The most well-known high IQ society (HIS hereafter) is Mensa. But did you know that there are many more—much more exclusive—high IQ societies? In his book The Genius in All of Us: Unlocking Your Brain’s Potential (Adam, 2018) Adam chronicles his quest to raise his IQ score using nootropics. (Nootropics are supposed brain-enhancers, such as creatine that supposedly help in increasing cognitive functioning.) Adam discusses his experience taking the Mensa test (Mensa “is Mexican slang for stupid woman“; Adam, 2018) and talking to others who did with him on the same day. One highschool student he talked to wanted to put that he was a Mensa member on his CV; yet another individual stated that they accepted a challenge from a family member, since other members were in Mensa, she wanted to show that she had what it took.
Adam states that they were handed two sheets of paper with 30 questions, to be answered in three or four minutes, with questions increasing in difficulty. The first paper, he says, had a Raven-like aspect to it—rotating shapes and choosing the correct shape that’s next in the sequence. But, since he was out of time for the test, he says that he answered “A” to the remaining questions when the instructor wasn’t looking, since he “was going to use cognitive enhancement to cheat later anyway” (Adam, 2018: 23). (I will show Adam’s results of his attempted “cognitive enhancement to cheat” on the Mensa exam at the end of this article.) The shapes-questions were from the first paper, and the second was verbal. On this part, some words had to be defined while others had to be placed into context, or be placed into a sentence in the right place. Adam (2018: 23) gives an example of some of the verbal questions:
Is ‘separate’ the equivalent of ‘unconnected’ or ‘unrelated’? Or ‘evade’ — is it the same as ‘evert’, ‘elude’ or ‘escape’?
[Compare to other verbal questions on standard IQ tests:
‘What is the boiling point of water?’ ‘Who wrote Hamlet?’ ‘In what continent is Egypt?’ (Richardson, 2002: 289)
‘When anyone has offended you and asks you to excuse him—what ought you do?’ ‘What is the difference between esteem and affection?’ [this is from the Binet Scales, but “It is interesting to note that similar items are still found on most modern intelligence tests” (Castles, 2013).]]
So it took a few weeks for Adam’s results to get delivered to his home. His wife opened the letter and informed him that he had gotten into Mensa. (He got in despite answering “A” after the time limit was up.) This, though, threw a wrench into his plans: his plan was to use cognitive enhancers (nootropics) to enhance his cognition and attempt to score higher and get into Mensa that way. However, there are much more exclusive IQ clubs than Mensa. Adam (2018: 30) writes:
Under half of the Mensa membership, for example, would get into the Top One Percent Society (TOPS). And fewer than one in ten of those TOPS members would make the grade at the One in a Thousand Society. Above that the names get cryptic and the spelling freestyle.
There’s the Epida society, the Milenija, the Sthiq Society, and Ludomind. The Universal Genius Society takes just one person in 2,330, and the Ergo Society just one in 31,500. Members of the Mega Society, naturally, are one in a million. The Giga Society? One in a billion, which means, statistically, just seven people on the planet are qualified to join. Let’s hope the know about it. If you are friends with one of them, do tell them.
At the top of the tree is the self-proclaimed Grail Society, which sets its membership criteria so high — one in 76 billion — that it currently has zero members. It’s run by Paul Cooijmans, a guitarist from the Netherlands. About 2,000 people have tried and failed to join, he says. ‘Be assured that no one has come close.’
Wow, what exclusive clubs! Mensans are also more likely to have “psychological and physiological overexcitabilities” (Karpinski et al, 2018) such as ADHD, autism, and other physiologic diseases. How psycho and socially awkward a few members of Mensa are is evidenced in this tweet thread.
How spooooky. Surely the high IQ Mensans have un-thought-of ways of killing that us normies could never fathom. And surely, with their high IQs, they can outsmart the ones who would attempt to catch them for murder.
