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Vygotsky’s Socio-Historical Theory of Learning and Development, Knowledge Social Class, and IQ
4050 words
Three of the main concepts that Soviet psychologist Lev Vygotsky is known for is cultural and psychological tools, private speech, and the zone of proximal development (ZPD). The ZPD is the distance between what a learner can do with and without help—the gap between actual and potential development. Vygotsky’s socio-historical theory of learning and development states that human development and learning take place in certain social and cultural contexts. When one thinks about how knowledge acquisition occurs, quite obviously, one can surmise that knowledge acquisition (learning) and human development take place in specific cultural and social contexts and so knowledge is culture-dependent (Richardson, 2002).
In this article, I will discuss the intersection of culture and Vygotsky’s concepts of private speech, cultural and psychological tools, and the zone of proximal development along with how these relate to IQ. Basically, the argument will be that what one is exposed to in childhood and during development will dictate how one performs on a test, and that the ZPD predicts school performance better than “IQ.”
What is culture and where does it come from?
This question is asked a lot by “HBDers” and I think it is a loaded question. It is a loaded question because they are fishing for a specific kind of answer—they want you to answer that culture derives from a people’s genetic constitution. This, though, fails. It fails because of how culture is conceptualized. Culture is simply what is socially transmitted by groups of people. It is physically visible (public) though the meaning of each cultural thing is invisible—it is private to the people who espouse the certain culture.
The basic source culture is values, beliefs, and norms. Cultures lay down strict norms of what is OK and what isn’t, like for example the foods they eat and along with it beliefs and attitudes shared by the social group. So a basic definition of culture would be: beliefs and ways of life that a social group shares—it is a human activity which is socially transmitted. Knowing this, we can see how learning and in some ways development, can be culturally-loaded. Since a culture dictates not only what is learned, but also how to think in a certain culture, we can then begin to see how different cultures lead people to think in different ways and along with it how different cultures lead to differences in not only knowledge but the acquisition of that knowledge.
UNESCO defines culture as “the set of distinctive spiritual, material, intellectual and emotional features of society or a social group, that encompasses, not only art and literature but lifestyles, ways of living together, value systems, traditions and beliefs” (UNESCO, 2001). (What is Culture?)
the term “culture” can refer to the set of norms, practices and values that characterize minority and majority groups (Stanford Encyclopedia of Philosophy, Culture)
Material culture consists of tangible objects that people create: tools, toys, buildings, furniture, images, and even print and digital media—a seemingly endless list of items. … Non-material culture includes such things as: beliefs, values, norms, customs, traditions, and rituals (Culture as Thought and Action)
Since society consists of individuals who then become a group living in a certain region, then it stands to reason that learning and human development are due to these kinds of cultural and social interactions between individuals which make up a certain society and therefore culture. The types of things that allow me to survive, learn, and grow in one culture won’t allow me to survive, learn, and grow to the same degree in another culture.
Now that I’ve touched on what culture is, where does it come from? Why are there different cultures? Quite simply, cultures are different because people are different and although different cultures are comprised of individuals, these individuals themselves comprise a group. These groups of people live in different environments/ecologies (physical environment), and so considerations of these ecologies lead not only to a group to begin to construct a society that is necessarily in-tune with the environment, it also leads to “mental environments” between the people that comprise the group in question. So then we can say that culture comes from the way that groups of people live their lives.
If we think about culture as thought and action, then we can begin to get at what culture really is. Values and beliefs influence our thought, attitudes, and behavior. “Culture influences action…by...shaping a repertoire or “toolkit” of habits, skills, and styles from which people construct “strategies of action“” (Swidler, 1986). Action is distinct from behavior, in that action is future- or goal-directed whereas behavior is due to antecedent conditions. That is, actions are done for reasons, to actualize a goal of the agent that is performing the action. Crudely, culture can be then said to be what a group of people does. Culture is “human-created environment, artifacts, and practices” (Vasileva and Balyasnikova, 2019).
