 113) writes:
Okay, suppose you note a correlation between levels of aggression and levels of testosterone among these normal males. This could be because (a) testosterone elevates aggression; (b) aggression elevates testosterone secretion; (c) neither causes the other. There’s a huge bias to assume option a while b is the answer. Study after study has shown that when you examine testosterone when males are first placed together in the social group, testosterone levels predict nothing about who is going to be aggressive. The subsequent behavioral differences drive the hormonal changes, not the other way around.
Brooks and Reddon (1996) also only show relationships with testosterone and aggressive acts; they show no causation. This same relationship was noted by Dabbs (2000; another Lynn 2013 citation) in prisoners. More violent prisoners were seen to have higher testosterone, but there is a caveat here too: being aggressive stimulates testosterone production so of course they had higher levels of testosterone; this is not evidence for testosterone causing aggression.
Another problem with that paragraph quoted from Lynn (2013) is that it’s a just-so story. It’s an ad-hoc explanation. You notice something with data you have today and then you imagine a nice-sounding story to attempt to explain your data in an evolutionary context. Nice-sounding stories are cool and all and I’m sure everyone loves a nicely told story, but when it comes to evolutionary theory I’d like theories that can be independently verified of the data they’re trying to explain.
My last problem with that paragraph from Lynn (2013) is his final citation: he cites it as evidence that the reduction of testosterone affects penis length…..but his citation (Widodsky and Green, 1940) is a study on rats… While these studies can give us a wealth of information regarding our physiologic systems (at least showing us which types of avenues to pursue; see my previous article on myostatin), they don’t really mean anything for humans; especially this study on the application of testosterone to the penis of a rat. See, the fatal flaw in these assertions is this: would a, say, 5 percent difference in testosterone lead to a larger penis as if there is a dose-response relationship between testosterone and penis length? It doesn’t make any sense.
Lynn (2013), though, says that Rushton’s theory doesn’t propose that there is a direct causal relationship between “intelligence”‘ and penis length, but just that they co-evolved together, with testosterone reduction occurring when Homo sapiens migrated north out of Africa they needed to cooperate more so selection for lower levels of testosterone subsequently occurred which then shrunk the penises of Rushton’s Caucasian and Mongoloid races.
Lynn (2013) then discusses two “new datasets”, one of which is apparently in Donald Templer’s book Is Size Important (which is on my to-read list, so many books, so little time). Table 1 below is from Lynn reproducing Templer’s ‘work’ in his book.
The second “dataset” is extremely dubious. Lynn (2013) attempts to dress it up, writing that “The information in this website has been collated from data obtained by research centres and reports worldwide.” Ethnicmuse has a good article on the pitfalls of Lynn’s (2013) article. (Also read Scott McGreal’s rebuttal.)
Rushton attempted to link race and penis size for 30 years. In a paper with Bogaert (Rushton and Bogaert, 1987), they attempt to show that blacks had larger penises than whites who h ad longer penises than Asians which then supposedly verified one dimension of Rushton’s theory. Rushton (1988) also discusses race differences in penis size, citing a previous paper by Rushton and Bogaert, where they use data from Alfred Kinsey, but this data is nonrepresentative and nonrandom (see Zuckermann and Brody, 1988 and Weizmann et al, 1990: 8).
Still others may attempt to use supposed differences in IGF-1 (insulin-like growth factor 1) as evidence that there is, at least, physiological evidence for the claim that black men have larger penises than white men, though I discussed that back in December of 2016 and found it strongly lacking.
Rushton (1997: 182) shows a table of racial differences in penis size which was supposedly collected by the WHO (World Health Organization). Though a closer look shows this is not true. Ethnicmuse writes:
ANALYSIS: The WHO did not study penis sizes. It relied on three separate studies, two of which were not peer-reviewed and the data was included as “Appendix III” (which should have alerted Rushton that this was not an original study). The first study references Africans in the US (not Africa!) and Europeans in the US (not Europe!), the second Europeans in Australia (not Europe!) and the third, Thais.
So it seems to be bullshit all the way down.
Ajmani et al (1985) showed that 385 healthy Nigerians had an average penile length of 3.21 inches (flaccid). Orakwe and Ebuh (2007) show that while Nigerians had longer penises than other ethnies tested, the only statistical difference was between them and Koreans. Though Veale et al (2014: 983) write that “There are no indications of differences in racial variability in our present study, e.g. the study from Nigeria was not a positive outlier.”
Lynn and Dutton have attempted to use androgen differentials between the races as evidence for racial differences in penis size (this is another attempt at a physiological argument to attempt to show the existence of racial differences in penis size). Edward Dutton attempted to revive the debate on racial differences in penis size during a 2015 presentation where he, again, showed that Negroids have higher levels of testosterone than Caucasoids who have higher levels of androgens than Mongoloids. These claims, though, have been rebutted by Scott McGreal who showed that populations differences in androgen levels are meaningless while they subsequently fail to validate Rushton and Lynn’s claims on racial differences in penis size.
Finally, it was reported the other day that condoms from China were too small in Zimbabwe, per Zimbabwe’s health minister. This led Kevin MacDonald to proclaim that this was “More corroboration of race differences in penis size which was part of the data Philippe Rushton used in his theory of r/K selection (along with brain size, maturation rates, IQ, etc.)” This isn’t “more corroboration” for Rushton’s long-dead theory; nor is this evidence that blacks have longer penises. I don’t understand why people make broad and sweeping generalizations. It’s one country in Africa that complained about smaller condoms from a country in East Asia, therefore this is more corroboration for Rushton’s r/K selection theory? The logic doesn’t follow.
Asians have small condoms. Those condoms go to Africa. They complain condoms from China are too small. Therefore Rushton’s r/K selection theory is corroborated. Flawed logic.
In sum, Lynn (2013) didn’t verify Rushton’s theory regarding racial differences in penis size and I find it even funnier that Lynn ends his article talking about “falsification’ stating that this aspect of Rushton’s theory has survived two attempts at falsification, therefore, it can be regarded as a “progressive research program“, though obviously, with the highly flawed “data” that was used, one cannot rationally make that statement. Supposed hormonal differences between the races do not cause penis size differences; even if blacks had levels of testosterone significantly higher than whites (the 19 percent that is claimed by Lynn and Rushton off of one highly flawed study in Ross et al, 1986) they still would not have longer penises.
The study of physical differences between populations is important, but sometimes, stereotypes do not tell you anything, especially in this case. Though in this instance, the claim that blacks have the longest penis lies on shaky ground, and with what evidence we do have for the claim, we cannot logically make the inference (especially not from Lynn’s (2013) flimsy data). Richard Lynn did not “confirm” anything with this paper; the only thing he “confirmed” are his own preconceived notions; he did not ‘prove’ what he set out to.
Testosterone is a fascinating hormone—the most well-known hormone to the lay public. What isn’t well-known to the lay public is how the hormone is produced and the reasons why it gets elevated. I’ve covered racial differences in testosterone in regards to crime, penis size and Rushton’s overall misuse of r/K selection theory. In this article, I will talk about what raises and decreases testosterone, as well as speak about racial differences in testosterone again since it’s such a fun topic to cover.
JP Rushton writes, in his 1995 article titled Race and Crime: An International Dilemma:
One study, published in the 1993 issue of Criminology by Alan Booth and D. Wayne Osgood, showed clear evidence of a testosterone-crime link based on an analysis of 4,462 U.S. military personnel. Other studies have linked testosterone to an aggressive and impulsive personality, to a lack of empathy, and to sexual behavior.
Booth and Osgood (1993: 93) do state that “This pattern of results supports the conclusions that (I) testosterone is one of a larger constellation of factors contributing to a general latent propensity toward deviance and (2) the influence of testosterone on adult deviance is closely tied to social factors.” However, as I have extensively documented, the correlation between testosterone and aggression is extremely low (Archer, 1991; Book et al (2001); Archer, Graham-Kevan and Davies, 2005), and therefore cannot be the cause of crime.