A woman named Jamie Loftus got into Mensa and she says that you get a discount on Hertz car rentals, a link to the Geico insurance website, you get access to the Mensa dating site “Mensa Match” (there is also an “IQ” dating site called https://youandiq.com/), an email address, a cardboard membership card, and access to Mensa events in your area. Oh, and of course, you have to pay to take the test and pay yearly to stay in. (Also read Loftus’ other articles on her Mensa experience: one where she describes the death threats she got, and another in which she describes how Mensans would like her to not write bad things about them (Mensans). Seems like Mensans are in their “feels” about being attacked for their little—useless—club.)
One of the founders of Mensa—Lancelot Ware—stated that he “get[s] disappointed that so many members spend so much time solving puzzles” (quoted in Tammet, 2009: 40). If Mensa were anything but “members [who] spend so much time solving puzzles“, then I think Ware would have stated as much. While the other founder of Mensa—Ronald Berrill— “had intended Mensa as “an aristocracy of the intellect”, and was unhappy that a majority of Mensans came from humble homes” (the Wikipedia article on Mensa International cites Serebriakoff, 1986 as the reference for the quote).
So, when it comes to HISs, what do they bring to the world? Or is it just a dues-paid club so that the people on top can get money from people attempting to stroke their egos saying “Yea, I scored high on a test and am in a club!”
The supervisor of the Japanese Intelligence Network (JIN) writes (his emphasis):
Currently, the ESOTERIQ society has seven members and the EVANGELIQ has one member.
I can perfectly guarantee that the all members exactly certainly undoubtedly absolutely officially keep authentic the highest IQ score performances.
Especially, the EVANGELIQ is the most exclusive high IQ society which has at least one member.
Do you think the one member of EVANGELIQ talks to himself a lot? From the results of Karpinski et al (2018), I would hazard the guess that, yes, he does. Here is a list of 84 HISs, and there is an even more exclusive club than the Grail Society: the Terra Society (you need to score 205 on the test where the SD is 15 to join).
So is there a use for high IQ societies? I struggle to think of one. They seem to function as money-sinks—to sucker people into paying their dues just because they scored high on a test (with no validity). The fact that one of the founders of Mensa was upset that Mensa members spend so much time doing puzzles is very telling. What else do they do with their ‘talent’ other than solve puzzles all day? What has the Mensa group—and any of the other (quite possible, but 84 are linked above) hundreds of HISs—done for the world?
Adam—although he guessed at the end of the first Mensa exam (the Raven-like one)—got into Mensa due to his second Mensa test—the verbal one. Adam eventually retook the Mensa exam after taking his nootropic cocktails and he writes (2018: 207):
The second envelope from Mensa was waiting for me when I returned from work, poking out beneath a gas bill. I opened the gas bill first. Its numbers were higher than I expected. I hoped the same would be true of the letter that announced my new IQ.
It was. My cognitively enhanced score on the language test had crept up to 156, from 154 before. And on the Culture Fair Test [the Raven-like test], the tough one with the symbols, it had soared to 137, from 128. That put me on the ninety-ninth percentile on both.
My IQ as measured by the symbols test — the one I had tried to improve on using the brain stimulation — was now 135, up from 125, and well above the required threshold for Mensa Membership.
Adam used Modafinil (a drug used to treat sleeplessness due to narcolepsy, obstructive sleep apnea, and shift work sleep disorder) and electrical brain stimulation. So Adam increased his scores, but he—of course—has no idea what causes his score increases: the nootropic, the electrical stimulation, practice, already having an idea of what was on the test, etc.
In any case, that’s ancillary to the main discussion point in this article: What has Mensa—and other HISs—done for the world? Out of the hundreds of HISs in the world, have they done anything of note or are they just a club of people who score highly on a test who then have to pay money to be in the club? There is no value to these kinds of ‘societies’; they’re just a circlejerk for good test-takers. Mensans have a higher chance of having mental disorders, which is evidenced by the articles above by Jamie Loftus, where they threaten her life with their “criminal element”.
So, until I’m shown otherwise, Mensa and other HISs are just a circlejerk where people have to pay to be in the club—and that’s all it is.