How culture, then, comes into play in Vygotsky’s socio-historical theory of learning and development is now clear—the ways that people interact with others in a specific culture then dictates the knowledge that they acquire which then shapes their mental abilities. This theory is a purely developmental theory. The socio-historical theory makes three claims: Social interaction plays a role in learning, knowledge acquisition, and development; language is an essential cultural/psychological tool in learning, and learning occurs within the zone of proximal development (ZPD). How that I have shown how I will be using the term “culture”, it is clear that what it means for Vygotsky’s theory of human learning and development is relevant. Now I will discuss cultural and psychological tools and then turn to those three aforementioned tenets that make up the theory.
Psychological and cultural tools
Psychological tools are symbols, signs, text and language, to name a few. They are internally oriented, but in their external appearance take their form in the aforementioned ways. Language and mathematics are two kind of psychological tools, but we can also rightly say they they are cultural tools as well (in the case of language).
Cultural tools are tools specific to a culture which allows an individual to navigate that culture. Cultural tools don’t determine thinking but they do constrain it, since the “information about the expected or appropriate actions in relation to a particular performance in a community. This is indirectly social in that it is not interpersonal, though it nevertheless stems from the social context” (Gauvain, 2001:129). Language can be seen as both a cultural and psychological tool; humans are born into culturally- and linguistically-mediated environments, and so they are immediately immersed in culture from the day they are born (Vasileva and Balyasnikova, 2019).
Cultural tools include historically evolved patterns of co-action; the informal and institutionalized rules and procedures governing them; the shared conceptual representations underlying them; styles of speech and other forms of communication; administrative, management and accounting tools; specific hardware and technological tools; as well as ideologies, belief systems, social values, and so on (Vygotsky, 1988).(Richardson, 2002: 288)
Robbins (2005: 146) writes:
Another important concept within sociocultural theory, which we can highlight through Rogoff’s (1995, 1998) contextual or community focus of analysis, is the use of cultural tools (both material and psychological) in the development of understanding. As Lemke (2001) points out, we grow and live within a range of different contexts, and our lives within these communities and institutions give us tools for making sense of, and to, those around us. Vygotsky described psychological tools as those that can be used to direct the mind and behaviour, while technical tools are used to bring about changes in other objects (Daniels, 2001). Commonly cited examples of cultural tools include language, different kinds of numbering and counting, writing schemes, mnemonic technical aids, algebraic symbol systems, art works, diagrams, maps, drawings, and all sorts of signs (John-Steiner & Mahn, 1996; Stetsenko, 1999).
So cultural tools, then, become “internalized in individuals as the dominant ‘psychological tools’” (Richardson, 2002: 288).
Social interaction plays a role in learning
This seems quite intuitive. As a human develops, they begin to take cues from their overall environment and those that are rearing them. They are immersed in a specific culture immediately from birth. They then begin to internalize certain aspects of the environment around them, and then begin to internalize the specific cultural and psychological tools inherent to that specific culture.
Tomasello (2019: 13) states that his theory is that “uniquely human forms of cognition and sociality emerge in human ontogeny through, and only through, species-unique forms of sociocultural activity” and so it is not only Vygotskian, but neo-Vygotskian. So children are in effect scaffolded by the culture they are immersed in, which is how “more knowledgeable others” (MKO) affect the learning trajectory of the child. A MKO is an individual who has a better understanding of, or a higher ability than, the learner. So MKOs aren’t merely for teaching children, they are strewn throughout the world teaching less knowledgeable others. These MKOs guide individuals in their ZPD, since the MKO would have greater access to certain knowledge that the LKO wouldn’t, they would then be able to guide the LKO in their learning, able to provide instruction to the LKO so they could then perform a certain task. Learning to play baseball, right a bike, lift weights, are but a few ways that MKOs guide the development and task-acquisition of children—these are perfect examples of the concept of “scaffolding.”
Although Vygotsky never used the term “scaffolding”, it’s a direct implication of his socio-historical theory of learning and development. The concept of scaffolding has been argued to be related to the ZPD, but see Shabani, Khatib, and Ebadi (2010) and Xi and Lantolf (2021) for criticism of this relationship. However, it has been experimentally shown that the concept of scaffolding along with the ZPD can be used to extend a student’s ZPD for critical thinking (Wass, Harland, and Mercer, 2011). That is, the students can better reach their potential and therefore become independent learners.