Another reason why testosterone is not the cause of aggression/deviant behavior is due to what times most crimes are committed at. Therefore, testosterone cannot possibly be the cause of crime. I’ve also shown that, contrary to popular belief, blacks don’t have higher levels testosterone than whites, along with the fact that testosterone does not cause prostate cancer, that even if blacks did have these supposed higher levels of the hormone, that it would NOT explain higher rates of crime.
Wu et al (1995) show that Asian Americans had the highest testosterone levels, African Americans were intermediate and European Americans were last, after adjustments for BMI and age were made. Though, I’ve shown in larger samples that, if there is any difference at all (and a lot of studies show no difference), it is a small advantage favoring blacks. We then are faced with the conclusion that this would not explain disease prevalence nor higher rates of crime or aggression.
Testosterone, contrary to Rushton’s (1999) assertion, is not a ‘master switch’. Rushton, of course, cites Ross et al (1986) which I’ve tirelessly rebutted. Assay times were all over the place (between 10 am and 3 pm) with testosterone levels being highest at 8 am. The most important physiological variable in Rushton’s model is testosterone, and without his highly selected studies, his narrative falls apart. Testosterone doesn’t cause crime, aggression, nor prostate cancer.
The most important take away is this: Rushton’s r/K theory hinges on 1) blacks having higher levels of testosterone than whites and 2) that these higher levels of testosterone then influence higher levels of aggression which lead to crime and then prostate cancer. Even then, Sridhar et al (2010) meta-analyzed 17 articles which talk about racial differences in prostate cancer survival rates. They state in their conclusion that “there are no differences between African American and Whites in survival from prostate cancer.” Zagars et al (1998) show that there were no significant racial differences in serum testosterone. Furthermore, when matched for major prognostic factors “the outcome for clinically local–regional prostate cancer does not depend on race (6,7,14–19). Moreover there appear to be no racial differences in the response of advanced prostate cancer to androgen ablation (29,47). Our study provides further evidence that racial differences in disease outcome are absent for clinically localized prostate cancer” (Zagars et al, 1998: 521). So it seems that these two studies also provide further support that Rushton et al were wrong in regards to prostate cancer mortality as well.
Rushton (1997 185) writes:
In any case, socialization cannot account for the early onset of the traits, the speed of dental and other maturational variables, the size of the brain, the number of gametes produced, the physiological differences in testosterone, nor the evidence on cross-cultural consistency.
There are no racial differences in testosterone and if there were, social factors would explain the difference between the races. However, as I’ve noted in the past, testosterone levels are high in young black males with low educational attainment (Mazur, 2016). The higher levels of testosterone in blacks compared to whites (which, if you look at figure 1 the levels are not high at all) is accounted for by honor culture, a social variable. Furthermore, the effects of the environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Environmental factors greatly influence testosterone (Booth et al, 2006), so Rushton stating that “socialization cannot account for the early onset” of “physiological differences in testosterone” is clearly wrong since environmental influences can be seen in infants as well as adults. Testosterone is strongly mediated by the environment; this is not up for debate.
Testosterone is one of many important hormones in the body; the races do not differ in the variable. So, therefore, all of Rushton’s ‘r/K predictions’, which literally hinge on testosterone (Lynn, 1990) fall apart without this ‘master switch’ (Rushton, 1999) driving all of these behaviors. Any theories of crime that include testosterone as a main driver in crime need to be rethunk; numerous studies attest to the fact that testosterone does not cause crime. Racial differences in testosterone only appear in small studies and the studies that do show these differences get touted around all the while, all of the better, larger analyses don’t get talked about because it goes against a certain narrative.
Finally, there is no inevitability of a testosterone decrease in older men. So-called “age-related declines” in the hormone are largely explained by smoking, obesity, chronic disease, marital status, and depression (Shi et al, 2013), and even becoming a father explains lower levels of testosterone (Gray, Yang, and Pope, 2006). On top of that, marriage also reduces testosterone, with men who went from unmarried to married showing a sharp decline in testosterone over a ten-year period (Holmboe et al, 2017). This corroborates numerous other studies showing that marriage lowers testosterone levels in men (Mazur and Michalek, 1998; Nansunga et al, 2014) But some of this decrease may be lessened by frequent sexual intercourse (Gettler et al, 2013). So if you live a healthy lifestyle, the testosterone decrease that plagues most men won’t occur to you. The decreases are due to lifestyle changes; not explicitly tied to age.
People are afraid of higher levels of testosterone at a young age and equally as terrified of lowering testosterone levels at an old age. However, I’ve exhasutively shown that testosterone is not the boogeyman, nor the ‘master switch’ (Rushton, 1999) it’s made out to be. There are no ‘genes for’ testosterone; its production is indirect through DNA. Thusly, if you keep an active lifestyle, don’t become obese, and don’t become depressed, you can bypass the so-called testosterone decrease. Fear mongering on both sides of the ‘testosterone curve’ are seriously blown out of proportion. Testosterone doesn’t cause crime, aggression, nor prostate cancer (even then, large meta-analyses show no difference in PCa mortality between blacks and whites).
The fear of the hormone testosterone is due to ignornace of what it does in the body and how it is produced in the body. If people were to understand the hormone, they would not fear it.
I thought I’d address what E.O. Wilson’s thoughts on Rushton’s theory and clarify some things on endemic disease and cold winter and how they relate to this r/K paradigm. Proponents of Rushton may look to it and say ‘Well, E.O. Wilson said X, so therefore the reason why it’s not accepted is Y!” However, this comes from a faulty misunderstanding of what Wilson said.
I think Phil is an honest and capable researcher. The basic reasoning by Rushton is solid evolutionary reasoning; that is, it is logically sound. If he had seen some apparent geographic variation for a non-human species – a species of sparrow or sparrow hawk, for example – no one would have batted an eye. … when it comes to [human] racial differences, especially in the inflamed situation in this country, special safeguards and conventions need to be developed.
This little blurb does not address anything, really. Yes, it does address the fact that people attacked Rushton for his research on human racial differences. What it does not address is Rushton’s incorrect application of the theory, as covered yesterday. So, bringing up Wilson’s thoughts on Rushton and the controversy surrounding his theory is a moot point.
I don’t understand why people cannot just accept that Rushton was wrong with his misuse of the theory. Notice how I never said anything about his data—I only talked about his misuse of the theory. People act as if both his data and theory need to be correct, well, why can’t one be right and the other wrong (the data and the theory)? Because that’s how it is in reality.
Rushton’s data was largely correct, however, his misapplication of r/K theory shows that he just saw, for instance, current TFRs (total fertility rates) and just arbitrarily placed Africans as r and Eurasians as K, when looking at what Rushton said about both environments—tropical and cold—would lead to K selection for the tropics, since Rushton asserts that endemic and infectious disease is a selective agent (with no references) while Asia was ‘unbearably cold (also with no reference). This characterization of Pleiositicine environments as ‘hot and endemic disease’ and ‘unbearably cold’ has literally no basis in reality.
Tropical environments are more challenging than cold/temperate ones (Dobzhansky, 1950: 221). Knowing this, Rushton’s assertion of cold winters selecting for higher levels of intelligence in Eurasians compared to Africans is wrong since life is easy nowhere. This characterization of life being ‘easy’ in tropical environments has no basis in reality. It’s like people assume that in the tropics you can just laze around all day while fruits fall onto your lap and you have to do nothing that’s cognitively demanding. This is not true at all. Just look at how a savanna looks, does that look ‘easy’ to live in?