A fallacy is an error in reasoning that makes an argument invalid. The “interactionism fallacy” is the fallacy—coined by Gottfredson (2009)—that since genes and environment interact, that heritability estimates are not useful—especially for humans (they are for nonhuman animals where environments can be fully controlled; see Schonemann, 1997; Moore and Shenk, 2016). There are many reasons why this ‘fallacy’ is anything but a fallacy; it is a simple truism: genes and environment (along with other developmental products) interact to ‘construct’ the organism (what Oyama, 2000 terms ‘constructive interactionism—“whereby each combination of genes and environmental influences simultaneously interacts to produce a unique result“). The causal parity thesis (CPT) is 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 (see Noble, 2012 for a similar approach). 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’.
Genes need the environment. Without the environment, genes would not be expressed. Behavior geneticists claim to be able to partition genes from environment—nature from nurture—on the basis of heritability estimates, mostly gleaned from twin and adoption studies. However, the method is flawed: since genes interact with the environment and other genes, how would it be possible to neatly partition the effects of genes from the effects of the environment? Behavior geneticists claim that we can partition these two variables. Behavior geneticists—and others—cite the “Interactionism fallacy”, the fallacy that since genes interact with the environment that heritability estimates are useless. This “fallacy”, though, confuses the issue.
Behavior geneticists claim to show how genes and the environment affect the ontogeny of traits in humans with twin and adoption studies (though these methods are highly flawed). The purpose of this “fallacy” is to disregard what developmental systems theorists claim about the interaction of nature and nurture—genes and environment.
Gottfredson (2009) coins the “interactionism fallacy”, which is “an irrelevant truth [which is] that an organism’s development requires genes and environment to act in concert” and the “two forces are … constantly interacting” whereas “Development is their mutual product.” Gottfredson also states that “heritability … refers to the percentage of variation in … the phenotype, which has been traced to genetic variation within a particular population.” (She also makes the false claim that “One’s genome is fixed at birth“; though this is false, see epigenetics/methylation studies.) Heritability estimates, according to Phillip Kitcher are “‘irrelevant’ and the fact that behavior geneticists persist
in using them is ‘an unfortunate tic from which they cannot free themselves’ (Kitcher,
2001: 413)” (quoted in Griffiths, 2002).
Gottfredson is engaging in developmental denialism. Developmental denialism “occurs when heritability is treated as a causal mechanism governing the developmental reoccurrence of traits across generations in individuals.” Gottfredson, with her “interactionism fallacy” is denying organismal development by attempting to partition genes from environment. As Rose (2006) notes, “Heritability estimates are attempts to impose a simplistic and reified dichotomy (nature/nurture) on non-dichotomous processes.” The nature vs nurture argument is over and neither has won—contra Plomin’s take—since they interact.
Gottfredson seems confused, since this point was debated by Plomin and Oyama back in the 80s (Plomin’s review of Oyama’s book The Ontogeny of Information; see Oyama, 1987, 1988; Plomin, 1988a, b). In any case, it is true that development requires genes to interact. But Gottfredson is talking about the concept of heritability—the attempt to partition genes and environment through twin, adoption and family studies (which have a whole slew of problems). For example, Moore and Shenk (2016: 6) write:
Heritability statistics do remain useful in some limited circumstances, including selective breeding programs in which developmental environments can be strictly controlled. But in environments that are not controlled, these statistics do not tell us much.
Susan Oyama writes in The Ontogeny of Information (2000, pg 67):
Heritability coefficients, in any case, because they refer not only to variation in genotype but to everything that varied (was passed on) with it, only beg the question of what is passed on in evolution. All too often heritability estimates obtained in one setting are used to infer something about an evolutionary process that occurred under conditions, and with respect to a gene pool, about which little is known. Nor do such estimates tell us anything about development.
Characters are produced by the interaction of nongenetic and genetic factors. The biological flaw, as Moore and Shenk note, throw a wrench into the claims of Gottfredson and other behavior geneticists. Phenotypes are ALWAYS due to genetic and nongenetic factors interacting. So the two flaws of heritability—the environmental and biological flaw (Moore and Shenk, 2016)—come together to “interact” to refute such simplistic claims that genes and environment—nature and nurture—can be separated.