What this means is that culture is significant in learning, language is necessary for culture, and people learn from others in their communities. Interacting with other people while developing, and even after, are how humans develop. Since we are a social species, it stands to reason that these concepts like MKOs and the significance of the cultural context in the acquisition of certain skills and learning play a significant role in the development of all children and even adults. Thus, each stage of the development of a child builds upon a previous stage, and so, play could also be seen as a form of learning—a form of sociocultural learning. Imaginative play, then, allows the self-regulation of children and also challenges them just enough in their ZPD.
Private speech
“Private speech” is when a child talks to themselves while they are performing a task (Alderson-Day and Fernyhough, 2015). It is one’s “inner speech”, their own “voice” in their heads. It is the act of talking to one’s self as they perform a task, and this is ubiquitous around the world, implying that it is a hallmark of human cognizing (Vissers, Tomas, and Law, 2020). This is basically the “voice” you head in your head as you live your daily life. It is, of course, a natural consequence of thinking and talking. Speech acts are a natural process of think acts, as Vygotsky argued, which is similar to Davidson’s (1982) argument against the possibility of animal mentality since for organisms to be thinking and rational they must be able to express numerous thoughts and interpret the speech of others. This kind of speech, furthermore, has been shown to been related to working memory and cognitive reflexivity (Skipper, 2022).
The zone of proximal development
The ZPD is what a learner can and cannot do without help. Vygotsky originally developed it to oppose the concept of “IQ” (Neugeurela, Garcia, and Buescher, 2015; Kazemi, Bagheri, and Rassei, 2020; Offori-Attah, 2021). This concept is perhaps the most-used and discussed concept that Vygotsky forwarded. Central to this concept, which is a part of Vygotsky’s overall theory of child development, is imitation. Imitation is a goal-directed activity, and so it is an action. There is intention behind the imitation because the imitator is copying what the MKO is doing. But Vygotsky was using “imitation” in a way that is not normally used. To be able to imitate, one has to be able to be able to do carry out the imitation of what they are seeing from the MKO. So Vygotsky’s concept of the ZPD is that a child can learn something that he doesn’t know how to do by imitating an MKO, having the MKO guide them through to complete the task. It has been argued that ZPD can improve a learner’s thinking ability, along with making learning more relevant and efficient to the learner since it gives the learner the ability to learn from instruction and having a MKO guide them to compete a task, which then becomes internalized (Abdurrahman, Abdullah, and Osman (2019).
So the ZPD indicates what a child can do independently, and then they are given harder, guided problems which they then imitate and further internalize. MKOs are able to recognize where a child is in their development and can help them then complete harder tasks. The ZPD is related to learning not only in school but also in play (Hakkarainen and Bredikyte, 2008). For instance, the Strong Museum of Play states that “Learners develop concepts and skills through meaningful play. Play supports physical, emotional, cognitive, and social development.” Children definitely learn from play, and this interactive kind of learning also has them better understand their body, since play is in part a physical activity (a guided, goal-directed, intention). Play is” developmentally beneficial (Eberle, 2014; UNICEF, 2018), and it is beneficial and related to the ZPD since a child can learn to do something either from a peer or coach that knows how to do the action they want to learn and then internalize. An individual that is playing is an active participant in their own learning. Play, in effect, creates the ZPD (Hakkarainen and Bredikyte, 2014). Though Vygotsky’s conception of “play” is different than used in common parlance. Play
is limited to the dramatic or make-believe play of preschoolers. Vygotsky’s play theory therefore differs from other play theories, which also include object-oriented exploration, constructional play, and games with rules. Real play activities, according to Vygotsky, include the following components: (a) creating an imaginary situation, (b) taking on and acting out roles, and (c) following a set of rules determined by specific roles (Bodrova & Leong, 2007). (Scharer, 2017: 63)
Further, “symbolic play may scaffold development because it facilitates infants’ communicative success by promoting them to ‘co-constructors of meaning’” (Creaghe and Kidd, 2022). “Play creates a zone of proximal development of the child. In play a child always behaves beyond his average age, above his daily behavior; in play it is as though he were a head taller than himself” (Vygotsky, 1978, 102 quoted in Gray and Feldman, 2004: 113).
