I was alerted to an article on the website (Ir)”RationalWiki” which in their own words “critique[s] and challenge[s] pseudoscience and the anti-science movement, explore[s] authoritarianism and fundamentalism, and analyze[s] how these subjects are handled in the media.” Unfortunately, it seems like the one who wrote this article (and is still adding to it) just selectively read certain articles and quote mined them.
The article on this website about me is an unfair mischaracterization of my views. Quotes will follow from the article with my comments.
In the opening paragraph they write:
NotPoliticallyCorrect is an Alt-right blog that promotes racialist pseudoscience and white nationalism; the owner posts as RaceRealist using the euphemism “racial realist” coined by the white supremacist J. P. Rushton who is extensively quoted on the blog.
- I’m not alt-right nor am I a white nationalist.
- I don’t promote ‘racialist pseudoscience’ nor do I promote ‘white nationalism’.
- Correct, Rushton did coin the term ‘race realist’, but he was not a ‘white supremacist’.
They continue, quoting an article of mine that I wrote almost two years ago titled Non-Western People are Abnormal to Our Society. I still stand by everything that I wrote in that article.
A racist crank obsessed with controversial topics such as race and IQ and eugenics, RaceRealist argues in a 2016 blog essay “Non-Western People are Abnormal to Our [Western] Societies” and its comments that “MENA” and “SSA’s” (i.e. people from the Middle-East, North Africa and Sub-Saharan Africa) as well as other non-Westerners are somehow abnormal to the US and Europe:
They then quote me:
MENA and SSA people are abnormal to Western societies. It’s clear that, on average, full-on acclimation is not possible.
One only needs to look at what is occurring in Western European countries to see that, on average, this is true.
In the same essay, RaceRealist goes on to post crude racism, such as “Negros” are biologically inferior:
Quoting me writing:
The same can be said for Negros[sic] in America as well. They are deviant, dysfunctional, they cause distress in our country and finally, they pose a danger to us, our families and societies as a whole. Just like those immigrants we have come into our countries who cannot assimilate because it’s not in their biology.
Except everything I wrote here was logically sound (last sentence notwithstanding). Look at the 4 d’s of abnormal psychology (which is the next quote they provide):
The “4 d’s of abnormality” and how they relate to our culture and the current culture/biology of those non-Western immigrants coming into our country is extremely telling. It’s clear that those people cannot assimilate into our societies because of differing biology and differing locations in which they evolved in. We chose our environments based on our biology. Environment increasingly depends on their genes, rather than being the cause of their exogenous behavior.
The 4 d’s of abnormality are deviance, dysfunction, distress and danger. Everything I wrote and then provided examples for in regards to the 4 d’s of abnormality are sound.
You can read my article Diversity in the Social Context for more evidence for this argument.
They then quote my article The Evolution of Jewish Nepotism writing:
RaceRealist is an anti-Semite who dislikes Ashkenazi Jews, accusing them of “derogating other ethnicities”; when discussing Ashkenazi Jews, he bizarrely maintains their higher average IQ is partly a product of “breeding with beautiful Roman women a few thousand years ago”, for which there exists no evidence.
I admit it is conjecture. Evidence exists for Jewish men migrating to Rome to mate with Roman women (Atzmon et al, 2010). I never stated that I ‘dislike Ashkenazi Jews’. In regards to the derogation, it’s true. Close-knit ethnic groups derogate the out-group (Sampasivam et al, 2016). Further, oxytocin promotes human ethnocentrism, which caused in-group favoritism and out-group derogation (Drew et al, 2010). In-groups derogate out-groups. Read the literature.
And the final thing the page shows is my tweet saying that “I finally made it on (Ir)”RationalWiki””:
to which they wrote:
Just because I have the numbers “88” in my handle doesn’t make me “alt-right” nor does it make me a “white nationalist.” I thought about changing it, then I realized that it’s good to weed out the people who aren’t serious about discussion and just look for things to discredit people that are meaningless to the conversation at hand. It tells you a lot about someone when they bring up irrelevant things. I’m not a white nationalist, nor am I an alt-righter. Just because I write about politics rarely and use them as an example (like in my article The Rise of Ethnocentrism and the Alt-Right: The Rebirth of Selfish Genes which I also disavow now that I realize that ‘selfish genes’ are a metaphor; Noble, 2011; Noble, 2013; Noble et al, 2014).
Take a look at the tags it tagged the article with: “Alt-righters, Pseudoscience, Racists, Internet kooks, Psuedoscience promoters, Alt-right, Internet Hate Sites.” Not an alrighter, I don’t push psuedoscience, I’m not a ‘racist’ (whatever that means). If you don’t like what I write, respond to any article you disagree with and explain why with logical, rational arguments. This piece is garbage and mischaracterizes my views using selective quotations (which, even then, failed to prove their point. No, numbers after a username are not evidence).
All in all, this article is garbage. It says that Rushton is ‘extensively quoted’, which is true for what I wrote in the beginning of this blog’s history, but not so for the past, say, 18 months. Rushton has been the target of my attacks on penis size, testosterone, and my personal favorite, r/K selection theory. But sure, go and dig in the archives for old articles to quote mine. This article written about me is dumb, doesn’t characterize my views correctly (calls me a ‘white nationalist’ and ‘alt-righter’). Selectively quote certain articles, assert that Rushton is ‘extensively quoted’ when I hardly discuss him anymore and when I do it’s about testosterone/to rebut him. (Ir)RationalWiki should think about reading a bit of my blog before characterizing me as something I’m not.
For the record, I don’t care about politics. I am not alt-right. I am not a white nationalist. I’m not an anti-semite. This will be updated to cover whatever else they decide to write about me. Hopefully it’s at least a bit closer to reality next time, because this article sucks.
Black-white differences in physiology can tell a lot about how the two groups have evolved over time. On traits like resting metabolic rate (RMR), basal metabolic rate (BMR), adiposity, heart rate, Vo2 max, etc. These differences in physiological variables between groups, then, explain part of the reason why there are different outcomes in terms of life quality/mortality between the two groups.
Right away, by looking at the average black and average white, you can see that there are differences in somatype. So if there are differences in somatype, then there must be differences in physiological variables, and so, this may be a part of the cause of, say, differing obesity rates between black and white women (Albu et al, 1997) and even PCOS (Wang and Alvero, 2013).
Resting metabolic rate
Resting metabolic rate is your body’s metabolism at rest, and is the largest component of the daily energy budget in modern human societies (Speakman and Selman, 2003). So if two groups, on average, differ in RMR, then one with the lower RMR may have a higher risk of obesity than the group with the higher RMR. And this is what we see.
Black women do, without a shadow of a doubt, have a lower BMR, lower PAEE (physical activity energy expenditure) and TDEE (total daily expenditure) (Gannon, DiPietro, and Poehlman, 2000). Knowing this, then it is not surprising to learn that black women are also the most obese demographic in the United States. This could partly explain why black women have such a hard time losing weight. Metabolic differences between ethnic groups in America—despite living in similar environments—show that a genetic component is responsible for this.
There are even predictors of obesity in post-menopausal black and white women (Nicklas et al, 1999). They controlled for age, body weight and body composition (variables that would influence the results—no one tell me that “They shouldn’t have controlled for those because it’s a racial confound!”) and found that despite having a similar waist-to-hip ratio (WHR) and subcutaneous fat area, black women had lower visceral fat than white women, while fasting glucose, insulin levels, and resting blood pressure did not differ between the groups. White women also had a higher Vo2 max, which remained when lean mass was controlled for. White women could also oxidize fat at a higher rate than black women (15.4 g/day, which is 17% higher than black women). When this is expressed as percent of total kcal burned in a resting state, white women burned more fat than black women (50% vs 43%). I will cover the cause for this later in the article (one physiologic variable is a large cause of these differences).
We even see this in black American men with more African ancestry—they’re less likely to be obese (Klimentidis et al 2016). This, too, goes back to metabolic rate. Black American men have lower levels of body fat than white men (Vickery et al, 1988; Wagner and Heyward, 2000). All in all, there are specific genetic variants and physiologic effects, which cause West African men to have lower central (abdominal) adiposity than European men and black women who live in the same environment as black men—implying that genetic and physiologic differences between the sexes are the cause for this disparity. Whatever the case may be, it’s interesting and more studies need to be taken out so we can see how whatever gene variants are *identified* as protecting against central adiposity work in concert with the system to produce the protective effect. Black American men have lower body fat, therefore they would have, in theory, a higher metabolic rate and be less likely to be obese—while black women have the reverse compared to white women—a lower metabolic rate.