For instance, as Moore (2016) writes, though “twin study methods are among the most powerful tools available to quantitative behavioral geneticists (i.e., the researchers who took up Galton’s goal of disentangling nature and nurture), they are not satisfactory tools for studying phenotype development because they do not actually explore biological processes.” (See also Richardson, 2012.) This is because twin studies ignore biological/developmental processes that lead to phenotypes.
Gamma and Rosenstock (2017) write that the concept of heritability that behavioral geneticists use is “is a generally useless quantity” while “the behavioral genetic dichotomy of genes vs environment is fundamentally misguided.” This brings us back to the CPT; there is causal parity to all processes/interactants that form the organism and its traits, thus the concept of heritability that behavioral geneticists employ is a useless measure. Oyama, Griffiths, and Gray (2001: 3) write:
These often overlooked similarities form part of the evidence for DST’s claim of causal parity between genes and other factors of development. The “parity thesis” (Griffiths and Knight 1998) does not imply that there is no difference between the particulars of the causal roles of genes and factors such as endosymbionts or imprinting events. It does assert that such differences do not justify building theories of development and evolution around a distinction between what genes do and what every other causal factor does.
Behavior geneticists’ endeavor, though, is futile. Aaron Panofsky (2016: 167) writes that “Heritability estimates do not help identify particular genes or ascertain their functions in development or physiology, and thus, by this way of thinking, they yield no causal information.” (Also see Panofsky, 2014; Misbehaving Science: Controversy and the Development of Behavior Genetics.) So, the behavioral genetic method of partitioning genes and environment does not—and can not—show causation for trait ontogeny.
Now, while people like Gottfredson and others may deny it, they are genetic determinists. Genetic determinism, as defined by Griffiths (2002) is “the idea that many significant human characteristics are rendered inevitable by the presence of certain genes.” Using this definition, many behavior geneticists and their sympathizers have argued that certain traits are “inevitable” due to the presence of certain genes. Genetic determinism is literally the idea that genes “determine” aspects of characters and traits, though it has been known for decades that it is false.
Now we can take a look at Brian Boutwell’s article Not Everything Is An Interaction. Boutwell writes:
Albert Einstein was a brilliant man. Whether his famous equation of E=mc2 means much to you or not, I think we can all concur on the intellectual prowess—and stunning hair—of Einstein. But where did his brilliance come from? Environment? Perhaps his parents fed him lots of fish (it’s supposed to be brain food, after all). Genetics? Surely Albert hit some sort of genetic lottery—oh that we should all be so lucky. Or does the answer reside in some combination of the two? How very enlightened: both genes and environment interact and intertwine to yield everything from the genius of Einstein to the comedic talent of Lewis Black. Surely, you cannot tease their impact apart; DNA and experience are hopelessly interlocked. Except, they’re not. Believing that they are is wrong; it’s a misleading mental shortcut that has largely sown confusion in the public about human development, and thus it needs to be retired.
Most traits are the product of genetic and environmental influence, but the fact that both genes and environment matter does not mean that they interact with one another. Don’t be lured by the appeal of “interactions.” Important as they might be from time to time, and from trait to trait, not everything is an interaction. In fact, many things likely are not.
I don’t even know where to begin here. Boutwell, like Gottfredson, is confused. The only thing that needs to be retired because it “has largely sown confusion in the public about human development” is, ironically, the concept of heritability (Moore and Shenk, 2016)! I have no idea why Boutwell claimed that it’s false that “DNA and experience [environment] are hopelessly interlocked.” This is because, as Schneider (2007) notes, “the very concept of a gene requires an environment.” Since the concept of the gene requires the environment, how can we disentangle them into neat percentages like behavior geneticists claim to do? That’s right: we can’t. Do be lured by the appeal of interactions; all biological and nonbiological stuff constantly interacts with one another.