The scaffolding occurs due to the relationship between play, the ZPD and what an individual then internalizes and then becomes embedded in their muscle memory. This is where MKOs come into play. When one is first learning to work out, they may seek out a personal knowledgeable in the mechanics of the human body to learn how to lift weights. Through instruction, they then begin to learn and then internalize the movements in their heads, and then they can just perform the lift well after successive attempts of doing a certain motion. Or take baseball. Baseball coaches would be the MKOs, and they then teach children to play baseball and they learn how to hit pitches, catch balls, throw and how to be a part of a team. Through the action of play, then, one can reach their ZPD and even extend it.
ZPD and IQ
Further, Vygotsky showed that the whether or not one has a large or small ZPD better “predicts” performance than does “IQ” and he also noted that those who scored higher on IQ tests “did so at the cost of their zone of proximal development“, since they exhaust their ZPD earlier leaving a smaller ZPD.
Vygotsky reported that not only did the size of the children’s ZPD turn out to correlate well with their success in school (large ZPD children were more successful than small ZPD children) but that ZPD size was actually a better predictor of school performance than IQ. (Poehner, 2008: 35; cf Smirni and Smirni, 2022)
It has even been experimentally demonstrated that children with high IQs have a smaller ZPD, children with low IQs have a larger ZPD (Kusmaryono and Kusmaningsih, 2021). It has also been shown that those who received ZPD scaffolding instruction improved more and even outperformed the other group on subsequent IQ tests after a first test was administered (Stanford-Binet and Mensa) (Ghelot, 2021). The responsiveness to remediation, and not “IQ” was a better predictor of school performance (Amini, Hassaskhah, and Sibet, 2017) and the degree of responsiveness wasn’t related to high or low IQ, since some learners had a high responsiveness and low score while others had a high score but low responsiveness (Poehner, 2017: 156). Those who took a test in one year and did not get better in subsequent years, Vygotsky argued, merely meant that they were not pushed outside of what they already know. So children with large ZPD were more likely to be successful irrespective of IQ while children with small ZPD were less likely to be successful, irrespective of IQ. Though the concepts of ZPD and IQ are seen as not contradictory, but related (Modarresi and Jeddy, 2021), quite clearly since “IQ” isn’t a measure of learning ability it merely shows what one has learned and so has been exposed to while the ZPD shows how one would do into the future due to how large their ZPD is. It shows not only where someone has reached, but also shows where they can reach. Thus, instead of the (undeserved) emphasis of IQ, we should therefore put the ZPD in its place, since it is a dynamic (relational) assessment and not a standardized test (Din, 2017).
What’s class got to do with it?
Since children acquire knowledge and beliefs based on their class background (what they are exposed to in their daily lives as they grow), then it follows that children will be differentially prepared for taking certain kinds of tests. So if the content on the tests is biased toward a group, then it is biased against a group. It is biased against a group since they are not exposed to the relevant material and kinds of thinking needed to be able to perform the test in a sufficient manner. Knowing what we now know about the acquisition of cultural and psychological tools, we can state that “high IQ may simply be an accident of immersion in middle-class cultural tools (aspects of literacy, numeracy, cultural knowledge, and so on) … the environment is made up of socially structured devices and cultural tools, and in which development consists of the acquisition of such cultural tools” (Richardson: 1998: 163-164). It is due to these considerations that culture-fair IQ tests are an impossibility, since people are encompassed in different cultures (what amount to learning environments where they acquire knowledge and cultural and psychological tools) are therefore an impossibility since abilities are cultural devices—culture-free tests are therefore an illusion (Cole, 2002; Richardson, 2002).
So if there are different cultural groups, then they by definition have different cultures. If they have different cultures, then they have different experiences (of course), and so, they acquire different kinds of knowledge and along with it cultural and psychological tools. It is then we can then rightly state that therefore different cultural groups would then be differentially prepared for doing certain tasks. And so, if one’s culture is more dominant and if one culture’s way of thinking is more prevalent, then it follows that people will be prepared for a certain test at different stages of being able to perform the tasks or answer the questions. Social status, also, isn’t merely just related to material things, it also influences how we think and act (Richardson and Jones, 2019) and so emotional and motivational—affective—factors would therefore play a role in one’s test score, since they are constructed from a narrow range of test items, constructed to get the results that were a priori to the test constructors. So since one’s class is related to affective factors, since IQ tests reflect mere class-specific items, it follows that the “affective state is one of the most important aspects of learning” (Shelton-Strong and Maynard, 2018). It is then, by using the concepts of cultural and psychological tools (which occur in social relations) that we can then rightly state that IQ tests are best looked at as mere class surrogates.