Skeletal muscle fiber
Skeletal muscle fibers are the how and why of black domination in explosive sports. This is something I’ve covered in depth. Type II fibers contract faster than type I. This has important implications for certain diseases that black men are more susceptible to. Though the continuous contraction of the fibers during physical activity leads to a higher disease susceptibility in black men—but not white men (Tanner et al, 2001). If you’re aware of fiber type differences between the races (Ama et al, 1986; Entine, 2000; Caeser and Henry, 2015); though see Kerr (2010’s) article The Myth of Racial Superiority in Sports for another view. That will be covered here in the future.
Nevertheless, fiber typing explains racial differences in sports, with somatype being another important variable in explaining racial disparities in sports. Two main variables that work in concert are the somatype (pretty much body measurements, length) and the fiber type. This explains why blacks dominate baseball and football; this explains why ‘white men can’t jump and black men can’t swim’. Physiological variables—not only ‘motivation’ or whatever else people who deny these innate differences say—largely explain why there are huge disparities in these sports. Physiology is important to our understanding of how and why certain groups dominate certain sports.
This is further compounded by differing African ethnies excelling in different running sports depending on where their ancestors evolved. Kenyans have an abundance of type I fibers whereas West Africans have an abundance of type II fibers. (Genetically speaking, ‘Jamaicans’ don’t exist; genetic testing shows them to come from a few different West African countries.) Lower body symmetry—knees and ankles—show that they’re more symmetrical than age-matched controls (Trivers et al, 2014). This also goes to show that you can’t teach speed (Lombardo and Deander, 2014). Though, of course, training and the will to want to do your best matter as well—you just cannot excel in these competitions without first and foremost having the right physiologic and genetic make-up.
Further, although it’s only one gene variant, ACTN3 and ACE explain a substantial percentage of sprint time variance, which could be the difference between breaking a world record and making a final (Papadimitriou et al, 2016). So, clearly, certain genetic variants matter more than others—and the two best studied are ACTN3 and ACE. Some authors, though, may deny the contribution of ACTN3 to elite athletic performance—like one researcher who has written numerous papers on ACTN3, Daniel MacArthur. However, elite sprinters are more likely to carry the RR ACTN3 genotype compared to the XX ACTN3 genotype, and the RR ACTN3 genotype—when combined with type II fibers and morphology—lead to increased athletic performance (Broos et al, 2016). It’s also worth noting that 2 percent of Jamaicans carry the XX ACTN3 genotype (Scott et al, 2010), so this is another well-studied variable that lends to superior running performance in Jamaicans.
In regards to Kenyans, of course when you are talking about genetic reasons for performance, some people don’t like it. Some may say that certain countries dominate in X, and that for instance, North Africa is starting to churn out elite athletes, should we begin looking for genetic advantages that they possess (Hamilton, 2000)? Though people like Hamilton are a minority view in this field, I have read a few papers that there is no evidence that Kenyans possess a pulmonary system that infers a physiologic advantage over whites (Larsen and Sheel, 2015).
People like these three authors, however, are in the minority here and there is a robust amount of research that attests to East African running dominance being genetic/physiologic in nature—though you can’t discredit SES and other motivating variables (Tucker, Onywera, and Santos-Concejero, 2015). Of course, a complex interaction between SES, genes, and environment are the cause of the success of the Kalenjin people of Kenya, because they live and train in such high altitudes (Larsen, 2003), though the venerable Bengt Saltin states that the higher Vo2 max in Kenyan boys is due to higher physical activity during childhood (Saltin et al, 1995).
The last variable I will focus on (I will cover more in the future) is blood pressure. It’s well known that blacks have higher blood pressure than whites—with black women having a higher BP than all groups—which then leads to other health implications. Some reasons for the cause are high sodium intake in blacks (Jones and Hall, 2006); salt (Lackland, 2014; blacks had a similar sensitivity than whites, but had a higher blood pressure increase); while race and ethnicity was a single independent predictor of hypertension (Holmes et al, 2013). Put simply, when it comes to BP, ethnicity matters (Lane and Lip, 2001).
While genetic factors are important in showing how and why certain ethnies have higher BP than others, social factors are arguably more important (Williams, 1992). He cites stress, socioecologic stress, social support, coping patterns, health behavior, sodium, calcium, and potassium consumption, alcohol consumption, and obesity. SES factors, of course, lead to higher rates of obesity (Sobal and Stunkard, 1989; Franklin et al, 2015). So, of course, environmental/social factors have an effect on BP—no matter if the discrimination or whatnot is imagined by the one who is supposedly discriminated against, this still causes physiologic changes in the body which then lead to higher rates of BP in certain populations.
Poverty does affect a whole slew of variables, but what I’m worried about here is its effect on blood pressure. People who are in poverty can only afford certain foods, which would then cause certain physiologic variables to increase, exacerbating the problem (Gupta, de Wit, and McKeown, 2007). Whereas diets high in protein predicted lower BP in adults (Beundia et al, 2015). So this is good evidence that the diets of blacks in America do increase BP, since they eat high amounts of salt, low protein and high carb diets.
Still, others argue that differences in BP between blacks and whites may not be explained by ancestry, but by differences in education, rather than genetic factors (Non, Gravlee, and Mulligan, 2012). Their study suggests that educating black Americans on the dangers and preventative measures of high BP will reduce BP disparities between the races. This is in-line with Williams (1992) in that the social environment is the cause for the higher rates of BP. One hypothesis explored to explain why this effect with education was greater in blacks than whites was that BP-related factors, such as stress, poverty and racial discrimination (remember, even if no racial discrimination occurs, any so-called discrimination is in the eye of the beholder so that will contribute to a rise in physiologic variables) and maybe social isolation may be causes for this phenomenon. Future studies also must show how higher education causes lower BP, or if it only serves as other markers for the social environment. Nevertheless, this is an important study in our understanding of how and why the races differ in BP and it will go far to increase our understanding of this malady.
This is not an exhaustive list—I could continue writing about other variables—but these three are some of the most important as they are a cause for higher mortality rates in America. Understanding the hows and whys of these variables will have us better equipped to help those who suffer from diseases brought on by these differences in physiological factors.
The cause for some of these physiologic differences come down to evolution, but still others may come down to the immediate obesogenic environment (Lake and Townshend, 2006) which is compounded by lower SES. Since high carbs diets increase BP, this explains part of the reason why blacks have higher BP, along with social and genetic factors. Muscle fiber typing is set by the second trimester, and no change is seen after age 6 (Bell, 1980). Resting metabolic rate gap differences between black and white women can be closed, but not completely, if black women were to engage in exercise that use their higher amounts of type II muscle fibers (Tanner et al, 2001). This research is important to understand differences in racial mortality; because when we understand them then we can begin to theorize on how and why we see these disparities.
Physiologic differences between the races are interesting, they’re easily measurable and they explain both disparities in sports and mortality by different diseases. Once we study these variables more, we will be better able to help people with these variables—race be dammed. Race is a predictor here, only because race is correlated with other variables that lead to negative health outcomes. So once we understand how and why these differences occur, then we can help others with similar problems—no matter their race.
Do you need to look at genetic differences between races to see if race is real? Some may argue that you do, and when you do you’ll see that genetic variation is too small to say that race exists. However, other arguments exist that do not look at genetic differences between races, but look at geographic ancestry, reproductive isolation between races, and morphologic differences. Those three variables are enough to prove the existence of race without looking at genetic differences between races. They do correspond to genetic differences between races. The four concepts I will briefly lay out are from Michael Hardimon, professor of philosophy at University of California, San Diego. The concepts are the racialist concept of race, minimalist concept of race concept, populationist concept of race, and the socialrace concept of race. One doesn’t need to look at the racialist concept of race to prove the existence of race, which I will prove below.
Michael Hardimon published Rethinking Race: The Case for Deflationary Realism earlier this year. In the book, he makes the case that race exists if minimalist race exists (I will get into what minimalist race entails below). Nevertheless, race deniers will say that even by looking at variables such as morphology, reproductive isolation, and geographic ancestry, race as a concept is scientifically invalid. This is patently false.
Concepts of race
The racialist concept of race
Hardimon’s first race concept is the racialist concept. The racialist concept (keep in mind, this is, as Hardimon writes on page 17 of his book Rethinking Race “the specific concept I have dubbed “the racialist concept” which “is hierarchal“) as defined by Hardimon holds that “racialist race is the idea of a fundamental division between groups and individuals” (Hardimon, 2017: 17). I think that Hardimon strawmans the racialist concept as he as defined it, but that’s for another day.