Boutwell’s claims are nonsense. It would be worth it to quote Richard Lewontin’s forward in the 2000 2nd edition of Susan Oyama’s The Ontogeny of Information (emphasis Lewontin’s):
Nor can we partition variation quantitatively, ascribing some fraction of variation to genetic differences and the remainder to environmental variation. Every organism is the unique consequence of the reading of its DNA in some temporal sequence of environments and subject to random cellular events that arise because of the very small number of molecules in each cell. While we may calculate statistically an average difference between carriers of one genotype and another, such average differences are abstract constructs and must not be reified with separable concrete effects of genes in isolation from the environment in which the genes are read. In the first edition of The Ontogeny of Information Oyama characterized her construal of the causal relation between genes and environment as interactionist. That is, each unique combination of genes and environment produces a unique and a priori unpredictable outcome of development. The usual interactionist view is that there are separable genetic and environmental causes, but the effects of these causes acting in combination are unique to the particular combination. But this claim of ontogenetically independent status of the causes as causes, aside from their interaction in the effects produced, contradicts Oyama’s central analysis of the ontogeny of information. There are no “gene actions” outside environments, and no “environmental actions” can occur in the absence of genes. The very status of environment as a contributing cause to the nature of an organism depends on the existence of a developing organism. Without organisms there may be a physical world, but there are no environments. In like the manner no organisms exist in the abstract without environments, although there may be naked DNA molecules lying in the dust. Organisms are the nexus of external circumstances and DNA molecules that make these physical circumstances into causes of development in the first place. They become causes only at their nexus, and they cannot exist as causes except in their simultaneous action. That is the essence of Oyama’s claim that information comes into existence only in the process of ontogeny. (Oyama, 2000: 16)
There is an “interactionist consensus” (see Oyama, Griffiths, and Grey, 2001; What is Developmental Systems Theory? pg 1-13): the organism and the suite of traits it has is due to the interaction of genetic/environmental/epigenetic etc. resources at every stage of development. Therefore, for organismal development to be successful, it always requires the interaction of genes, environment, epigenetic processes, and interactions between everything that is used to ‘construct’ the organism and the traits it has. Thus “it makes no sense to ask if a particular trait is genetic or environmental in origin. Understanding how a trait develops is not a matter of finding out whether a particular gene or a particular environment causes the trait; rather, it is a matter of understanding how the various resources available in the production of the trait interact over time” (Kaplan, 2006).
Lastly, I will shortly comment on Sesardic’s (2005: chapter 2) critiques on developmental systems theorists and their critique of heritability and the concept of interactionism. Sesardic argues in the chapter that interaction between genes and environment, nature and nurture, does not undermine heritability estimates (the nature and nurture partition). Philosopher of science Helen Longino argues in her book Studying Human Behavior (2013):
By framing the debate in terms of nature versus nurture and as though one of these must be correct, Sesardic is committed to both downplaying the possible contributions of environmentally oriented research and to relying on a highly dubious (at any rate, nonmethodological) empirical claim.
In sum, the “interactionist fallacy” (coined by Gottfredson) is not a ‘fallacy’ (error in reasoning) at all. For, as Oyama writes in Evolution’s Eye: A Systems View of the Biology-Culture Divide “A not uncommon reaction to DST is, ‘‘That’s completely crazy, and besides, I already knew it” (pg 195). This is exactly what Gottfredson (2009) states, that she “already knew” that there is an interaction between nature and nurture; but she goes on to deny arguments from Oyama, Griffiths, Stotz, Moore, and others on the uselessness of heritability estimates along with the claim that nature and nurture cannot be neatly partitioned into percentages as they are constantly interacting. Causal parity between genes and other developmental resources, too, upends the claim that heritability estimates for any trait make sense (not least for how heritability estimates are gleaned for humans—mostly twin, family, and adoption studies). Developmental denialism—what Gottfredson and others often engage in—runs rampant in the “behavioral genetic” sphere; and Oyama, Griffiths, Stotz, and others show how we should not deny development and we should discard with these estimates for human traits.
Heritability estimates imply that there is a “nature vs nurture” when it is “nature and nurture” which are constantly interacting—and, due to this, we should discard with these estimates due to the interaction of numerous developmental resources; it does not make sense to partition an interacting, self-organizing developmental system. Claims from behavior geneticists—that genes and environment can be separated—are clearly false.