There are also a few more things I’d like to talk about in regards to Rushton’s theory, mainly on endemic disease and why it is an agent of K-selection; not r. Even then, r characteristics probably wouldn’t be able to evolve in the savanna (Miller, 1991: 670). The thing is, populations that evolve in disease-ridden places are expected to select for high population growth—increasing r. However, populations in other areas would increase K as they would be selected for survival and not disease resistance. So if disease was a main difference in so-called r/K differences between populations, r-selected people would be more disease resistant AND they would live longer lives (Miller, 1991: 672).
Case closed, right? Wrong. Miller (1991) writes: “If differences in disease rates do prove to be part of the explanation, the theory would not be an r vs K selection theory, because resistance to disease and a long life span are considered K characteristics, rather than r characteristics” (pg: 672). It is also doubtful that conditions in Africa are much more variable in comparison to other continents.
Furthermore, if an alien observed us with no prior knowledge of our species and only had Pianka’s (1970) paper to go off of, he would conclude that Mongoloids would be r-selected due to the cold winter temperatures which bring a high mortality rate. This is the direct opposite of what Rushton claimed.
Miller states at the end of the article that these differences between populations clearly need explaining. However, the explanation is not r vs. K selection, as Afrosapiens and I showed yesterday, Rushton reversed r and K for the three races, making Africans r when they really would be K and making Mongoloids K, when in reality they would be r. Miller addresses other possibilities, such as testosterone, citing Ellis and Nyborg (1992) for racial differences in testosterone, however, he notes that the difference is only 3 percent which wouldn’t account for racial differences in behavior. (Also recall my critique of having no measure of central adiposity.) I’ve definitively shown that even if the races did differ largely in testosterone that it would not account for disease acquisition nor higher rates of crime.
from Anderson (1991: 53)
Above are the agents of selection, their defining characteristics, and independent and dependent variables. Notice how for r-selection the typical agents of selection are temperature extremes, drought, and natural disaster. For K-selection, the usual agents of selection are limited food supply, endemic infectious disease, and predation. Alpha-selection selects for competitive ability and is thus closer to K than r. Limited resources that can be collected or guarded such as shelter or food are agents of selection.
Clearly, as you can see, if this theory did apply to the human races, Mongoloids would be r and Africans would be K. Endemic disease is an agent of K-selection, not r. This is because endemic disease usually imposes density-dependent selection while cold winters impose density-independent selection. Furthermore, and perhaps most importantly, intelligence can be selected for due to agents of r- or K-selection! Rushton had no reason to add intelligence as a ‘K trait’, as Pianka did not even add it to his continuum. Further, Pianka gave no experimental rationale as to why he placed those traits on r or K (Graves, 2002: 135)! So due to this, Rushton’s claims are wrong and people should stop pushing his r/K theory.
Clearly, Rushton reversed r and K selection and wrongly applied them to the races of man. The three races he describes are NOT local populations, so any inferences made off of any so-called evolutionary environment are not warranted because he did not use the right variable (r or K) for Africans or Eurasians. However, some people may not want to admit that Rushton—and by extension, them—were wrong so they will attempt whatever kind of mental gymnastics possible to attempt to prove that Rushton was ‘right’. As I’ve already said, I don’t have a problem with Rushton’s data; I have a problem with his misapplication of r/K to humans—which I’ve made a strong case that he was wrong and didn’t know what he was talking about in terms of ecology and evolution.
Rushton’s theory was no longer viable 3 years after it was proposed when Judith Anderson got her hands on it, writing the paper Rushton’s Racial Comparisons: An Ecological Critique of Theory and Method. There is literally no saving his application of r and K to humans because he used it wrong! I don’t care what E.O. Wilson said, because he didn’t address Rushton’s application of r/K to human races. He only said if he noticed this variation between another species that no one would have batted an eye. That says absolutely nothing about Rushton’s erroneous application of r/K selection to the races of man.
I hope any HBDers reading this will stop and think for a moment before stating that Eurasians are K and Africans are r. This canard needs to stop in this sphere and I hope I set the wheels in motion to end it.
Today is the 4th anniversary of Jensen’s death, with the 4th anniversary of Rushton’s being three weeks ago on October 2nd. The fact that two of the biggest names in the IQ game, and race science game died in a 3-week span was crushing to the truth. When they were pushing their theories on racial differences in intelligence, they had their classes stormed in on and they pretty much couldn’t teach. All of this, in a country where so-called ‘freedom of speech exists’, we can have people shout others down when they speak uncomfortable truths when they don’t like what they’re hearing. BUT, just because those truths don’t want to be heard does not change the reality of them. Rushton and Jensen were pretty much explaining why black Americans have less academic achievement over whites. But when a genetic explanation is brought up instead of the Left’s want for there to be a fully environmental, ‘racism’ explanation they storm classrooms and protest against the so-called ‘fascists’ who are just reporting what they find.
In Rushton’s article The New Enemies of Evolutionary Science, he extensively talks about the derision he faced from students while he gave his lectures. It was so bad that he couldn’t teach:
Behind the scenes, however, I became the target of a witch hunt by some of the administrators. Dismayingly, my dean, a physical anthropologist, publicly declared that I had lost my scientific credibility and spearheaded an attack on me in the newspapers. She issued a series of preemptive statements making plain her negative opinion of me and my work. “What evidence is there for this ranked ordering of the evolution of the human races?” she wrote. “None.” Claiming that her views represented only her academic opinion she emphasized that she was not speaking in any administrative capacity. Her letter was nonetheless widely interpreted in the media as a refutation by my “boss.” Henceforth, in order to support me, a person would now have to go up against the dean in addition to prevailing opinion. Next, the chair of my department gave me an annual performance rating of “unsatisfactory” citing my “insensitivity.” This was a remarkable turnaround because it occurred for the same year in which I had been made a Fellow of the prestigious John Simon Guggenheim Foundation. My previous twelve years of annual ratings had been “good” or “excellent.” Indeed, my earlier non-controversial work had made me one of the most cited scholars at my university.
Some radical and black students mobilized and held rallies, even bringing in a member of the African National Congress to denounce me. In one demonstration, a mob of 40 people stormed through the psychology department, banging on walls and doors, bellowing slogans through bull horns, drawing swastikas on the walls, and writing on my door “Racists Pig Live Here.”
The administration responded by barring me from the classroom and ordering me to lecture by videotape on the pretext that they could not protect me from the lawlessness of students. Again I launched formal grievances. After a term of enforced teaching by videotape, I won the right to resume teaching in person, though then I was required to run a gauntlet of demonstrators shouting protests and threats. Only after several forced cancellations of my classes did the administration warn the demonstrators that further action would lead to suspension and legal action. That brought the protests to a halt.
This sounds just like today huh? Seems like much hasn’t changed in the past 30 years. The amount of derision that Rushton faced just for his areas of research interest speaks volumes. Clearly, people are scared of the truth about human nature, whether individually or racially/ethnically. The fact that Rushton couldn’t teach because his classes kept getting interrupted shows that people don’t care about factual data, especially when it hurts their feelings or conflicts with any type of egalitarian nonsense they have in their heads. Once challenged, they get mad, scream ‘racist’ and simply do anything in their power to make life a living hell for the person who dares to speak non-politically correct things. But, and a huge but, just because one stops, for the time being, this from being spoken of, DOES NOT make the racial differences between groups go away. People look for any and all types of environmental explanations to attempt to explain away racial IQ gaps and other racial differences both physically and mentally, but they don’t hold up to the genetic explanation, which was shouted down by people who don’t want their fragile reality broken.
The same thing, of course, happened to Arthur Jensen:
In the 1990s protesters in London pelted him with tomatoes at a lecture hall. “Jensenism” became a term of rebuke, used against those who championed theories about whites’ superiority. “Jensenism,” evolutionary biologist Stephen Jay Gould once declared, rested “on a rotten edifice.”
AR: Well, the sorts of things that you’ve been telling me, the sorts of things you’ve been doing research about, can you and do you freely teach these things in your classes?