He also says that the racialist concept “is closely associated with racism” while the terms racialism and racism are “sometimes used interchangeably” (Hardimon, 2017: 17).
His argument against the racialist concept of race (as he defines it) is as follows (Hardimon, 2017: 21):
A third line of argument starts from the idea that in order for racialist races to exist, certain things must be true of human genetics, namely the following:
(a) The fraction of human genetic diversity between populations must exceed the fraction of diversity between them.
(b) The fraction of human genetic diversity within populations must be small.
(c) The fraction of diversity between populations must be large.
(d) Most genes must be highly differentiated by race.
(e) The variation in genes that underlie obvious physical differences must be typical of the genome in general.
(f) There must be several important genetic differences between races apart from the genetic differences that underlie obvious physical differences.
Note: (b) says that racialist races are genetically racially homogeneous groups; (c)-(f) say that racialist races are distinguised by major biological differences.
Call (a)-(f) the racialist concept of race’s genetic profile.
Now that his argument against the racialist concept (as he defines it) is laid out, you can see why I said that I think he strawmans the racialist concept. But I’ll get into that another day.
He then cites Lewontin’s (1972) analysis of blood groups by race as evidence against the racialist concept. Lewontin found that 85.4 percent of total human variation fell within populations. He also found that populations that populations classically defined as human races (Caucasians, Africans, Mongoloids, South Asian Aborigines, American Indians, and Oceanians) accounted for 8.3 percent of total human variation. Total variation between the classically defined races accounted for 6.3 percent of the variance.
It’s worth noting that the numbers given by Lewontin are true; where he goes wrong is assuming that there is no taxonomic significance for race based on the data he got from his analysis. “Call this Lewontin’s cleaver,” writes Hardimon on page 22.
Then in 2002, 31 years after Lewontin published his analysis, A.W.F. Edwards published his paper Human Genetic Diversity: Lewontin’s Fallacy. (Edwards, 2003). In the paper, Edwards argues that Lewontin’s conclusion is incorrect. Edwards (2003: 800-801) writes in his conclusion (emphasis mine):
There is nothing wrong with Lewontin’s statistical analysis of variation, only with the belief that it is relevant to classification. It is not true that ‘‘racial classification is … of virtually no genetic or taxonomic significance’’. It is not true, as Nature claimed, that ‘‘two random individuals from any one group are almost as different as any two random individuals from the entire world’’, and it is not true, as the New Scientist claimed, that ‘‘two individuals are different because they are individuals, not because they belong to different races’’ and that ‘‘you can’t predict someone’s race by their genes’’. Such statements might only be true if all the characters studied were independent, which they are not.
Of course, Lewontin’s conclusion is fallacious because small genetic differences do not entail that racial classification that race has no taxonomic significance (Richard Dawkins accepts the taxonomic existence of race). As you can see from the quote from Edwards, he does not object to Lewontin’s analysis of the races, he objects to his conclusion—namely that races do not exist based on the within-race variation being greater than between-race variation.
On page 22-23, Hardimon writes about Edwards’ objection to Lewontin’s conclusion:
Lewontin’s locus-by-locus analysis (which does not consider the possibility of a correlation between individual loci) does not preclude the possibility that individual loci might be correlated in such a way that people could be grouped into traditional racial categories. The underlying thought is that racial classification would have “taxonomic significance” were it possible to group people into traditional racial categories by making use of correlations between individual loci. However, Lewontin’s argument that there are no racialist races because the component of within-race genetic variation is larger than the component of between-race variation is untouched by Edwards’s objection.
In 2002, Rosenberg et al, in their paper Genetic Structure of Human Populations confirmed Lewontin’s analysis. They looked at 377 autosomal loci in 1,056 individuals from 52 populations and found that within-population differences between major groups (Africa, Europe, Asia, the Middle East, Central and South Asia, East Asia, Oceania, and America) accounted for 3-5 percent of genetic variation while genetic differences between individuals accounted for 93-95 percent of genetic variation. So Rosenberg et al (2002) confirmed Lewontin’s (1972) analysis—though do recall that Lewontin’s conclusion is incorrect. According to Hardimon’s interpretation of the racialist concept of race, both Lewontin’s and Rosenberg et al’s analysis disprove the racialist concept of race, but that doesn’t mean that there is no scientific basis for the biological reality of race (Hardimon, 2012).
The minimalist concept of race
The minimalist concept of race is similar to the racialist concept, though there are some stark differences. It does not say that there are intrinsic differences between races—call them essences if you will), but it does say that you can distinguish races by patterns of different physical features such as skin color, hair type, nose shape, morphology, etc, which then correspond to differences in geographic ancestry in geographically, genetically isolated breeding populations.
The minimalist concept of race further states that (i) races are distinguised from other races by patterns of visible physical features; (ii) the members are linked by a common ancestry which is peculiar to members of the group; and (iii) this group must originate from a distinct location.
The minimalist concept of race does not require: that the fraction of human genetic diversity between minimalist races is larger than the fraction of diversity within them; it is compatible with within-race diversity being large and between-race diversity being small; it does not require most genes to be highly differentiated by race; it does not require the existence of a lot genetic differences between races that underlie more than the phenotypic differences already noticed; the concept does not imply that there can be predictions made from yet unstudied characteristics; it finally does not require any genetic differences between races other than those found in the genes that underlie differences in physical appearance between race. This is called the minimalist concept of biological race (Hardimon, 2017: 66) and it survives all objections from Lewontin’s and Rosenberg et al’s analysis of between-race genetic variation.
This is my favorite race concept, personally, because it covers any and all objections from the race-denialist crowd—people who deny any genetic differences between races—because the only genetic differences it counts on are those physical traits that are already noticed.
Hardimon (2017: 29) writes:
Such readers should feel free to regard the minimalist concept of race, that is, as a concept that, though in many respects similar to the ordinary concept, is nonetheless distinct from it. What I would insist on is that minimalist races (groups satisfying the minimalist concept of race) are *races* (that is races so properly called)—either because the minimalist concept of race just is the ordinary concept of race or because it captures enough of the ordinary concept of race for minimalist races to be counted as races. My view is that if it can be shown that minimalist races exist, races exist. And if it can be shown that *minimalist race* is real, race is real.
The populatonist concept of race
The populationist concept of race is a nonessentialist, non-hierarchical concept of race that slightly differs from the minimalist concept of race. The populationist concept of race can be said to be a scientific concept of race (as can the minimalist concept) because it characterizes races as groups belonging to different groups of biological descent, they are distinguished by patterns of phenotypic differences, and these phenotypic differences trace back to geographically separated and genetically isolated founding populations.
The populationist concept of race also holds that “A race is a subdivision of Homo sapiens—a group or population that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographical ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population” (Hardimon, 2017: 99). So with these criteria, you can see that even if you do not accept the racialist concept of race (as Hardimon defines it), you can still be a race realist. The populationist concept is likely to exist, and if the populationist concept of race exists then race is real.
Defining race as geographically and reproductively isolated breeding populations that share a common line of biological descent with similar phenotypic characters is as barebones a concept of race as you can get—and it is perfectly in line with how most people view races on the basis of phenotypic characterization. The populationist concept of race supposes that numerous concepts from the racialist concept of race are true—but do not presuppose any to-be-studied differences between those races. The strength of the populationist argument, as you can see, is very strong and it holds up to numerous lines of criticism very well. Although both the populationist and minimalist race concepts do not presupposed any to-be-studied differences between races, this still is not good enough for race deniers.
It is clear that without even looking at the brain and physiological differences between races, that race does indeed exist and it does—contrary to popular belief—have implications for people’s health of certain races.
The socialrace concept of race
Finally, the last concept of race laid out by Hardimon is the concept of socialrace. The concept of socialrace takes a race to be a racialist race, it refers to a position that is occupied by a social group that is a socialrace, and the socialrace concept refers to the system of social positions that are socialraces. This concept of race is, clearly, different from the minimalist and populationist race concepts but does indeed correlate with popular notions of race (and would correlate with the minimalist and populationist concept of race very well). The socialrace concept is, basically, what is believed to be racialist races.
The concept of socialrace is a concept of race as a social group (Hardimon, The Ontology of Race: 31)
The socialrace concept differs from the minimalist and populationist concept of race in that it looks at so-called social—not biological—correlates of race. Though, still, the socialrace concept can be said to show the reality of race since how one socially defines themselves correlates almost perfectly with geographic ancestry (which is a prerequisite for the existence of the minimalist concept of race and the populationist concept of race) (Tang et al, 2005). They showed that self-identified racial categories lined up almost perfectly with geographic ancestry (99.86 percent of the time). So, as you can see, the concept of socialrace also gives credence to the existence of the minimalist and populationist concepts of race.