Five years away is always five years away. When one makes such a claim, they can always fall back on the “just wait five more years!” canard. Charles Murray is one who makes such claims. In an interview with the editor of Skeptic Magazine, Murray stated to Frank Miele:
I have confidence that in five years from now, and thereafter, this book will be seen as a major accomplishment.
This interview was in 1996 (after the release of the soft cover edition of The Bell Curve), and so “five years” would be 2001. But “predictions” such as this from HBDers (that the next big thing for their ideology, for example) is only X years away happens a lot. I’ve seen many HBDers make claims that only in 5 to 10 years the evidence for their position will come out. Such claims seem strangely religious to me. There is a reason for that. (See Conley and Domingue, 2016 for a molecular genetic refutation of The Bell Curve. While Murray’s prediction failed, 22 years after The Bell Curve’s publication, the claims of Murray and Herrnstein were refuted.)
Numerous people throughout history have made predictions regarding the date of Christ’s return. Some have used calculations to ascertain the date of Christ’s return, from the Bible. We can just take a look at the Wikipedia page for predictions and claims for the second coming of Christ where there are many (obviously failed) predictions of His return.
Take John Wesley’s claim that Revelations 12:14 referred to the day that Christ should come. Or one of Charles Taze Russell’s (the first president of the Watch Tower Society of Jehova’s Witnesses) claim that Jesus would return in 1874 and be ruling invisibly from heaven.
Russell’s beliefs began with Adventist teachings. While Russell, at first, did not take to the claim that Christ’s return could be predicted, that changed when he met Adventist author Nelson Barbour. The Adventists taught that the End Times began in 1799, Christ returned invisibly in 1874 with a physical return in 1878. (When this did not come to pass, many followers left Barbour and Russell states that Barbour did not get the event wrong, he just got the fate wrong.) So all Christians that died before 1874 would be resurrected, and Armageddon would begin in 1914. Since WWI began in 1914, Russell took that as evidence that his prediction was coming to pass. So Russell sold his clothing stores, worth millions of dollars today, and began writing and preaching about Christ’s imminent refuted. This doesn’t need to be said, but the predictions obviously failed.
So the date of 1914 for Armageddon (when Christ is supposed to return), was come to by Russell from studying the Bible and the great pyramids:
A key component to the calculation was derived from the book of Daniel, Chapter 4. The book refers to “seven times“. He interpreted each “time” as equal to 360 days, giving a total of 2,520 days. He further interpreted this as representing exactly 2,520 years, measured from the starting date of 607 BCE. This resulted in the year 1914-OCT being the target date for the Millennium.
Here is the prediction in Russell’s words “…we consider it an established truth that the final end of the kingdoms of this world, and the full establishment of the Kingdom of God, will be accomplished by the end of A.D. 1914” (1889). When 1914 came and went (sans the beginning of WWI which he took to be a sign of the, End Times), Russell changed his view.
Now, we can liken the Russell situation to Murray. Murray claimed that in 5 years after his book’s publication, that the “book would be seen as a major accomplishment.” Murray also made a similar claim back in 2016. Someone wrote to evolutionary biologist Joseph Graves about a talk Murray gave; he was offered an opportunity to debate Graves about his claims. Graves stated (my emphasis):
After his talk I offered him an opportunity to debate me on his claims at/in any venue of his choosing. He refused again, stating he would agree after another five years. The five years are in the hope of the appearance of better genomic studies to buttress his claims. In my talk I pointed out the utter weakness of the current genomic studies of intelligence and any attempt to associate racial differences in measured intelligence to genomic variants.
(Do note that this was back in April of 2016, about one year before I changed my hereditarian views to that of DST. I emailed Murray about this, he responded to me, and gave me permission to post his reply which you can read at the above link.)