Jensen: I sure do. I soft-pedaled things 20 years ago, and even then, there were great protests. I had students who would drop the course if these things were brought up even in a very mild way, in a hypothetical way. Students today wonder what all the shouting was about.
AR: Is that so?
Jensen: Yes, it’s rather hard to get students to believe that there were these protests and so on. They take a lot of this for granted. Oh, there’s been a great change in the students in that respect … But even in 1969-1970, I never saw a black in any of these demonstrations.
AR: Is that right?
Jensen: Not a one.
AR: They were SDS [Students for a Democratic Society]-types?
Jensen: All SDS and Progressive Labor Party, mainly. I tried to put them out when they tried to audit my course, because they were hecklers, and so some of the SDS people would sign up for the course. Of course, then they’d have to do the assignments and take the exams.
Interestingly enough, they usually were the top students in the course because they did so much outside reading to try and give me a bad time. They would go out and read everything Galton wrote! They were bright students. They just happened to be political radicals. “
Years ago, if I gave talks at the APA or the American Educational Research Association, the least little thing you’d say, people would get up on the floor and start denouncing you. I haven’t run into that for a long time, except in Canada and Australia. There’s about a ten year cultural lag in those places, I think, on this topic.
AR: I guess nowadays, as compared to fifteen or twenty years ago, you’re not a notorious presence on campus? People don’t say, “There goes Jensen!” You just don’t get that anymore?
Jensen: No, no. I used to. I used to have to be accompanied around campus by two campus policemen. In fact, they told me not to leave my office and go to the library, or any place, except to go to the men’s room around the corner, but not anywhere else without calling the campus police. They’d whiz across campus in a car and they’d be here in just a couple of minutes and walk with me wherever I wanted to go. One year I had two campus policemen, plain clothes men, in all my classes. They audited my courses.
He had to be escorted around campus by two campus police, all because of his research areas of interest. Why did Jensen have to be protected by two men in plain clothes just for talking about his scientific research? There is a clue in what he said: the Students for a Democratic Society (SDS) and the Labor Party, not coincidentally, leftists who like to censor free, true speech when it doesn’t match to their false views of egalitarianism. But as we know, just because the causes for racial differences aren’t spoken of, that doesn’t mean that they go away. Is race a causal factor in intelligence? Yes, it is. ‘Discrimination’, a so-called ‘stereotype threat’ is not the cause for lower black intelligence. Rushton and Jensen showed that the races differ by 1.2 SDs at the most, and that it was 80 percent genetic in nature (Rushton and Jensen, 2005: 279). Were the public to accept truths such as this and not any false ‘truths’ such as what the left puts out, Rushton and Jensen would not have received the derision they did when they were publishing and pushing their theories decades ago. I recall a specific poster that I saw on AmRen a few years back talking about how Jensen was a ‘racist’ and along with Shockley, both needed to be fired and lose their jobs because they just so happened to speak these uncomfortable truths.
When I met Phil in person for the first time the following year, I could not believe that a man so intensely hated in public (nearly always by idiots who did not know him personally and who did not know anything about science) could be so gentle, genial, and generous in person. His very kind and mild manners always impressed me, especially in stark contrast to how people thought and assumed he was.
There is one very small consolation in Phil’s tragically early death: Phil was not an artist, he was a scientist. When an artist dies, his art dies with him, which is why there has not been (and will never be) Beethoven’s 10th Symphony or Guernica II. Unlike art, however, science is cumulative. The rest of us can honor his memory and his scientific legacy by continuing his work. Phil was simultaneously a tremendous role model and a very tough act to follow. He was a model of scientific integrity. Unlike Galileo, he never recanted.
Science is cumulative. He, Jensen, Murray, Herrnstein, Gottfredson, Lynn et al are Modern Day Galileos. They spoke out against this leftist paradigm that has persisted in universities for decades, and even while shown extreme derision, they never recant their statements because they know they are just speaking the truth. Any allegations of so-called ‘racism’ are just that: allegations with no factual backing behind them. The fact that they need to be called childish words such as ‘racist’ and they need to have their lectures and classes interrupted by ‘protests’ speaks volumes on the research they were doing. The fact that the left has nothing to say except untrue vitriol shows who was right. When you have to attempt to silence someone because you don’t like what they’re saying or it ‘offends you’, that says volumes about your character than the one’s character you’re trying to spew vitriol at.
The fact of the matter is, no matter what anyone or any entity does to attempt to hide racial differences in intelligence, or any other trait for that matter, the truth will always come out. When answers one receives don’t line up to what one sees in his day-to-day life, one goes and looks for the truth. And that truth is that some races aren’t as intelligent as others which leads to differences in scholastic achievement and life success. These differences persist through the generations and when a downtrodden individual (no matter the race) realizes that those have a better social standing then they, they make mental leaps in their head that ‘they’re being held down’ or ‘the man is out to get them’ not even thinking that it’s their own innate ability that’s holding them down in comparison to the other group.
Rushton and Jensen will be fully vindicated one day. It’s only a matter of time. David Piffer showed that IQ alleles differ in frequency between races, meaning that a FULL vindication of Rushton, Jensen, Gottfredson, Murray, Herrnstein, Lynn, Kanazawa et al are going to come soon.
RIP to two great men who had a huge effect on my worldview and the reasons for differences around the world. I only hope that others rise up to continue their work and prove, once and for all, that they were right.
Edit, 7/18/17: r/K selection theory has been rebutted.
r/K theory doesn’t apply to humans and if it did, Mongoloids would be r and Africans would be K. Cold with is an agent of r selection while endemic disease is an agent of K selection. Rushton used a debunked “continuum” for the basis for his theory and completely changed r and K. However it’s wrong. Rushton was wrong. Anonymous Conservative is wrong. Anyone who uses those two in reference to r/K is wrong by proxy since r/K is a debunked paradigm.
Japan has had a population crisis for a few years. Japan’s fertility rate was 1.4 in 2014. To have enough children to keep the population stable, the Total Fertility Rate (TFR) needs to be 2.1. As a country industrializes and becomes more prosperous, the TFR drops as higher IQ follows better nutrition. As a nation industrializes and becomes more complex, the attention of the populace shifts from one of having children and a family to one of success and intellectualism. As this occurs, the birth rate drops because the more intelligent a population is, the more likely it is for them to pursue higher education or monetary achievement. Clearly, the main reason Japan has concerns with their TFR is due to their high intelligence.
The Japan Times reported yesterday that almost half of single young men and women were virgins. A survey of Japanese men and women aged 18-34 found that 70 percent of unmarried men and 60 percent of unmarried women were not in a relationship. Also discovered, 42 percent of the men and 42.4 percent of the women admitted to being virgins. The survey was taken before in 2010, with 36.2 percent of men and 38.7 percent of women admitting to being virgins.
These surveys have been carried out every 5 years since 1987. Then, the rate of men who said they had no partner was 48.6 percent and for women it was 39.5 percent. The survey, which was conducted last June and accounted for 8,754 single people and 6,598 married couples across Japan, also found that 90 percent of the respondents wanted to get married “sometime in the future”, but for some people, this turns out to be a mistake. Moreover, 30 percent of the 2,760 men and 26 percent of the 2,570 women polled said they were not currently looking for a relationship. The increase in singles was most noted in the 20s, when women are the most fertile. The Prime Minister of Japan, Shinzo Abe also said he wants to increase the birthrate from 1.4 to 1.8 by 2025.
Lastly, the study found that the number of children for couples marries for 15 to 19 years was 1.94, a record low. This study did not ask questions about same-sex partners, but what we are concerned about is the TFR and how it’s driven by evolution, so this is a non-factor.
Japan’s population is dramatically shrinking. In 2010, they had a population of 128 million but by their 2015 census, they had a population of 127 million. This is due to the increase in virgins and an aging population. Why is this happening?