This concept of race—as its name implies—does not talk race is a biological manner, but a social one, as its name implies. However, due to the extremely high chance that one’s self-identified race (their socialrace) lines up with the geographic ancestry of the classical races, we can see that the socialrace concept further buttresses the argument for the existence for the reality of the minimalist concept of race and the populationist concept of race.
The socialrace concept is kind of like Templeton (2014) defines race: that human races exist in a cultural sense, but not biologic sense. I have shown, though, that races exist in a cultural, social, and biological sense with the arguments presented in this article. Socialrace, culturalrace, whatever you want to call it, it is evidence for the existence of race.
Race exists whether or not the racialist position of race (as Hardimon defines it) is true or not. The minimalist concept of race and populationist concept of race show that race is real while the concept of socialrace further lends credence to the biological models of the minimalist and populationist concept of race. Even still, people who deny race because the genetic distance between races is too small for their to be any meaningful differences between them do not accept that three arguments above (sans the racialist concept) for the existence of race. They’ll still talk about the genetic differences between them and, say, morphology, but the minimalist concept of race and the populationist concept of race define race in enough of a way that genetic differences do not need to be looked at—we can only look at reproductive isolation, morphology, geographic ancestry and physical differences between minimalist and populationist races such as hair, nose, and skin color along with morphological differences.
Minimalist and populationist races exist and are a biological reality. We can take those two concepts to be a scientific basis for race. While we can take the concept of socialrace not as a biological concept, but as a social concept and we can then say that socialrace is socially real while being a significant social reality. That social reality is manifested by noticing different racial phenotypes, along with differences in SES, educational attainment, etc, and placing different races in different average social positions, which would correlate with the concepts of race mentioned above. This also correlated nearly perfectly with geographic ancestry. So, I’m saying it again, the existence of race as a social reality is real; the existence of socialrace buttresses the arguments for both the existence of the minimalist concept of race and the populationist concept of race—both of which are scientific concepts of race.
Minimalist races exist, and is a superficial biological reality, populations races may exist and if they exist, they are a relatively superficial biological reality. Socialraces exist and are a social reality which also lend credence to the minimalist and populationist concepts. I personally am privy to the minimalist race concept because it is shown to be real, so race is real.
In sum, race exists whether you look at genetic differences between races or not, morphology, geographic ancestry, reproductive and genetic isolation are all you need to prove the existence of race. There is a scientific concept of race, and the minimalist and populationist race concepts provide the existence for it, while the socialrace concept does as well. It is clear that for a scientific concept of race, you only need phenotypic variation, morphologic variation between races,
(Also read the American Rennaisance review for the book, A Tactical Retreat for Race Denial. I think it is balanced and fairly written, though a bit biased and doesn’t account for Hardimon’s views well enough in my opinion.)
Back in July I wrote about how there is controversy on whether or not MtF transgenders should compete with ‘bio women’ and whether or not their anthropometry or hormones gave them an advantage over biological women (I am aware that T levels decrease once they go on HRT, just a lot of them still have T ranges in near the low end of the new numbers for men). Well I am reading The Sports Gene by Jerry Epstein and he brings up two (anecdotal) examples of MtF transgenders who take HRT and see a decrease in performance due to decreased T:
No scientist can claim to know the precise impact of testosterone on any individual athlete. But a 2012 study that spent three months following female athletes from a range of sports—including track and field and swimming—showed that elite-level competitors had testosterone levels that consistently remained more than twice as high as those of the nonelites. And there are powerful anecdotes as well.
Joanna Harper, fifty-five, is a medical physicist who was born a male and later transitioned to living as a woman. Harper also happens to be a nationally accomplished age-group runner, and when she started hormone therapy in August 2004 to suppress her body testosterone and physically transition to female [Note from RR: I, of course, do not agree with the use of ‘her’ and that ‘she’ ‘physically transition[ed] to female’] like any good scientist, she took data. Harper figured she would slow down gradually, but was surprised to find herself getting slower and weaker by the end of the first month. “I felt the same when I ran,” she says. “I just couldn’t go as fast.” In 2012, Harper won the U.S. national cross-country title for the fifty-five-to-fifty-nine age group, but age and gender-graded performance standards indicate that Harper is precisely as competitive now as a female as she was as a male. That is, as a female, Harper is just as good relative to women as she was relative to men before her transition, but she’s far slower than her former, higher-testosterone self.
In 2003, as a man, Harper ran Portland’s Helvetia Half-Marathon in 1:23:11. In 2005, as a woman, she ran the same race in 1:34:01. Harper’s male time was about fifty seconds faster than her female time. She has compiled data from five other runners who have transitioned from male to female, and all show the same pattern of precipitous speed decline. One runner competed in the same 5K for fifteen years straight, eight times as a man and then seven times as a woman following testosterone suppression therapy; always faster than nineteen minutes as a man, and always slower than twenty minutes as a woman. (Epstein, 2013: 78) [Keep in mind that I have the nook version so the physical copy may have this on a different page.
Yes this is anecdotal evidence that testosterone gave an advantage while ‘male’ and then when they ‘transitioned’ to ‘female’ it showed that they became weaker, but still at the top level of women’s performance. Knowing this—how this man had an advantage ‘as a man’ and kept the same relative advantage when he ‘transitioned to a woman’ is a large clue that testosterone does infer an inherent advantage to athletes who have more of the hormone surging through their body.
Testosterone is known to affect skeletal muscle growth, but the mechanisms by which testosterone affects muscle growth are not known (Bhasin, Woodhouse, and Storer, 2001). Also, women with very high androgen levels—whether it’s due to endogenous or exogenous testosterone—have a 2.5 to 5 percent advantage over women who have androgen levels in the normal range (Berman, 2017). So the difference in performance—between women at least—with high and low levels of testosterone is not too great, though that 2.5 to 5 percent advantage most likely would come into play at the very end of the race.
Also recall that I previously wrote that, per the IOC guidelines, a ‘MtF’ needs to ‘declare herself’ a woman for at least four years while taking HRT for 1-2 years to be able to compete with ‘the gender they think they are’. Well, the testosterone levels that the IOC states is ‘OK’ for ‘MtFs’ is still in the low range of the new testosterone guidelines for men! Testosterone most definitely does give an advantage in sports. Think of sports as a modern day test of survival. Basically, those good at sports—such as football and basketball for instance—would have been better able to form hunting parties in our evolutionary past. So while forming these parties, testosterone rose since testosterone raises while men are in groups as well as preparing for competition (Booth et al, 1989). So since our modern body plans sprang up around 2 mya with the appearance of Homo erectus in the fossil record, we can logically infer that cooperation and testosterone—among other things—were needed to be successful hunters.
So if you look at most sports as just a way for men to have a competitive spirit and simulate fighting/hunting with other men, then it makes it clear that testosterone does infer an advantage in sports. For instance, there is a clear relationship between testosterone and explosive jumping (Cardinale and Stone, 2006). These relationships are very clear, have large effects yet bodies like the IOC disregard these findings, allowing MtFs to compete with real women, even when the data and verbal argumentation against letting them compete are logically sound.
Studies do state, of course, that the relationship between high testosterone and athletic performance hasn’t been proven, they also haven’t been refuted either (Sudai, 2017). In fact, all you need to look at is traits that are influenced by testosterone—height, size of limbs, fat mass, shoulder width/size (the most androgen receptors lie in the shoulders and traps muscles, so to tell if someone is juicing, they will have low levels of body fat but ‘3-D delts’ and large traps) etc. So just by looking at a few simple traits and then comparing anatomy with females who have high testosterone compared to women who do not have high levels of testosterone, we can draw the logical conclusion that testosterone does increase sports performance for both men and women, and we have both anecdotal and experimental evidence for the assertion.
In sum, the anecdotal evidence from Epstein’s book is a good start. However, we will need more than anecdotal evidence to prove that testosterone truly does give individuals an advantage if they do have higher testosterone levels than their competition. As larger studies get done, these effects will begin to get teased out. I am certain that testosterone will be found to give a huge advantage in terms of sports, and since sports are a way for us to compete with each other, impress women, gauge other males’ fighting skills, and began as a way to hone skills used to hunt and fight (Lombardo, 2012). Sports began as a way for us to develop the skills needed to survive and hunt, among other things, and so, to hunt, you need to have high levels of testosterone to give that ‘boost’. So if sports began as a way to gauge potential rivals and allies, and as a way to hone/improve fighting skills, then we can logically state that testosterone does give an advantage in sports competition.