Emil Kirkegaard stated on Twitter:
Do you wanna bet that future genomics studies will vindicate us? Ashkenazim intelligence is higher for mostly genetic reasons. Probably someone will publish mixed-ethnic GWAS for EA/IQ within a few years
Notice, though “within a few years” is vague; though I would take that to be, as Kirkegaard states next, three years. Kirkegaard was much more specific for PGS (polygenic scores) and Ashkenazi Jews, stating that “causal variant polygenic scores will show alignment with phenotypic gaps for IQ eg in 3 years time.” I’ll remember this; January 6th, 2022. (Though it was just an “example given”, this is a good example of a prediction from an HBDer.) Nevermind the problems with PGS/GWA studies (Richardson, 2017; Janssens and Joyner, 2019; Richardson and Jones, 2019).
I can see a prediction being made, it not coming to pass, and, just like Russel, one stating “No!! X, Y, and Z happened so that invalidated the prediction! The new one is X time away!” Being vague about timetables about as-of-yet-to-occur events it dishonest; stick to the claim, and if it does not occur….stop holding the view, just as Russel did. However, people like Murray won’t change their views; they’re too entrenched in this. Most may know that I over two years ago I changed my views on hereditarianism (which “is the doctrine or school of thought that heredity plays a significant role in determining human nature and character traits, such as intelligence and personality“) due to two books: DNA Is Not Destiny: The Remarkable, Completely Misunderstood Relationship between You and Your Genes and Genes, Brains, and Human Potential: The Science and Ideology of Intelligence. But I may just be a special case here.
Genes, Brains, and Human Potential then led me to the work of Jablonka and Lamb, Denis Noble, David Moore, Robert Lickliter, and others—the developmental systems theorists. DST is completely at-ends with the main “field” of “HBD”: behavioral genetics. See Griffiths and Tabery (2013) for why teasing apart genes and environment—nature and nurture—is problematic.
In any case, five years away is always five years away, especially with HBDers. That magic evidence is always “right around the corner”, despite the fact that none ever comes. I know that some HBDers will probably clamor that I’m wrong and that Murray or another “HBDer” has made a successful prediction and not immediately change the date of said prediction. But, just like Charles Taze Russell, when the prediction does not come to pass, just make something up about how and why the prediction didn’t come to pass and everything should be fine.
I think Charles Murray should change his name to Charles Taze Russel, since he pushed back the date of the prediction so many times. Though, to Russel’s credit, he did eventually recant on his views. I would find it hard to believe that Murray would; he’s too deep in this game and his career writing books and being an AEI pundit is on the line.
So I strongly doubt that Murray would ever come outright and say “I was wrong.” Too much money is on the line for him. (Note that Murray has a new book releasing in January titled Human Diversity: Gender, Race, Class, and Genes and you know that I will give a scathing review of it, since I already know Murray’s MO.) It’s ironic to me: Most HBDers are pretty religious in their convictions and can and will explain away data that doesn’t line up with their beliefs, just like a theist.
The claim that “Men are stronger than women” does not need to be said—it is obvious through observation that men are stronger than women. To my (non-)surprise, I saw someone on Twitter state:
“I keep hearing that the sex basis of patriarchy is inevitable because men are (on average) stronger. Notwithstanding that part of this literally results from women in all stages of life being denied access to and discourage from physical activity, there’s other stuff to note.”
To which I replied:
“I don’t follow – are you claiming that if women were encouraged to be physically active that women (the population) can be anywhere *near* men’s (the population) strength level?”
I then got told to “Fuck off,” because I’m a “racist” (due to the handle I use and my views on the reality of race). In any case, while it is true that part of this difference does, in part, stem from cultural differences (think of women wanting the “toned” look and not wanting to get “big and bulky”—as if it happens overnight) and not wanting to lift heavy weights because they think they will become cartoonish.
Here’s the thing though: Men have about 61 percent more muscle mass than women (which is attributed to higher levels of testosterone); most of the muscle mass difference is allocated to the upper body—men have about 75 percent more arm muscle mass than women which accounts for 90 percent greater upper body strength in men. Men also have about 50 percent more muscle mass than women, while this higher percentage of muscle mass is then related to men’s 65 percent greater lower body strength (see references in Lassek and Gaulin, 2009: 322).