This is, of course, driven by r/K Selection Theory. Rushton thought of r/K Selection Theory, also known as Differential K theory, in 1985 with a paper titled Differential K Theory: The Sociobiology of Individual and Group Differences. Organisms can be r-selected, K-selected or somewhere in between. Humans as a species are K-selected, but some human races and ethnies are more K-selected than others.
Africans are r-selected, meaning that they have many children while not investing too much time in their offspring. They evolved to be r-selected to offset the high mortality rate due to the harshness of Sub-Saharan Africa. Due to this, black girls have an earlier menarche (period) so they can reproduce more to a) offset the high mortality rate and b) have a chance to reproduce more due to the high mortality rate. This is driven by disease, malnutrition, and parasitic load, which also drop IQ and contribute to the high birth rate since lower IQ populations have more children.
Caucasians are in the middle of r and K, and have fewer children and put more energy into caring for each one. This goes back to evolving in the Ice Age where cooperation and altruism were needed. More attention to children was needed for Eurasians evolving back then due to the harsh conditions of the Ice Age. So, a higher IQ evolved, and along with the higher IQ came a bigger brain. The bigger brains of Eurasians led to children being born earlier, and a bigger brain allowed for better care for the children along with numerous other positive variables to help survive in the harsh weather. Moreover, genes from Neanderthals are responsible for a 1 percent decrease in historic fitness (biological fitness) in Eurasian populations.
Orientals (Japanese, Chinese, Koreans) are further K than Caucasians are. This is reflected in brain size, where more K-selected populations have bigger brains, thus they can think further into the future and maximize care for their children. The opposite holds true for blacks. This is reflected in modern-day, first-world life where blacks have too many children to care for on their own accord and whites and Orientals have fewer children and put more investment into their children .
It’s not only Japan that’s having this problem with birthrates. It’s all of the West and East Asia. Higher IQ societies do have a longer life expectancy, while lower IQ societies have a lower one. Then, as described above, the lower IQ populations have more children to offset the mortality rate.
Japan’s birthrate concerns are due largely in part to genetic factors. This is currently occurring in all high IQ populations. Those populations have a large elderly population, with the young demographic quickly shrinking. Seeing this gradient throughout the world with IQ and fertility rates, we can make some general conclusions:
- Low IQ populations have more children while high IQ populations have less children.
- High IQ populations are more likely to have a large subset of virgins, as seen with this article. Lower IQ populations lose their virginity earlier.
This can be seen with the CLASH (CLimate, Aggression and Self-control in Humans) model (Van Lange, Rinderu, and Bushmen 2016). According the the CIA World Fact book 2014, in countries closer to the equator, the average age of first birth for a female was 20 years of age (the countries were the Gaza strip, Liberia, Bangladesh, Kenya, Mali, Tanzania, Uganda and various other middle African countries). Conversely, for countries further away from the equator, the average age of first birth was 28 years of age (Japan, Canada, and most European countries). Those populations that evolved in warmer climates where the changes in season are minimal with unpredictable harshness tend to enact faster life history strategies than those in colder climates.
Moreover, a slower life history strategy (K-selection), under a predictable environment would be better to enhance inclusive fitness. There is a growing body of evidence that predictable environments promote K-selection “in terms of lower mortality, morbidity, delayed reproduction, and a higher contribution towards one’s social capital.” This can be seen with the trends in Western and East Asian countries.
The trend that Japan is facing can be reversed with incentives for reproduction. However, the more intelligent a society is, the fewer children it will have due to evolutionary pressures. Is there a happy medium between IQ and fertility rates, where the population isn’t too dumb and the fertility rates aren’t too low? I’ll explore that in the future.
(Note, 6/24/17: Rushton’s r/K selection in applications to human races is dead. It’s been dead for almost 30 years after and ecologist critiqued his method and use of ecological theory in application to human races. Now, that doesn’t meant that everything written below—or even on my whole blog—is fully wrong, just that the attempted explanation is wrong. It still holds that Eurasians have worse fitness than Africans, which is partly due to deleterious Neanderthal variants, however, r/K theory does not explain it.)
Science Daily reported last week that Neanderthals left humans a genetic burden, which is having less offspring. Of course, these deleterious alleles only introgressed into non-African populations due to Africans not leaving Africa. This manifests itself today in birth rates within countries and between them based on the ethnic/racial mix. And (not) coincidentally, the areas with the highest rate of children are in sub-Saharan Africa.
The Neanderthals existed in small bands, so inbreeding was common. Due to this inbreeding, Neanderthals were more homogenous than we are today. When humans migrated out of Africa, they encountered the inbred Neanderthals who they interbred with. Harmful genetic variants acquired from Neanderthals are shown to reduce the fitness of populations with certain deleterious alleles. There are of course tradeoffs with everything in life. Increased intelligence and being better able to weather the Ice Age, among numerous other factors, were positive things gained from interbreeding with Neanderthals. Negative effects were the acquisition of deleterious alleles which still persist today in non-African hominids. These deleterious alleles decreased biological fitness which manifests itself in the birthrate of Eurasian populations throughout the world (the Germann and Japanese birthrate is 1.3 for reference).
Harris and Nielson also hypothesize that since Neanderthals existed in small bands that natural selection was less effective, allowing for weakly harmful mutations to pass on and not get weeded out over the generations. However, when introduced back into humans these effects become lost over time due to a large population with natural selection selecting against the deleterious Neanderthal alleles. Using a computer program, Harris and Nielson quantify how much of a negative effect the Neanderthal genome had on modern populations. The conclusion of the results was that Neanderthals are 40 percent LESS genetically fit than modern humans.
The researchers’ simulations also suggest that humans and Neanderthals mated more freely, which leads more credence to the idea that Neanderthals got absorbed into the Homo Sapien population and not mostly killed off. The estimation for Neanderthal DNA in modern hominids from the simulation was around 10 percent, which then continued to drop as the Neanderthal-Homo Sapiens hybrids interbred with those who hardly had any Neanderthal DNA. More evidence also shows that the percentage of Neanderthal DNA was higher in the past in Eurasians as well. Which makes sense since Asians have on average 20 percent more Neanderthal DNA than Europeans due to a second interbreeding event.
However, Harris and Nielson end up concluding that non-Africans historically had a 1 percent loss in biological fitness due to Neanderthal genetics. Moreover, a better immune system came from Neanderthal genetics. Skin color is another trait inherited from Neanderthals as well.
Along with the acquisition of deleterious Neanderthal alleles, early Eurasians also encountered the same environment as the Neanderthals. Those selection pressures, along with interbreeding due to small bands lead to a decrease in the number of children had. Fewer children are easier to care for as well as show more attention to. All of these variables in that environment lead to fewer children produced. It’s a better evolutionary strategy to have fewer children in more northerly climes than in more southerly ones due to the differing selection pressures. Environmental effects are also one reason why birthrates are lower for populations that evolved in northerly climes (Neanderthals and post-OoA hominids). Harsh winters lead to a decreased population size, as evidenced by the Inuit and Eskimoes, which their low population size didn’t allow for selection for high IQ despite having the same brain size as East Asians.
I couldn’t help but think that, yet again, for the second time in two weeks, one of JP Rushton’s theories was confirmed. This confirms one of the many variables of Rushton’s r/K Selection Theory. Just like I covered how Piantadosi and Kidd corroborated Rushton’s theory of brain size and earlier child birth. Neanderthals had bigger brains than we do today, and knowing what we know about the correlation between IQ, brain size and early childbirth, I would assume that Neanderthals also had earlier childbirths as well,.
Along with these deleterious gene variants from Neanderthals, other variables that contribute to the decline in Eurasian populations also include higher IQ as well, as JP Rushton says, is an extreme way to have control over their environment and individuality. These traits are seen in higher IQ populations in comparison to lower IQ populations. We could also make the inference that since Eurasian children have bigger heads, that multiple childbirths would be taxing on the Eurasian woman’s birth canal while it would be less taxing on the African woman’s.