Conclusion
Basically, “in order to understand the individual, one must first understand the social relations in which the individual exists” (Wertsch, 1985: 63). Vygotsky’s theory is one in which the mind is formed and constructed through social and cultural interactions with those who are already immersed in the culture that the individual’s mind is developing in. And so, by using the concepts of cultural and psychological tools, we can then see how and why different classes are differentially prepared for taking tests, which is then reflected in the score outcomes. Since growing individuals learn what they are exposed to and they learn from those who are already immersed in the culture at large, then it follows that individuals learn culturally-specific forms of learning and thusly acquire different “tool sets” in which they then navigate the social world they are in. The concepts of private speech, cultural and psychological tools, MKO, scaffolding and the ZPD all coalesce to a theory of learning and development in which the learner is an active participant in their development, and so, these things also combine to show how and why groups score differently on IQ tests.
Knowledge is the content of thought, and the ability to speak is how we convey thoughts to others and how we actualize the thoughts we have into action. Thus all higher human cognitive functioning is social in nature (van der Veer, 2009). Though it is wrongly claimed that IQ is shown to be a measure of learning potential, it is rightly said that the ZPD is social in nature (Khalid, 2015). IQ doesn’t show one’s learning potential, it merely shows what one was or was not exposed to in regard to the relevant test items (Lavin and Nakano, 2017). Culture is a fluid and dynamic experience (Rublik, 2017) in which one is engrossed in the culture they are born into, and so, by understanding this, we can then understand why different groups of people score differently on IQ tests, without the need for genes or biological processes.
Though there have been good criticisms of Vygotsky’s socio-historical theory of learning and development. Though much of Vygotsky’s theorizing has led to predictions and do have some empirical support (Morin, 2012). One argument against the ZPD is that it doesn’t explain development or how it really occurs. If you think about development from a Vygotskian perspective, we see that it is as much of a cultural and social activity than is mere individual learning. By learning from people more knowledgeable than themselves, they are then able to learn how to do something, and through repetition, able to do it on their own without the MKO.
The fact of the matter is, IQ tests aren’t as good as either teacher assessment (Kaufman, 2019) or the ZPD in predicting where a learner will end up. It is for these reasons (and more) we should stop using IQ tests and we should us the relational ZPD. (One can also look at the ZPD as related to considerations from relational developmental systems theory as well; Lerner, 2011, 2013; Lerner, Johnson, and Buckingham, 2015; Ettekal et al, 2017; Bell, 2019). It is for these reasons that standardized tests should not be used anymore, and we should use tests of dynamic assessment. The empirical research on the issue bears out this claim.
The Case for Reparations for Black Americans
2050 words
Introduction
“Reparations” refers to the act or process of righting a historical wrong. Should we give reparations to black Americans, being that they are the descendants of slaves and thusly the reparations that would have been owed to them would be owed to their descendants? Also note that the slaves worked for free for hundreds of years, so untold amounts of money were stolen from them, so should we pay reparations to their descendants? Note that in most cases “should” claims and questions are moral claims and questions. Thus, this issue is one of morality. There is also the issue of Jim Crow laws and segregation. In this article I will argue that since the US government has given reparations to other groups it has wronged in the past, so too should black Americans receive reparations from the US government. Though I will not state exactly what or how much they should receive, I will cite some literature that speaks about it. I will merely argue that they should receive reparations. I will discuss one pro-argument and one anti-argument for reparations, and then give my own.
Reparations given to other groups in the past
Throughout the history of the United States, many heinous acts have been performed. Over the last 500+ years since colonialism, these people have been massacred and have had their identities almost erased systematically. In 1946, a commission was formed to hear grievances from Native Americans. The US government set aside 1.3 billion dollars for 173 tribes in 1946, but of course has been dodgy on payments. There is even a more recent push for reparations for Native Americans in California.