Talk about anything (reasonable).
In honor of Movember, I’m going to take some time this month to write about prostate cancer, it’s causes and how to prevent it (doctor supervision, etc). Since ‘charities’ like the Susan G. Komen Foundation are very shady and all eyes go to them Movember gets looked over. Movember is to raise awareness for prostate cancer and other diseases that plague men. Also read I Will Not Be Pinkwashed: Komen’s Race is for Money, Not the Cure.
See also my articles on race and prostate cancer:
Also on prostate cancer, one meta-analysis show there is no B-W PCa gap:
This meta-analysis concludes that there are no racial differences in the overall and prostate cancer–specific survival between African American and White men.
While another study shows the same:
Although African-American patients tend to have higher pretreatment PSA levels than white patients, the outcome for the disease is similar in the two groups when stratified by known pretreatment prognostic factors. Our data provide no evidence for the hypothesis that prostate cancer in African-Americans is intrinsically more virulent than in whites.
Steve Sailer published an article the other day titled Wieseltier vs. “The Bell Curve” and I left a comment saying that psychological traits are not normally distributed. Two people responded to me, and I replied back but Sailer didn’t approve my two comments. I have a blog, so I can post it here.
They do actually exist.
“Human resource management: Human Resource Management (HRM) is the term used to describe formal systems devised for the management of people within an organization. The responsibilities of a human resource manager fall into three major areas: staffing, employee compensation and benefits, and defining/designing work.”
Organizational behavior: “the study of the way people interact within groups. Normally this study is applied in an attempt to create more efficient business organizations. The central idea of the study of organizational behavior is that a scientific approach can be applied to the management of workers.”
Industrial and organizational psychology: “This branch of psychology is the study of the workplace environment, organizations, and their employees. Technically, industrial and organizational psychology – sometimes referred to as I/O psychology or work psychology – actually focuses on two separate areas that are closely related.”
We conducted 5 studies involving 198 samples including 633,263 researchers, entertainers, politicians, and amateur and professional athletes. Results are remarkably consistent across industries, types of jobs, types of performance measures, and time frames and indicate that individual performance is not normally distributed—instead, it follows a Paretian (power law) distribution. Assuming normality of individual performance can lead to misspecified theories and misleading practices. Thus, our results have implications for all theories and applications that directly or indirectly address the performance of individual workers including performance measurement and management, utility analysis in preemployment testing and training and development, personnel selection, leadership, and the prediction of performance, among others.
Even most types of job performance and performance measures don’t fit a normal curve.
You say, “…psychological traits aren’t normally distributed.”
But the abstract you linked says,
…individual performance is not normally distributed.
Yes, those of us who have had the misfortune to manage work groups know all about 80/20. This is performance, not “psychological traits.”
Psychological tests aren’t a measure of performance? Traits like IQ only show a normal distribution because the normal distribution is built into the tests (see below).
The other one linked says,
… at many physiological and anatomical levels in the brain, the distribution of numerous parameters is in fact strongly skewed . . .
Okay. The cylinders in the straight-six engine of my BMW lean over to one side, but that doesn’t seem to effect the horsepower. This is a physical trait.
So, what of those “psychological traits”? Like IQ? Granted, it is a kind of performance, one of taking IQ tests, but the results have a normal distribution, and it’s not the kind of performance being measured in the study referenced anyway. IQ, by definition, is a “psychological trait,” and it has a normal distribution.
IQ tests have been constructed so that the scores will exhibit a bell curve distribution. That is, the tests themselves are constructed to reveal differences that are already presumed. IQ tests are constructed with the assumption that the scores are normally distributed, however, the normal distribution is built into the test. Items that 50 percent of the testees get right are kept, along with the smaller proportion of items that many testees get right. (See Richardson, 2002 for more information.) Even most psychological constructs are not normally distributed. This is like g being supposedly physiological when—if it were—it wouldn’t mimic any known physiologic process in the body.
Buzsaki and Muzuseki (2014) review data that sensory acuity, reaction time, memory word usage and sentence lengths are not normally distributed. Basic physiologic processes, too, are not normally distributed, like visual acuity, resting heart rate, metabolic rate, etc. And this makes sense, because those traits are crucial to human survival and therefore need to be malleable. Hormones raise, for instance, during a life-or-death situation, and that is what is needed for survival. So, therefore, few physiological traits are normally distributed.
Honestly, I don’t know what your point is, but I don’t disagree with what you have shown me. I know it’s true, but I’m just too far left on your ski jump curve of losers to grasp why you responded to me that way.
Wieseltier was referring to The Bell Curve, in which results have a normal distribution.
Rigbt, the IQ book. But tests are constructed with the assumption of a normal distribution, but psychological traits are not normally distributed. Read Mizsukei and Buzsaki’s work.
Burt (1967) writes:
A detailed analysis of test results obtained from a large sample of English children (4,665 in all), supplemented by a study of the meagre data already available, demonstrates beyond reasonable doubt that the distribution of individual differences in general intelligence by no means conforms with strict exactitude to the so-called normal curve.
In sum, IQ tests are constructed with the assumption that whatever is being tested lies on a bell curve. Clearly, since they are constructed in such a way, the results are forced to fit a normal distribution. But, as seen above, most traits that are critical to survival are not normally distributed, so why should intelligence/IQ be the same? The data from Buzsaki and Mizuseki (2014) show that “skewed … distributions are fundamental to structural and functional brain organization.”
(Also read The Myth of the Bell Curve and The Unicorn, The Normal Curve, and Other Improbable Creatures. where Micceri shows that achievement measures in “language arts, quantitative arts/logic, sciences, social studies/history, and skills such as study skills grammar, and punctuation” are not normally distributed. Human performance does not follow a bell curve. Also read The Bell Curve Is A Myth — Most People Are Actually Underperformers. The Bell Curve in Psychological Research and Practice: Myth or Reality?: “If IQ scores distribute normally, this does not mean that intelligence equally distribute normally in the population.” … “ In this way, a normal distribution in summated test scores, for example, would be seen as the sign of the presence of an error sufficient to give scores the characteristic bell shape, not as the proof of a good measurement.“)
In my last article on brain size and IQ, I showed how people with half of their brains removed and people with microcephaly can have IQs in the normal/above average range. There is a pretty large amount of data out there on microcephalics and normal intelligence—even a family showing normal intelligence in two generations despite having dominantly inherited microcephaly.
Microcephaly is a condition in which an individual has a head circumference of 2 SD below the mean. Though most would think that would doom all microcephalics to low IQs, 15 percent of microcephalics have IQs in the normal range. This is normally associated with mental retardation, but this is a medical myth (Skoyles and Sagan, 2002: 239), though there are numerous cases of microcephalics having normal IQs (Dorman, 1991). Numerous studies show that it’s possible for normal people to have small brains. Giedd et al (1996) showed a wide variation in head circumference. Of the 104 individuals who had their heads scanned, volume for the cerebellum ranged from 735 cc in a 10 year old boy to 1470 cc in a 14 year old boy (Skoyles, 1999: 4, para 12). Though Giedd et al (1996) did not report total brain volumes in their subjects, brain volume can be inferred. Skoyles (1999; 4, para 12) writes:
The cerebral cortex makes up only 86.4% of brain volume when measured by MRI (Filipek, Richelme, Kennedy & Caviness, 1994), so the total brain volume of the 10-year-old would be larger at 850.7 cc. Brains at 10 years are about 4.4% smaller than adult size (Dekaban & Sadowsky, 1978), suggesting that that brain would grow to an adult size of 888 cc. Even using the lower figure of 80% cerebrum to brain ratio derived from anatomical studies suggests a figure of only 960 cc.
The variation of 888 cc to 960 cc depending on which value for the cerebrum to brain ratio you use still shows that people can have brains 450-300 cc lower than average and still be ‘normal’.
Researchers began noticing many cases of both individuals and families exhibiting features of microcephaly—but they had normal intelligence (Simila, 1970;Seemanova et al, 1985; Rossi et al, 1987; Teebi et al, 1987; Sherrif and Hegab, 1988; Desch et al, 1990; Opitz and Holt, 1990; Evans, 1991; Heney et al, 1991; Green et al, 1995; Rizzo and Pavone, 1995; Teebi and Kurash, 1996; Innis et al, 1997; Kawame, Pagon, and Hudgens, 1997; Abdel-Salam et al, 1999; Digweed, Reis, and Sperling, 1999; Woods, Bond, and Enard, 2005; Ghaoufari-Fard et al, 2015). This is a pretty huge blow to the brain size/IQ correlation, for if people with such small heads can have normal IQs, why do we have such large brains that leave us with such large problems (Skoyles and Sagan, 2002: 240-244)?