This study also shows that Neanderthals also had less offspring due to being more intelligent. They had bigger brains than we do today, and since we know that higher IQ is correlated with fewer children conceived, we can say that they were pretty damn smart (they buried their dead 50,000 years ago. There was also a recent discovery of a 176,500-year-old Neanderthal constructions in a French cave). A main cause for the current trend in birthrates in Eurasian populations is due interbreeding with Neanderthals. These events also attributed more to the decline of the Neanderthals.
Deleterious Neanderthal alleles are yet another reason for lower Eurasian birthrates, which shows = that the current trend currently happening in the world with these populations is natural and evolutionarily based. I’ve said a few times that by showing positive things to women on television will increase the white birth rate, with Rushton cites National Socialist Germany as one example. By showing women happy with children, this lead to a massive boom in the German population. To ameliorate the effects of low natural birth rates, these positive things need to be shown on television to women to start to reverse the effects of low natural childbirths.
It’s been a great month for Rushton’s theories, with two of them being corroborated in one month. It’s only a matter of time before the denial of human nature is completely discarded from modern science. As the data piles up on human genetic diversity we will not be able to deny these clearly evident factors any longer.
In the past 100 years since the inception of the IQ test there have been racial differences in test scores. What causes these score differences? Genetics? Environment? Both? Recently it has come out that populations do differ in allele frequencies that affect intelligence. David Piffer’s “forbidden paper on population genetics and IQ” was rejected by the new editor of the journal Intelligence. In the paper, he shows how IQ alleles vary in frequency by population. One reviewer even said it should not be put up for review, which Piffer believes there was a hidden agenda or a closed minded attitude. He even puts reviewers comments and responds to them. He says science should be transparent, which is why he’s showing the researchers’ comments on his paper.
His December, 2015 paper titled: A review of intelligence GWAS hits: Their relationship to country IQ and the issue of spatial autocorrelation shows that there are differing allele frequencies in which IQ between populations that affect IQ which are then correlated highly with average IQ by country (r=.92, factor analysis showed a correlation of .86). There was also a “positive and significant correlation between the 9 SNPs metagene and IQ”(pg. 45). However, Piffer does conclude that since the 9 alleles are present within all populations (Africans, Latin Americans, Europeans, South Asians, and East Asians) that the intelligence polymorphisms don’t appear to be race-specific, but were already present in Homo Sapiens before the migration out of Africa. He then goes on to say that it’s extremely likely that the vast majority of alleles were subject do differential selection pressure which lead increases in cognitive abilities at different rates rates in different geographical areas (pg. 49). It’s of course known that differing populations faced differing selection pressures which then lead to genotypic changes which then affected the phenotype. It’s not surprising that genes that correlate strongly with intelligence have differing frequencies in different geographical populations; it’s to be expected with what we know about evolution and natural selection. Below is the scatter plot showing the relationship between polygenic score GWAS (Genome Wide Association Studies) hits and IQ:
The fact that these differences exist should not come as a shock to those who want to seek the truth, but as seen with how David Piffer didn’t even get consideration for a revision, this shows the bias in science to studies such as this that show racial differences in intelligence exist.
Piffer’s data also corroborates Lynn and Meisenberg’s (2010) finding of a correlation of .907 with measured and estimated IQ. This shows that the differing allele frequencies affect IQ, which then affect a countries GDP, GNP, and over all quality of life.
With a sample with a huge n (over 100,000 subjects) cognitive abilities tests were performed on verbal-numerical reasoning, memory and reaction time (a huge correlate for IQ itself, see Rushton and Jensen, 2005). Davies et al (2016) discovered that there were significant genome-wide SNP based associations in 20 genomic regions, with significant gene-based regions on 46 loci!! Once we find definitive proof that intelligence differences vary between individuals, as well as the loci and genomic regions responsible, we can then move on to difference in allele frequency in depth (which Piffer 2015 was one of the starts to this project).
Moreover, genes that influence intelligence determine how well axons are encased in myelin, which is the fatty insulation that coats our axons, allowing for fast signaling to the brain. Thicker myelin also means faster nerve impulses. The researchers used HARDI to measure water diffusion in the brain. If the water diffuses rapidly in one direction, that shows the brain has very fast connections. Whereas a more broad diffusion would indicate slower signaling, thus lower intelligence. It basically gives us a picture of an individuals mental speed. Thinking of reaction time tests where Asians beat whites who beat blacks, this could possibly show how differing process times between populations manifest itself in reaction time. Since myelin is correlated with fast connections, we can make the inference that Asians have more than whites who have more than blacks, on average. The researchers also say that it’s a long time from now, but we may be able to increase intelligence by manipulating the genes responsible for myelin. This leads me to believe that there must be racial differences in myelin as well, following Rushton’s Rule of Three.
Since the mother’s IQ is the best predictor of the child’s IQ, this should really end the debate on its own. Sure on average, intelligent black mothers would birth intelligent children, but due to regression to the mean, the children would be less intelligent than the mother. JP Rushton also says that regression works in the opposite way. Both blacks and whites who fall below their racial means will have children who regress to the means of 85 and 100 respectively, showing the reality of the genetic mean in IQ between the races.
Why would differing allele frequencies lead to the same cognitive processes in the brain in genetically isolated populations? I’ve shown that brain circuits vary by IQ genes, and populations do differ in this aspect, like all other differing genotypic/phenotypic traits.
East Asians have bigger brains, as shown by MRI studies. Rushton and Rushton (2001) showed that the three races differ in IQ, brain size, and 37 different musculoskeletal traits. We know that West Africans and West African-descended people have genes for fast twitch muscle fibers (Type II) (Nielson and Christenson, 2001). Europeans and East Asians have slow twitch muscle fibers (Type I) for strength and endurance. (East Africans have this as well, which allows for ability to run for distance, which fast twitch fibers do not allow for. The same is true for slow twitch fibers and sprinting events.) Bengt Saltin showed that European distance runners have up to 90 percent slow twitch fibers (see Entine, 2000)! So are genetic IQ differentials really that hard to believe? With all of these differing variables in regards to intelligence that all point to a strong genetic cause for individual differences in other genes that lead to stark phenotypic differences between the races, is it really not plausible that populations differ in intelligence, which is largely inherited?
Is it really plausible that differing populations would be the same cognitvely? That they would have the same capacity for intelligence? Even when evolution occurred in differing climates? The races/ethnicities differ on so many different variables with differing genes being responsible for it. Would IQ genes really be out of the question? Evolution didn’t stop from the neck up. Different populations faced different selection pressures, so different human traits then evolved for better adaption in that environment. Different traits clearly developed in genetically isolated populations that had no gene flow with each other for tens of thousands of years. These differing evolutionary environments for the races put different pressures on them, selecting some for high IQ alleles and others for low IQ alleles.
We are coming to a time where intelligence differences between populations will become an irrefutable fact. With better technology to see how differing genes or sets of genes affect our mind as well as physiology, we will see that most all human differences will come down to differing allele frequencies along with differing gene expression. Following Rushton’s simple rule based on over 60 variables, East Asians will have the most high IQ alleles followed by Europeans and then blacks. The whole battery of different cognitive abilities tests that have been conducted over the past 100 years show us that there are differences, yet we haven’t been able to fully explain it by GWAS and other similar techniques. Charles Murray says within the next 5 to 10 years we will have definitive proof that IQ genes exist. After that, it’s only a matter of time before it comes out that racial differences in IQ are due to differing allele frequency as well as gene expression.
“Philosophers of Science” attempt to stick their heads into the race/IQ debate to give their field more credence than it should get with the hard sciences. They use bad arguments like saying that “gene-environment interactions are widespread and hard to entangle” (Block, 1995), not knowing that identical twins reared apart grow up to be so similar (Rushton and Jensen, 2005, p. 279). The only time they should stick their heads in this debate is when they’re affirming that the methodology used to test IQ as well as racial differences in IQ are sound; otherwise, they do not have the training to assess this. Most “Philosophers of Science” defend claims that disintegrate when presented with the relevant scientific evidence (Sesarardic, 2000). I will be referencing this paper for the length of this article.