In WW2, about 127,000 Japanese were placed in internment camps, since it was worried that they would have been spying on America for Japan. (Most of these camps were near the west coast.) This was part of the anti-Asian sentiment of the time. In 1944 in Korematsu v. United States, SCOTUS upheld keeping Japanese Americans in these camps (a 6-3 decision). In 1988, the Regan administration gave $20,000 to each surviving internment camp prisoner, which is about $51,000 today. But the National Archives state:
The Japanese American Evacuation Claims Act of July 2, 1948, provided compensation to Japanese American citizens removed from the West Coast during World War II (WWII) for losses of real and personal property. Approximately 26,550 claims totaling $142,000 were filed. The program was administered by the Justice Department, which set a $100,000,000 limit on the total claims. Over $36,974,240 was awarded.
In the 1900s, America was under the spell of eugenic ideas. (Eugenic ideas go back centuries, to ancient Greece.) Eugenics wasn’t a theoretical or even mathematical idea, it was purely a social/political idea in that only the fit should breed (positive eugenics) and the unfit should not (negative eugenics). This then led to the forced sterilization, with “IQ” tests used as a vehicle for forced sterilization. The most famous case perhaps being that of Carry Buck, where a physician stated that her sterilization would be for the “good of society” since she scored low on an IQ test (the Binet)—Carrie had a mental age of 9 years while her mother Emma had a mental age of 7 years and 11 months, although Carrie’s daughter was actually quite a normal girl (Gould, 1984). Carrie was the first sterilization carried out in 1927 under a new law which states that epileptics and those who are feebleminded were to be sterilized. All in all, about 64,000 people were sterilized between 1907 and 1963, and the American Eugenics Society had sought to sterilize 1/10th of the US population (Farber, 2008). Some were even sterilized without their knowledge during the present day, showing gross misconduct on women’s bodily autonomy. Starting in 2022, the state of California paid out reparations to people who were sterilized during the eugenics movement and more recently people who were sterilized in their prison systems.
When it comes to reparations for black Americans, 77 percent of blacks agreed that descendants of enslaved people should receive reparations, while only 18 percent of whites agreed. About 3 in 10 US adults think that some form of reparations should be given to descendants of slavery, while about 68 percent believe that slavery descendants should not be paid, per Pew. It is estimated that it would take $10-12 trillion or $800,000 per black household to eliminate the black-white wealth gap. It has also been estimated that since the start of slavery, racism has cost blacks something along the lines of $70 trillion. Craemer et al (2020) argue that reparations should be something along the lines of $12-13 trillion. (Craemer estimates $20.3 trillion.) It has even been noted that wealth gaps between whites and blacks are associated with longevity differences between them, so reparations would close the gap some (Himmelstein et al, 2022). (Systemic racism also has a say in longevity differences, along with conscious or unconscious bias by physicians.) Nevertheless many white Americans reject the case for reparations due to, among other reasons, denying that there are lasting effects of slavery. , I won’t argue about how much reparations black Americans should receive, I will argue only if black Americans should receive reparations—and since other groups that were historically harmed in the US have received reparations, then it follows that black Americans should receive reparations.
As we can see from the above, the US government has given reparations to groups it has wronged in the past. But there is a good amount of philosophy on the morality of reparations and whether or not black Americans should receive reparations (which then becomes a moral argument). I will look at two of them—Bernard Boxill’s (2003) A Lockean Argument for Black Reparations (a pro-reparations argument) and Stephen Kershnar’s (2003) The inheritance-based claim for reparations (an anti-reparations argument). After I describe both arguments, I will then provide my own argument which I don’t think has been made in the literature that argues in favor of reparations for black Americans (though I won’t make any claims as to how much; I merely cited what some scholars have argued above.)
A pro-argument
Boxill developed two arguments in his paper—an inheritance argument and a counterfactual argument. Boxill (2003: 73) writes:
This reparation was never paid. Instead each white generation passed on its entire assets to the next white generation. I am not speaking of those few who inherited specific parcels of land or property from the supporters of slavery. I am speaking of whole generations. The whole of each generation of whites passed on its assets to the whole of the next white generation because each generation of whites specified that only whites of the succeeding generation were permitted to own or compete for the assets it was leaving behind. But as I have already shown, the slaves had titles to reparation against these assets. And we can assume that the present generation of African Americans are the slaves’ heirs. Hence the present generation of African Americans have inherited titles to a portion of the assets held by the present white population, with the qualification that they cannot insist on these titles if doing so would put the present white population in danger of perishing.