If we can have smaller heads—which would make childbirth easier and allow us to continue to have smaller pelves which would be conducive to endurance running since we are the running ape, why would brains have gotten so much larger from that of erectus (where modern people can have normal IQs with erectus-sized brains) if it is perfectly possible to have a brain on around the size of early erectus? In any event, these anomalies need an explanation, and Skoyles (1999) hypothesizes that people with smaller heads but normal IQs may have a lower capacity for expertise. This is something that I will look into in the future, as it may explain these anomalies, along with the true reason why our brains began increasing around 3 mya.
Sells (1977)—using the criteria of 2 SD below mean head size—showed that 1.9 percent of the children he tested (n=1009) had IQs indistinguishable from their normocephalic peers. Watemberg et al (2002) studied 1,393 patients. They found that almost half of their patients with microcephaly (15.4% of their patients studies had microcephaly) had IQs within the normal limits, while among those with sub-normal intelligence, 30 percent had borderline IQs or were mildly mentally retarded (it’s worth noting that l-glutamate can raise IQ scores by 5-20 points in the mild to moderate mental deficiency; Vogel, Braverman and Draguns, 1966 review numerous lines of evidence that glutamate raises IQ in mentally deficient individuals). Sassaman and Zartler (1982) showed that 31.9 percent of microcephalics had normal intelligence, 6.9 percent of them had average intelligence.
Head circumference does not directly correlate with IQ in microcephalic patients (Baxter et al, 2009). Dorman (1991: 268) writes: “Decreased head size may or may not be associated with lowered intelligence, indicating that small head size by itself does not affect intelligence. The presence of subgroups of microcephalic persons who typically have normal intelligence is sufficient to rule out a causal relationship between head size and intellect. … It can be added that reduction in brain size without such structural pathology, as mayvoccur in some genetic conditions or evenvas a result of normal variation, does not
affect intelligence. ”
Tenconi et al (1981) write: “We were able to examine five other members of this family (1-3; 11-1; 11-4; 11-5; 11-8) and found no abnormalities: they were of normal intelligence, head circumference, and ophthalmic evaluation. Members of the grandmother’s family who refused to be examined appeared to be of normal intelligence and head appearance and did not have any serious eye problems.”
Stoler-Poria et al (2010) write: “There was a K-ABC cognitive score < 85 (signifying developmental delay) in two (10%) children from the study group and in one (5%) child from the control group: one of the children in the study group (the one with HC below − 3 SD) scored significantly below the normal range (IQ = 70), while the other scored in the borderline range (IQ = 83); the child from the control group also scored in the borderline range (IQ = 84).” Whereas Thelander and Pryor (1968) showed that individuals with head circumferences 2-2.6 SDs below the mean had average IQs, though the smaller their HC, the lower their IQ. Ashwal et al (2009: 891) write: “The students with microcephaly had a similar mean IQ to the normocephalic group (99.5 vs 105) but had lower mean academic achievement scores (49 vs 70).” So it seems that microcephalics can have normal IQs, but have lower academic achievement scores.
Primary microcephalics have higher IQs than secondary microcephalics (Cowie, 1987). Primary microcephaly is microcephaly that one is born with whereas secondary microcephaly is acquired.
There is one case study of a girl with microcephaly where Tan et al (2014) write: “Most recent measures of general intelligence (performed at 6½ years of age) reveal a below average full scale IQ of 75 with greatest impairment in processing speed. On the Wechsler Preschool and Primary Scale of Intelligence III Revised (for children 2 years 6 m – 7 years 3 m), she obtained a Verbal IQ of 83, Nonverbal IQ of 75, and Processing speed 71. On the Wechsler Individual Achievement Testing (WIAT) she showed significant struggles in secondary language on tasks of early reading (SS 60), word reading (SS 70), reading comprehension (SS 69) and struggles in math on the task of numerical operations (SS 61) (WPPSI – R and WIAT mean = 100 and SD = 15). Parents report subjectively that differences in development relative to her sisters are becoming more apparent with time.”
It is not a foregone conclusion that if an individual has microcephaly that they will have a low IQ and be mentally retarded, as reviewed above, there are numerous cases of individuals with microcephaly and normal IQs, with this even being seen in families—that is, multiple families with normal IQs yet have microcephaly. Numerous people with Nijmegen breakage syndrome (a type of microcephaly) can have normal IQs. Rossi et al (1987) reported that for 6 Italian families (n=21 microcephalics) with autsomally inherited microcephaly, for those administered psychometric tests (n=12), all had normal IQs but one, with an IQ range of 99 to 112 for a mean of 99.3.
In conclusion, microcephalics can have normal IQs and live normal lives, despite having heads, on average, that are 2 SDs below the mean. These anomalies (and there are many, many more) need explaining. This is great evidence that a larger brain does not always mean a higher IQ, as well as yet more evidence that it was possible for Homo erectus to have an IQ in our range today, which means that we may not need brains our current size for our intellect and achievements. To conclude, I will provide a quote from Dorman (1991):
The normal intelligence found by SELLS in school children with small head size also militates against any straightforward relationship between diminished head size and lowered intelligence.
With the correlation between brain size and IQ being .4 (Gignac and Bates, 2017), this does not rule out the ‘outliers’ reviewed in this article. These cases deserve an explanation, for if large brains lead to high IQs, why do these people with heads significantly smaller have IQs in the normal range? (See Skoyles, 1999: 8, para 31 for an explanation for the brain size/IQ correlation.)
There are a few things I constantly see around the Internet that really irk me. One of those things is the meme that soy causes feminization in males. Some people may see a picture of a guy with soft facial features and they’ll say ‘oh that’s a soy boy.’ They do not show a good understanding of soy and its chemicals. As usual, overblown claims from people who have no specialty in what they’re talking about have an answer—just one they do not want to hear.
I have no idea when this craze of blaming soy and other foods on ‘feminization of males’ (I have done so a few years ago, though I realize my error now), but it’s starting to get out of hand. I see this around Twitter a lot; ‘oh it’s the soy making men beta’ or ‘they know exactly what soy does to men and they still push it!’. The whole scare about soy is that soy has phytoestrogens called isoflavones, and these phytoestrogens then may mimic estrogen production in the body. (It’s worth noting that phytoestrogens do not always mimic estrogens, despite some people’s protesting to me that “It has estrogen right in the name!”.)
Many men have blamed soy and phytoestrogens/isoflavones on their growing breasts, having a flaccid penis, slow beard growth (that’d be enough motivation for me to do something about it, to be honest), loss of hair on his arms and legs, and, he says “Men aren’t supposed to have breasts … It was like my body is feminizing.” So this man went to an endocrinologist and was told that he had gynecomastia—enlarged breasts in men. He got tested for a whole slew of maladies, but they all came back negative. Then the doctor told him to be very specific with his diet. The man then said that he was lactose intolerant and that he drank soy milk instead of cow’s milk. The doctor then asked him how much soy milk he drank per day, to which the man responded 3 quarts. Was soy the cause of his gynecomastia and other negative health effects? I don’t think so.
For men and boys, soy does not seem to have an effect on estrogen and other hormone levels, nor does it seem to have an effect on development and fertility:
A handful of individuals and organizations have taken an anti-soy position and have questioned the safety of soy products. In general, this position latches to statistically insignificant findings, understates how powerfully the research refutes many of the main anti-soy points, and relies heavily on animal research studies, which are medically irrelevant to human health.
Most of those people are ‘activists’ who do not understand the intricacies of what they are talking about. In the field of nutrition, it’s dumb to take studies done on animals nd then extrapolate that data to humans. It does not make sense.
There are reasons not to eat soy that do not go along with this dumb hysteria from people who do not know what they are talking about. One reasons is that, when compared to casein protein, soy protein is inferior (Luiking et al, 2005). Further, data is “inconsistent or inadequate in supporting most of the suggested health benefits of consuming soy protein or ISF” (Xiao, 2008). People may cite studies like Lephart et al (2002) where they write in their article Neurobehavioral effects of dietary soy estrogens:
Whether these observations hold true for the human brain remains to be established and will only become apparent from long-term clinical studies. One point that needs clarification relates to the timing of brain development in the rat, which differs from that in the human. (pg. 12)
Rats and humans are different; I don’t think I need to say that. Though people who cite these studies (uncritically) as ‘evidence’ that soy lowers T, causes infertility problems, and feminization just look to grab anything that affirms their fearmongering views.