Half of the paper analyzes Lewontin’s argument to Jensen in which he uses his now famous “seed argument” in which he says you can take two seeds from the same heterogeneous population and plant them in rich and poor soil and “. . . as a result, the phenotypic differences within each of the two groups of plants will be 100 percent heritable, but the difference between the two groups will be entirely due to differences in two environments (zero heritability).” The fact of the matter is, this argument is parroted by “Philosophers of Science” when Jensen never made that argument.
Jensen then systemically dismantled every environmental argument with empirical evidence that they don’t hold up.
Other researchers then made accusations of “racism” the reason for Jensen’s overlooking of this. James Flynn, a big opponent of the hereditarian hypothesis and Rushton and Jensen in general, say that Jensen is not a “racist”. There is also something called the “X-Factor”, which is when phenotypic differences between two groups can be explained by an environmental factor that has no within-group variation at all, a 0 heritability. Racism, however, is a poor excuse for the “X-Factor”. Both Flynn and Jensen rule out discrimination as being the cause for the “X-Factor” as well.
Simply put, Jensen doesn’t make inferences that the black-white IQ gap is genetically based on one or a few variables on their own, but everything put together, that’s where the remaining evidence put. “Philosophers of Science” don’t understand heritability coefficients to be saying what they do; they wouldn’t be saying that if they knew how they worked.
Sesardic brings up how Block (1995) only mentions three pieces of empirical evidence: The “Flynn Effect”, “data about caste-like minorities”, and the small amount of genetic variation between races.
- The Flynn Effect happens uniformly in all populations at a rate of 3 points per decade but has slowed considerably. This increase began starting around 1880, coinciding with the industrial revolution. Better nutrition increased brain size in all populations, which lead to an increase in IQ. The Flynn Effect is not on g, so to make any claims that the differences in IQ between blacks and whites, or global differences in IQ for that matter, can be changed with more favoring towards environmentalist positions are not consistent with the scientific literature. In 1945, the average white IQ in America was 85, the same as the average American black IQ today. Since the differences in IQ have stayed consistent despite better nutrition in all groups, this proves that the gap is genetic in origin. Just because a change in one group over time is due to an environmental change, doesn’t mean, or even make it probable, that a difference between 2 groups at the same time is due to an environmental change. Since the Flynn Effect does not occur on g, it should be a non-factor.
- Minorities are only “caste-like” because differences in IQ are heritable, leading to racial disparities in social class differences. We can see when we match blacks, whites, and “Hispanics” for IQ (100), that some differences disappear, other differences decrease dramatically, and even blacks and “Hispanics” beat out whites in a couple of variables. Through multiple IQ tests averaged over time as well as seeing that test differences between races stay mostly the same, we can then make the inference, with all of the other evidence, that racial and ethnic differences in IQ are mostly genetic in origin with the environment having very little effect. To say that “racism” or “stereotype threat” has any bearing on these racial differences in IQ is laughable because 1) stereotype threat is only replicable in the lab and 2) racism as a variable does not exist in IQ testing.
- The small amount of genetic variation between races as an argument for the non-existence of race is meaningless. There are around 3 billion base pairs in the human genome. The human races differ on around .1 percent of the genome, or around 3 million base pairs. This is more than enough genetic difference to show phenotypic differences (obviously) as well as genotypic differences (again, obviously). Richard Dawkins in the Ancestor’s Tale writes: “What is not correct is the inferene that race is therefore a meaningless concept.” Race is a perfectly valid concept, anyone who denies it has doesn’t know of all of the studies that show the existence of race and how it’s a scientifically taxonomic concept.
Sesardic then brings up how “Philosophers of Science” continuously cite The Mismeasure of Man and Steven Jay Gould in an attempt to denigrate scientists long dead. A few “glowing reviews” from two “Philosophers of Science”:
No one has done as much as Stephen J. Gould to expose race and intelligence studies for the garbage that they often are. (Brown 1998, 5)
Stephen Jay Gould has lucidly analyzed how filling the skulls with lead shot, and comparing the weights of the lead, could easily be infected with unconscious biases. (Kitcher 1997, 171)
The garbage that they often are? Steven Jay Gould is a long discredited ideologue who put his politics before actual science, ironically giving HIM the same bias he falsely accused Samuel Morton of having. James Flynn even says that Gould’s book evades all of Jensen’s best arguments (as most always happens with this debate) with his false belief that g is “reified” therefore leading to the study of race and IQ being meaningless since he has “rebutted the g factor”. I proved the existence of Spearman’s hypothesis the other day using Jensen’s writings that he empirically verified that Spearman’s hypothesis exists in 25 independent samples of blacks and whites along with the study by Dragt (2010) who used the method of correlated vectors to empirically prove the existence of Spearman’s hypothesis. In meta-analyses of Spearman’s hypothesis, he found that differences in intelligence between groups are largely based on cognitive complexity and any so-called “biases in mental testing” cannot account for these racial differences in cognitive ability.
In the definitive refutation of Steven Jay Gould’s “reanalysis” of Morton’s skulls, Lewis, et al definitively prove by remeasuring 308 of the 670 skulls that he had no implicit biases. They also found that if Morton’s biases were true, then there would be considerable overestimates of white skulls while there would be considerable underestiamates of non-white skulls. Ironincally enough, he considered his Egyptian skulls “Negroid” and overmeasured by 12 percent. He overmeasured three of those skulls, along with Seminole (by 8 percent) and native African Nergro (by 7 percent), falsifying the claim that Morton had a bias in measuring his skulls!! As I have brought up here numerous times, as Rushton has refuted him (and defended Morton’s results) as well as Jensen giving Gould a definitive rebuttal to his book. Gould should not be being cited seriously anymore. He should only be brought up as an example of extreme bias in the context of race as well as racial differences and a whole slew of other things that are politically motivated.
He finally rounds up the paper by bringing up how TJ Bouchard, showing that the Big Five Personality Traits have a high heritabilty, gets told that they are traits that carry a social judgment. However, we now know that 40-60 percent of the variation the Big Five is heritable, so this is a meaningless claim.
Sesardic ends the paper as follows:
Why is this small segment of contemporary philosophy of science in such a sorry state? On reflection, I prefer to leave this question as an exercise for the reader. My aim in this paper is to criticize a deviant philosophical trend, not to explain how it came about or why it spread.
My answer to this question is that most philosophers seem to be leftists. We can see with the vehement race denial that they want to believe so strongly that racial differences, as well as race as whole, does not exist. The fact that they attempt to say that these things are not a reality and based on faulty methodologies shows that they do not know what they are talking about. They show large misconceptions about heritability, and continuously cite Steven Jay Gould, even when Gould has been refuted numerous times as well it being shown that they don’t correctly understand heritability. They show large misconceptions of what is understood in the field of psychometrics and heritabilities and make faulty claims about the hereditarian hypothesis.
If the hereditarian hypothesis is to be refuted (it won’t), it will be from science and not philosophy or “Philosophers of Science”.
It seems like every day something new comes out that attempts to discredit the reality of g (This paper came out in 2012.). Steven Jay Gould (in)famously wrote in The Mismeasure of Man:
The argument begins with one of the fallacies—reification, or our tendency to convert abstract concepts into entities (from the Latin res, or thing). We recognize the importance of mentality in our lives and wish to characterize it, in part so that we can make the divisions and distinctions among people that our cultural and political systems dictate. We therefore give the word “intelligence” to this wondrously complex and multifaceted set of human capabilities. (emphasis mine)
“The results disprove once and for all the idea that a single measure of intelligence, such as IQ, is enough to capture all of the differences in cognitive ability that we see between people,”
“Instead, several different circuits contribute to intelligence, each with its own unique capacity. A person may well be good in one of these areas, but they are just as likely to be bad in the other two,”
Just like The Mismeasure of Man is “the definitive refutation to the argument of The Bell Curve”, right?