So this is how Boxill gets around a possible objection to the argument—many white Americans have inherited things from slave owners or who were complicit in slavery. This argument can be put in form like this:
(1) Slavery owners passed on assets to successive generations, with each generation passing on assets gained from slavery.
(2) Present-day black Americans are heirs to those who were enslaved.
(C) Therefore, the present white population owes reparations to the present black population in America since present white Americans are the heirs to assets that were gained through slavery of the descendants of present black Americans.
Danielson (2004) states the same, writing:
Some legal scholars suggest that the government should directly address the issue of reparations for slaves because America profited from slave labor for over two centuries, so America should compensate slaves for their labor. Slaves were deprived of fair wages for almost three hundred years and their descendents were therefore deprived of economic inheritance. The slave masters, ergo their descendents through inheritance, benefited from the withheld wages that rightfully belonged to their slaves.
So if a group of people that benefitted long ago from an action(s) still benefit today from said action(s), and the result of those actions was an untold amount of free and therefore stolen wages, it then follows that the group that benefitted from the action needs to pay reparations to the descendants of the group that was historically wronged.
An anti-argument
While Kershnar (1999) seems to provide a pro-argument for reparations based on inheritance, it seems that Kershnar (2002) has walked back on the claim and argues that inheritance-based claims for reparations fail. Kershnar (2002) argues that since slavery brought about the existence of black Americans, then without slavery there would be no black Americans and hence there would be no conversation about reparations. I don’t see how this matters—because the historical injustice DID happen, and so due to the moneys lost from free labor for hundreds of years, therefore, the case can be made that blacks are owed reparations.
He also argued that the US did not cause slavery, but it did permit it. This is true. However, it took a war to end slavery when the South attempted to secede from the US in order to continue the practice of slavery. It took the North winning the Civil War to abolish slavery. Though, the US government was implicit in slavery since its inception by allowing it to occur.
I will now provide and defense an argument that since other groups in the US were wronged in the past and have received reparations from the US government, so too should black Americans.
The case for reparations for black Americans argument
Here is my argument:
(P1) The US government has a history of giving reparations to people who have suffered injustices (like the Japanese and Natives).
(P2) Black Americans have suffered injustices (slavery, Jim Crow, segregation).
(C) So black Americans deserve reparations from the US government.
This argument uses modus ponens, so it is valid. P1 was argued for in the first section. P2 is common knowledge. So C would then follow—black Americans deserve reparations from the US government due to their ancestors being enslaved and the recent injustices they received in the 1900s during and after Reconstruction, leading up to the Civil Rights Movement of 1964. I don’t see how anyone could reject a premise and falsify the argument.
Conclusion
The legacy of slavery still continues today (most Americans today believe that the legacy of slavery still affects blacks today), and it’s partly reflected in low birth weights of black Americans (Jasienska, 2009). The untold negative effects of slavery have combined to further depress black Americans.
There is even a new bill in the works discussing what reparations for black Americans would look like, which will create a task force to study reparations for black Americans. One time has even argued that giving black Americans reparations would decrease COVID-19 transmission in black Americans (Richardson et al, 2021). One city—Evanston, Illinois—even enacted a plan to give reparations to black Americans and California has also stated that the legacy of slavery requires reparations too; they are now considering the next steps for reparations. Further, there is also a public health case for reparations. Seeing as the US Congress apologized for the enslavement of black Americans and segregation only in 2008, there is a better way to right these wrongs—not mere lip service—and that is to pay reparations to black Americans.
Slavery was a moral wrongdoing, and along with how blacks were treated after they were emancipated from the racist South (Jim Crow laws, segregation), this combines to create a powerful argument for the moral case for reparations for black Americans, since other groups in the country that were wronged received reparations, like victims of sterilization in the 1900s and new millennium, Japanese Americans during WW2, and Native Americans. Thus, it follows that black Americans, too, should receive reparations.