Jargin (2014) writes in his article Soy and phytoestrogens: possible side effects:
Feminizing effect of phytoestrogens and soy products may be subtle, detectable only statistically in large populations; it can be of particular importance for children and adolescents. This matter should be clarified by independent research, which can have implications for the future of soy in the agriculture.
If it’s only identifiable in statistically large populations, then it is meaningless. Though, East Asians seem to be adapted to soy and so (like all studies should note), these results should not be extrapolated to other races/ethnies (Jargin, 2014). I do agree with that assessment; I do not agree with the claim that these phytoestrogens would cause problems that would only be seen in statistically large populations.
If people want to use rat studies to show that soy supposedly raises estrogen levels, then I will use a rat study showing the opposite (Song, Hendrich, and Murphy, 1999). They showed that the effects of the isoflavones from soy were only weakly estrogenic. Further, Mitchell et al (2001) write in their article Effect of a phytoestrogen food supplement on reproductive health in normal males:
The phytoestrogen supplement increased plasma genistein and daidzein
concentrations to approx. 1 µM and 0.5 µM respectively; yet, there was no observable effect on endocrine measurements, testicular volume or semen parameters over the study period. This is the first study to examine the effects of a phytoestrogen supplement on reproductive health in males. We conclude that the phytoestrogen dose consumed had no effect on semen quality.
The men in this study took a daily isoflavone supplement containing 40 mg of isoflavone every day for two months and still did not show negative effects. Looking at rat studies and then extrapolating that to humans doesn’t make sense.
Finally, there was a large meta-analysis by Messina (2010) who writes:
The intervention data indicate that isoflavones do not exert feminizing effects on men at intake levels equal to and even considerably higher than are typical for Asian males.
And from the conclusion:
Isoflavone exposure at levels even greatly exceeding reasonable dietary intakes does not affect blood T or estrogen levels in men or sperm and semen parameters. The ED-related findings in rats can be attributed to excessive isoflavone exposure and to differences in isoflavone metabolism between rodents and humans. Thus, men can feel confident that making soy a part of their diet will not compromise their virility or reproductive health.
Now, I know that proponents of the hypothesis of soy feminizing males would say to me “Why don’t you just eat a bunch of soy and see what happens then, if it is fine for you?” Well, unlike most people, I eat a strict diet and soy is not part of it.
Soy isoflavones are currently being researched in regards to the prevention and treatment of diabetes, cardiovascular disease, cancer, osteoporosis, and neuroprotection (Kalaiselven et al, 2010), while the nutritional and health benefits of soy isoflavones are currently being studied (Friedman and Brandon, 2001; McCue and Shetty, 2004). Soy foods may also be optimal for bone health (Lanou, 2011).
In conclusion, as you can see, the claims of soy causing feminizing effects on men are largely overblown. People extrapolate data from rat studies to humans, which doesn’t make any sense. To paraphrase Dr. Jason Fung, imagine 2 lions are watching a deer eat. They see how strong and in shape the deer are eating grass. So the lions, noticing that the deer are healthy eating grass, begin to eat grass too thinking it is healthy and they die. One hundred years later, 2 deer are watching a lion eat meat and sees how strong, fast, and healthy it is. They then draw the conclusion that eating meat is healthy and will do the same for them and they eat meat and die. The point of the analogy is that just because studies on animals show X and therefore Y, that does not mean that it will hold for humans! This is something very simple for people to understand, though most do not.
Most people search for things to prove their assumptions without having an actual understanding of the biological mechanisms of what they’re talking about. People should learn some of the literature before they cite studies that supposedly back their biases, because they would then see that it is not as nuanced as they believe.
(Note: Diet changing under Doctor’s supervision only.)
Here is my reply to Jared Taylor’s new article over at AmRen Breakthroughs in Intelligence:
“The human mind is not a blank slate; intelligence is biological”
The mind is not a ‘blank slate’, though there is no ‘biological’ basis for intelligence (at least in the way that hereditarians believe). They’re just correlations. (Whatever ‘intelligence’ is.)
“there is no known environmental intervention—including breast feeding”
There is a causal effect of breast feeding on IQ:
While reported associations of breastfeeding with child BP and BMI are likely to reflect residual confounding, breastfeeding may have causal effects on IQ. Comparing associations between populations with differing confounding structures can be used to improve causal inference in observational studies.
Brion, M. A., Lawlor, D. A., Matijasevich, A., Horta, B., Anselmi, L., Araújo, C. L., . . . Smith, G. D. (2011). What are the causal effects of breastfeeding on IQ, obesity and blood pressure? Evidence from comparing high-income with middle-income cohorts. International Journal of Epidemiology, 40(3), 670-680. doi:10.1093/ije/dyr020
Breastfeeding is related to improved performance in intelligence tests. A positive effect of breastfeeding on cognition was also observed in a randomised trial. This suggests that the association is causal.
Horta, B. L., Mola, C. L., & Victora, C. G. (2015). Breastfeeding and intelligence: a systematic review and meta-analysis. Acta Paediatrica, 104, 14-19. doi:10.1111/apa.13139
“before long we should be able to change genes and the brain itself in order to raise intelligence.“
Which genes? 84 percent of genes are expressed in the brain. Good luck ‘finding’ them…
These results corroborate with the results from previous studies, which have shown 84% of genes to be expressed in the adult human brain …
Negi, S. K., & Guda, C. (2017). Global gene expression profiling of healthy human brain and its application in studying neurological disorders. Scientific Reports, 7(1). doi:10.1038/s41598-017-00952-9
“Normal people can have extraordinary abilities. Prof. Haier writes about a non-savant who used memory techniques to memorize 67,890 digits of π! He also notes that chess grandmasters have an average IQ of 100; they seem to have a highly specialized ability that is different from normal intelligence. Prof. Haier asks whether we will eventually understand the brain well enough to endow anyone with special abilities of that kind.”
Evidence that intelligence is not related to expertise.
“It is only after a weight of evidence has been established that we should have any degree of confidence in a finding, and Prof. Haier issues another warning: “If the weight of evidence changes for any of the topics covered, I will change my mind, and so should you.” It is refreshing when scientists do science rather than sociology.”
Even with the “weight of evidence”, most people will not change their views on this matter.
“Once it became possible to take static and then real-time pictures of what is going on in the brain, a number of findings emerged. One is that intelligence appears to be related to both brain efficiency and structure”
Patterns of activation in response to various fluid reasoning tasks are diverse, and brain regions activated in response to ostensibly similar types of reasoning (inductive, deductive) appear to be closely associated with task content and context. The evidence is not consistent with the view that there is a unitary reasoning neural substrate. (p. 145)
Nisbett R. E., Aronson J., Blair C., Dickens W., Flynn J., Halpern D. F., Turkheimer E. Intelligence: New findings and theoretical developments. American Psychologist. 2012;67:130–159. doi: 10.1037/a0026699.
“Early findings suggested that smart people’s brains require less glucose—the main fuel for brain activity—than those of dullards.”
Cause and correlation aren’t untangled; they could be answering questions in a familiar format, for instance, and this could be why their brains show less glucose consumption.
“It now appears that grey matter is where “thinking” takes place, and white matter provides connections between different areas of grey matter. Some brains seem to be organized with shorter white-matter connections, which appear to allow more efficient communication, and there seem to be sex differences in the ways the part of the brain are connected. One of the effects of aging is deterioration of the white-matter connections, which reduces intelligence.”
Read this commentary (pg. 162): Norgate, S., & Richardson, K. (2007). On images from correlations. Behavioral and Brain Sciences, 30(02), 162. doi:10.1017/s0140525x07001379
“Brain damage never makes people smarter”
This is wrong:
You would think that cutting out one-half of people’s brains would kill them, or at least leave them vegetables needing care for the rest of their lives. But it does not. Consider this striking story. A boy starts having seizures at 10 years of age when his right cerebral hemisphere atrophies. By the time he is 12, the left side of his body is paralyzed. When he is 19, surgeons decide to operate and remove the right side of his brain, as it is causing gits in his intact left one. You might think this would lower his IQ or leave him severely retarded, but no. His IQ shoots up 14 points, to 142! The mystery is not so great when you realize that the operation has gotten rid of the source of his fits, which had previously hampered his intelligence. When doctors saw him 15 years later, they described him as “having obtained a university diploma . . . [and now holding] a responsible administrative position with a local authority.”