In the above paper, they cite Gould twice writing:
It remains unclear, however, whether population differences in intelligence test scores are driven by heritable factors or by other correlated demographic variables such as socioeconomic status, education level, and motivation (Gould, 1981; . . .
They have been shown over numerous studies that population differences in intelligence are driven by heritable factors (Rushton and Jensen, 2005; Lynn and Vanhanen, 2006; Winick, Meyer, and Harris, 1975; Frydman and Lynn, 1988; Rushton, 2005)
More relevantly, it is questionable whether they relate to a unitary intelligence factor, as opposed to a bias in testing paradigms toward particular components of a more complex intelligence construct (Gould, 1981;
I will prove the existence of g in this article. There is also an empirical basis for the g factor.
It’s getting old now that researchers still think that they can “disprove g”, as a multitude of studies have already corroborated Spearman’s hypothesis as an empirical fact. That is, applying the scientific method, using the same hypothesis over a multitude of different studies and testing those predictions by experiment or further observation and modify the hypothesis when new information comes to light. Then, repeat the aforementioned steps until there are no discrepancies between the theory and experiment/observations.Then when consistency is obtained it then becomes a theory that provides a coherent set of premises that explain a class of events.
How many times has the Hampshire et al hypothesis been corroborated? I doubt it has been corroborated as many times as Spearman’s hypothesis has.
As I said the other day, Jensen tested Spearman’s hypothesis on 25 large independent samples, with each sample confirming Spearman’s hypothesis. Even matching blacks and whites for SES didn’t diminish the effect. Jensen then concludes that the overall chance for Spearman’s hypothesis being wrong is over 1 in a billion. Pretty high odds.
Even then, if this study were to be replicated the amount of times that Spearman’s hypothesis has, it still wouldn’t disprove g.
He (Gould) continues: “The fact that Herrnstein and Murray barely mention the factor-analytic argument forms a central indictment around The Bell Curve and is an illustration of its vacuousness.” Where, Gould asks, is the evidence that g “captures a real property in the head?
Murray states that they “barely brought up the factor-analytical argument” because it was out of date; Gould was using statistics on g that were 50 + years old. Also, a reviewer of his book for the journal Nature said that Gould’s “discussion of the theory of intelligence stops at the stage it was more than a quarter of a century ago.” Gould was using old arguments, and, as Arthur Jensen states in his response to Gould:
Of all the book’s references, a full 27 percent precede 1900. Another 44 percent fall between 1900 and 1950 (60 percent of those are before 1925); and only 29 percent are more recent than 1950.
More than half of Gould’s references in The Mismeasure of Man are outdated by more than 50 years. Clearly, he was attempting to denigrate the old studies of intelligence, i.e., phrenology, even though this recent paper in the journal Nature recently said:
The genomic regions identified include several novel loci, some of which have been associated with intracranial volume
So, we have several loci that are associated with intracranial volume; this shows that those skull studies of yesteryear weren’t crazy. Moreover, the fact that Rushton and Ankney (1996) “reviewed 32 studies correlating measures of external head size with IQ scores or with measures of educational and occupational achievement, and they found a mean r .20 for people of all ages, both sexes, and various ethnic backgrounds, including African Americans” shows that there is a correlation of .20, albeit not too high but there, with external head size and IQ. This shows that Gould’s argument on phrenology is bunk, as modern studies confirm that there is a slight correlation between head size and IQ, and therefore g.
The fact that researchers are still bringing up Gould’s arguments on g show that there really is no good argument to discount it. Basically, any and all arguments that attempt to discredit g are bunk as Spearman’s hypothesis has been empirically verified:
Conclusion: Mean group differences in scores on cognitive-loaded instruments are well documented over time and around the world. A meta-analytic test of Spearman’s hypothesis was carried out. Mean differences in intelligence between groups can be largely explained by cognitive complexity and the present study shows clearly that there is simply no support for cultural bias as an explanation of these group differences. Comparing groups, whether in the US or in Europe, produced highly similar outcomes.
Along with Jensen’s 25 large independent studies that showed that the probability that Spearman’s hypothesis is false is 1 in a billion, this proves that Spearman’s hypothesis is an empirical scientific fact.
Newman and Just, (2005) state in verbal and spatial conditions that the frontal cortex revealed greater activation for high-g in comparison to low-g, supporting the idea that g reflects functions of the frontal lobe. The “seat” of general intelligence is the prefrontal cortex (Cole, et al, 2011, Roth, 2011). This can also be verified with MRI scans that show that those who have higher g have bigger prefrontal cortexes than those with lower g.
Moreover, the fact that Colom, et al (2006) show that in their sample that neuroanatomic areas underlying the g factor could be found across the entire brain including the frontal, parietal, temporal and occipital lobes, shows that this factor is present throughout the brain and all are correlated with g and work together in concert to manifest intellectual ability.
Other researchers have also used the method of correlated vectors on functional Magnetic Resonance Imaging (fMRI), which measures brain activity by detecting changes associated with blood flow. This technique is proven useful due to the fact that cerebral blood flow and neuronal action are correlated. Lee, et al write:
In conclusion, we suggest that higher order cognitive functions, such as general intelligence, may be processed by the coordinated ability may be attributable to the functional facilitation rather than the structural peculiarity of the neural network for g. In addition, our results demonstrated that the posterior parietal regions including bilateral SPL and right IPS could be the neural correlates for superior general intelligence. These findings would be the early step toward the development of biological measures of g which leads to new perspectives for behavior interventions improving general cognitive ability.
They also used the MCV to find that the frontal and parietal lobes are associated with g. Even these studies show that g shows up throughout the brain and not in one solitary spot (though, the PFC is still the seat of intelligence), this shows yet another biological basis for g.
Hampshire, et al write:
Thus, these results provide strong evidence that human intelligence is a construct that emerges from the functioning of anatomically dissociable brain networks.
However, with the above studies confirming that the seat of intelligence is the prefrontal cortex, along with great g ability possibly be attributable to the functional facilitation rather than the structural peculiarity of the neural network for g, this shows, along with the study proving Spearman’s hypothesis, that g is a real and measurable thing. g’s seat is the prefrontal cortex, and exceptional g may possibly be attributed to the functional facilitation of the neural network for g . What all of these studies show is that all though the Hampshire paper showed how they “demonstrate that different components of intelligence have their analogs in distinct brain networks.” that a) higher order cognitive functions may be processed by the coordinated activation of widely distributed brain areas (disproving the above quote), b) the seat of g is the prefrontal cortex, c) those with more g have bigger prefrontal cortexes and therefore bigger brains since the prefrontal cortex is the ‘seat’ of intelligence and d) Spearman’s hypothesis has been corroborated numerous times by many different researchers not named Arthur Jensen.
Highfield (one of the researchers in the study) ends the article as follows:
“We already know that, from a scientific point of view, the notion of race is meaningless. Genetic differences do not map on to traditional measurements of skin colour, hair type, body proportions and skull measurements.
This is something that never ends; it always comes up no matter how many times it’s been said. People can say “race is a social construct” all they want, it doesn’t make it true as there is a biological reality to race.
Now we have shown that IQ is meaningless too,” Dr Highfield said.
When will people learn not to cite men who have smeared their legacy in an attempt to defame men who they disagreed with ideologically? Citing Steven Jay Gould in 2016 shows a bias to want to discredit g as a main factor for many things in life including SES, educational attainment, wealth attainment and so forth. The g factor is a measurable thing, with the seat of the factor being the prefrontal cortex. No amount of attempting to dispute this factor can be done, as it’s been empirically verified numerous times.