Men have around 24 pounds of skeletal muscle mass compared to women, though in this study, women were about 40 percent weaker in the upper body and 33 percent weaker in the lower body (Janssen et al, 2000). Miller et al (1993) found that women had a 45 percent smaller cross-section area in the brachii, 45 in the elbow flexion, 30 percent in the vastus lateralis, and 25 percent smaller CSA in the knee extensors, as I wrote in Muscular Strength by Gender and Race, where I concluded:
The cause for less upper-body strength in women is due the distribution of women’s lean tissue being smaller.
Men have larger fibers, which in my opinion is a large part of the reason for men’s strength advantage over women. Now, even if women were “discouraged” from physical activity, this would be a problem for their bone density. Our bones are porous, and so, by doing a lot of activity, we can strengthen our bones (see e.g., Fausto-Sterling, 2005). Bishop, Cureton, and Collins (1987) show that the sex difference in strength in close-to-equally-trained men and women “is almost entirely accounted for by the difference in muscle size.” Which lends credence to my claim I made above.
Lindle et al (1997) conclude that:
… the results of this study indicate that Con strength levels begin to decline in the fourth rather than in the fifth decade, as was previously reported. Contrary to previous reports, there is no preservation of Ecc compared with Con strength in men or women with advancing age. Nevertheless, the decline in Ecc strength with age appears to start later in women than in men and later than Con strength did in both sexes. In a small subgroup of subjects, there appears to be a greater ability to store and utilize elastic energy in older women. This finding needs to be confirmed by using a larger sample size. Muscle quality declines with age in both men and women when Con peak torque is used, but declines only in men when Ecc peak torque is used. [“Con” and “Ecc” strength refer to concentric and eccentric actions]
Women are shorter than men and have less fat-free muscle mass than men. Women also have a weaker grip (even when matched for height and weight, men had higher levels of lean mass compared to women (92 and 79 percent respectively; Nieves et al, 2009). So men had greater bone mineral density (BMD) and bone mineral content (BMC) compared to women. Now do some quick thinking—do you think that one with weaker bones could be stronger than someone with stronger bones? If person A had higher levels of BMC and BMD compared to person B, who do you think would be stronger and have the ability to do whatever strength test the best—the one with the weaker or stronger muscles? Quite obviously, the stronger one’s bones are the more weight they can bare on them. So if one has weak bones (low BMC/BMD) and they put a heavy load on their back, while they’re doing the lift their bones could snap.
Alswat (2017) reviewed the literature on bone density between men and women and found that men had higher BMD in the hip and higher BMC in the lower spine. Women also had bone fractures earlier than men. Some of this is no doubt cultural, as explained above. However, even if we had a boy and a girl locked in a room for their whole lives and they did the same exact things, ate the same food, and lifted the same weights, I would bet my freedom that there still would be a large difference between the two, skewing where we know it would skew. Women are more likely to suffer from osteoporosis than are men (Sözen, Özışık, and Başaran 2016).
So if women have weaker bones compared to men, then how could they possibly be stronger? Even if men and women had the same kind of physical activity down to the tee, could you imagine women being stronger than men? I couldn’t—but that’s because I have more than a basic understanding of anatomy and physiology and what that means for differences in strength—or running—between men and women.
I don’t doubt that there are cultural reasons that account for the large differences in strength between men and women—I do doubt, though, that the gap can be meaningfully closed. Yes, biology interacts with culture. So the developmental variables that coalesce to make men “Men” and those that coalesce to make women “Women” converge in creating the stark differences in phenotype between the sexes which then explains how the sex differences between the sexes manifest itself.
Differences in bone strength between men and women, along with distribution of lean tissue, differences in lean mass, and differences in muscle size explain the disparity in muscular strength between men and women. You can even imagine a man and woman of similar height and weight and they would, of course, look different. This is due to differences in hormones—the two main players being testosterone and estrogen (see Lang, 2011).
So yes, part of the difference in strength between men and women are rooted in culture and how we view women who strength train (way more women should strength train, as a matter of fact), though I find it hard to believe that even if the “cultural stigma” of the women who lifts heavy weights at the gym disappeared overnight, that women would be stronger than men. Differences in strength exist between men and women and this difference exists due to the complex relationship between biology and culture—nature and nurture (which cannot be disentangled).