Skoyles, J. R., & Sagan, D. (2002). Up from dragons: the evolution of human intelligence. New York: McGraw-Hill (pg. 282)
“Prof. Haier wants a concerted effort: “What if a country ignored space exploration and announced its major scientific goal was to achieve the capability to increase every citizen’s g-factor [general intelligence] by a standard deviation?””
Don’t make me laugh. You need to prove that ‘g’ exists first. Glad to see some commentary on epigenetics that isn’t bashing it (it is a real phenomenon, though the scope of it in regards to health, disease and evolution remains to be discovered).
As most readers may know, I’m skeptical here and a huge contrarian. I do not believe that g is physiological and if it were then they better start defining it/talking about it differently because I’ve shown that if it were physiological then it would not mimick any known physiological process in the body. I eagerly await some good neuroscience studies on IQ that are robust, with large ns, their conclusions show the arrow of causality, and they’re not just making large sweeping claims that they found X “just because they want to” and are emotionally invested in their work. That’s my opinion about a lot of intelligence research; like everyone, they are invested in their own theories and will do whatever it takes to save face no matter the results. The recent Amy Cuddy fiasco is the perfect example of someone not giving up when it’s clear they’re incorrect.
I wish that Mr. Taylor would actually read some of the literature out there on TBI and IQ along with how people with chunks of their brains missing can have IQs in the normal range, showing evidence that most a lot of our brain mass is redundant. How can someone survive with a brain that weighs 1.5 pounds (680 gms) and not need care for the rest of his life? That, in my opinion, shows how incredible of an organ the human brain is and how plastic it is—especially in young age. People with IQs in the normal range need to be studied by neuroscientists because anomalies need explaining.
If large brains are needed for high IQs, then how do these people function in day-to-day life? Shouldn’t they be ‘as dumb as an erectus’, since they have erectus-sized brains living in the modern world? Well, the human body and brain are two amazing aspects of evolution, so even sudden brain damage and brain removal (up to half the brain) does not show deleterious effects in a lot of people. This is a clue, a clue that most of our brain mass after erectus is useless for our ‘intelligence’ and that our brains must have expanded for another reason—family structure, sociality, expertise, etc. I will cover this at length in the future.
Last week a study was published stating that white men who exercised 3 times the recommendation of 1.5 hours (450 minutes, 7.5 hours) had a higher chance of getting coronary artery calcification (CAC), which is the accumulation of plaque and calcium in the arteries of the heart. You, of course see news headlines such as: “Physically active white men at high risk for plaque buildup in arteries“; “White Men Who Exercise Every Day Have 86 Per Cent Higher Risk of Heart Disease Than Black Men, Study Claims“; “Excessive Exercise May Harm The Heart, Study Suggests “; “Excessive exercise increases risk of arterial plaque buildup in white men“; (and my personal favorite headline about this study): “You can exercise yourself to death, says new study“. People just passing by and reading the title (like most do) may then conclude that “they’re saying not to exercise because of CAC.” No, this is not what they are saying at all.
The Coronary Artery Risk Development in Young Adults (CARDIA) study is one of the most important studies in the study of coronary heart disease that have been undertaken. It is a sample of men and women, about equal numbers of each race, from Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California. The study began in 1985-86 and there were follow-up examinations at “1987-1988 (Year 2), 1990-1991 (Year 5), 1992-1993 (Year 7), 1995-1996 (Year 10), 2000-2001 (Year 15), 2005-2006 (Year 20), 2010-2011 (Year 25), and 2015-2016 (Year 30).” The CARDIA website writes:
Data have also been collected on physical measurements such as weight and body composition as well as lifestyle factors such as dietary and exercise patterns, substance use (tobacco and alcohol), behavioral and psychological variables, medical and family history, and other chemistries (e.g., insulin).
So there is a goldmine of information to be gleaned from this data. The study that is getting press in the news uses data from this cohort.
The study is titled 25-Year Physical Activity Trajectories and Development of Subclinical Coronary Artery Disease as Measured by Coronary Artery Calcium by Laddu et al (2017). They studied three cohorts by the amount of time they exercised per week: below requirement, at requirements, or above requirements. It is recommended to exercise at least 150 minutes per week.
There were 3,175 men and women who participated in the CARDIA study between 1985 and 2011 who had CAC data available for 25 years. About 47.4 percent of the sample was black, with 56.6 being women. The cohort “consisted of 18.9% black men, 24.6% white men, 28.6% black women, and 28.0% white women” (Laddu et al, 2017).
Of the three activity levels they studies (below 150 minutes, 150 minutes, and over 150 minutes), they observed that white men who exercised 3 times the weekly recommendation (150 minutes(3)= 450 minutes=7.5 hours) had a higher chance of developing CAC. It’s worth noting that exercise time was self-reported (which is the only way I can see how something like this would work, are you supposed to follow people with a camera every day to see how long they engage in physical activity?).
In regards to the physical activity measurement, Laddu et al (2017) write:
At each of the 8 examinations, self-reported leisure-time PA was ascertained by the interviewer-administered CARDIA Physical Activity History Questionnaire.17 Participants were asked about the frequency of participation in 13 specific categories (8 vigorous intensity and 5 moderate intensity) of recreational sports, exercise, home maintenance, and occupational activities during the previous 12 months. Intensity for each activity was expressed as metabolic equivalents (METs), in which 1 MET is defined as the energy expended at rest, which is approximately equivalent to an oxygen consumption of 3.5 mL per 1 kg of body weight per minute.18Vigorous activities (≥6 METs) included running or jogging; racquet sports; biking; swimming; exercise or dance class; job lifting, carrying, or digging; shoveling or lifting during leisure; and strenuous sports. Moderate-intensity activities (3-5 METs) included nonstrenuous sports, walking and hiking, golfing and bowling, home exercises or calisthenics, and home maintenance or gardening.19 Each activity was scored according to whether it was performed for 1 hour or longer during any 1 month during the past year, the number of months it was performed at that level, and the number of months the activity was performed frequently. Each activity was then assigned an intensity score, ranging from 3 to 8 METs, and a duration threshold (ranging from 2-5 hours per week), above which participation was considered to be frequent.20
This is a good metric; though I would like to see a study that looks at just gym-going activity and death, time spent in the gym strength training/moderate to intense cardio. Nevertheless, white men who reported more physical activity had a higher chance of acquiring CAC. Though I can see people’s recall being hazy, people over/under reporting, etc etc.
White men who exercised 7.5 hours per week were 27 percent more likely to get CAC, whereas blacks who exercised that much were at no greater risk to acquire CAC when compared to whites (7.5 hours of exercise compared to less than 2.5 hours per week). Black women who exercised less than the recommendations had a higher chance of acquiring CAC. The researchers couldn’t ascertain why white men who exercised three times the recommendations had such a higher chance of acquiring CAC by the time they reached middle age, but Dr. Jamal Rana says “however this plaque buildup may well be of the more stable kind, and thus less likely to rupture and causes heart attack, which was not evaluated in this study.” The head author, Dr. Deepika Laddu also reiterated: “it does not suggest that anyone should stop exercising.” So people who just read these click bait headlines who say “They’re telling whites not to exercise!”, you’re wrong and you should read papers and not news articles.
This is the perfect example of people reading click baity, fear-mongering headlines and running with it. I saw some people saying “They’re telling us not to exercise!” No. If you were to read the paper and any serious news articles on the matter, you’d see that they do not recommend that people do not exercise. Now the question is, why do whites who exercise more than 7.5 hours per week have a higher chance of acquiring heart disease? I can think of a few explanations (though they are not satisfactory): 1) genes: which genes? Why? How do they interact with the body over time to lead to arterial calcification?; 2) dietary habits: I’d like to know what their diet was like and see their macro composition, carbohydrates, not saturated fat, causes heart disease (Siri-Tirino et al, 2010; de Souza et al, 2015) so that may be a huge contributing factor.
Nevertheless, this is yet another physiological race difference. Oddly enough, black men are more likely than white men to have hypertension (Hicken et al, 2013).
Even though black men, on average, have higher rates of hypertension than white men, white men who are physically active for 7.5 had a higher chance of acquiring CAC than those who exercised less than 2.5 hours per week. This effect wasn’t seen in black men who had physical activity at that level, which, of course, implies that differences in genes and SES underlie this difference. I await more papers into this matter into the mechanisms of how and why this occurs and will ruminate on this myself in the future. No, this study does not tell white men not to exercise.