Black-White Differences in Anatomy and Physiology: Black Athletic Superiority
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Due to evolving in different climates, the different races of Man have differing anatomy and physiology. This, then, leads to differences in sports performance—certain races do better than others in certain bouts of athletic prowess, and this is due to, in large part, heritable biological/physical differences between blacks and whites. Some of these differences are differences in somatotype, which bring a considerable advantage for, say, runners (an ecto-meso, for instance, would do very well in sprinting or distance running depending on fiber typing). This article will discuss differences in racial anatomy and physiology (again) and how it leads to disparities in certain sports performance.
Kerr (2010) argues that racial superiority in sport is a myth. (Read my rebuttal here.) In his article, Kerr (2010) attempts to rebut Entine’s (2000) book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It. In a nutshell, Kerr (2010) argues that race is not a valid category; that other, nongenetic factors play a role other than genetics (I don’t know if anyone has ever argued if it was just genetics). Race is a legitimate biological category, contrary to Kerr’s assertions. Kerr, in my view, strawman’s Entine (2002) by saying he’s a “genetic determinist”, but while he does discuss biological/genetic factors more than environmental ones, Entine is in no way a genetic determinist (at least that’s what I get from my reading of his book, other opinions may differ). Average physical differences between races are enough to delineate racial categories and then it’s only logical to infer that these average physical/physiological differences between the races (that will be reviewed below) would infer an advantage in certain sports over others, while the ultimate cause was the environment that said race’s ancestors evolved in (causing differences in somatotype and physiology).
Black athletic superiority has been discussed for decades. The reasons are numerous and of course, this has even been noticed by the general public. In 1991, half of the respondents of a poll on black vs. whites in sports “agreed with the idea that “blacks have more natural physical ability,“” (Hoberman, 1997: 207). Hoberman (1997) of course denies that there is any evidence that blacks have an advantage over whites in certain sports that come down to heritable biological factors (which he spends the whole book arguing). However, many blacks and whites do, in fact, believe in black athletic superiority and that physiologic and anatomic differences between the races do indeed cause racial differences in sporting performance (Wiggins, 1989). Though Wiggins (1989: 184) writes:
The anthropometric differences found between racial groups are usually nothing more than central tendencies and, in addition, do not take into account wide variations within these groups or the overlap among members of different races. This fact not only negates any reliable physiological comparisons of athletes along racial lines, but makes the whole notion of racially distinctive physiological abilities a moot point.
This is horribly wrong, as will be seen throughout this article.
The different races have, on average, differing somatotypes which means that they have different anatomic proportions (Malina, 1969):
| Data from Malina, (1969: 438) | n | Mesomorph | Ectomorph | Endomorph |
| Blacks | 65 | 5.14 | 2.99 | 2.92 |
| Whites | 199 | 4.29 | 2.89 | 3.86 |
| Data from Malina (1969: 438) | Blacks | Whites |
| Thin-build body type | 8.93 | 5.90 |
| Submedium fatty development | 48.31 | 29.39 |
| Medium fleshiness | 33.69 | 43.63 |
| Fat and very fat categories | 9.09 | 21.06 |
This was in blacks and whites aged 6 to 11. Even at these young ages, it is clear that there are considerable anatomic differences between blacks and whites which then lead to differences in sports performance, contra Wiggins (1989). A basic understanding of anatomy and how the human body works is needed in order to understand how and why blacks dominate certain sports over whites (and vice versa). Somatotype is, of course, predicated on lean mass, fat mass, bone density, stature, etc, which are heritable biological traits, thus, contrary to popular belief that somatotyping holds no explanatory power in sports today (see Hilliard, 2012).
One variable that makes up somatotype is fat-free body mass. There are, of course, racial differences in fat mass, too (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000). Lower fat mass would, of course, impede black excellence in swimming, and this is what we see (Rushton, 1997; Entine, 2000). Wagner and Heyward (2000) write:
Our review unequivocally shows that the FFB of blacks and whites differs significantly. It has been shown from cadaver and in vivo analyses that blacks have a greater BMC and BMD than do whites. These racial differences could substantially affect measures of body density and %BF. According to Lohman (63), a 2% change in the BMC of the body at a given body density could, theoretically, result in an 8% error in the estimation of %BF. Thus, the BMC and BMD of blacks must be considered when %BF is estimated.
While Vickery, Cureton, and Collins (1988) found that blacks had thinner skin folds than whites, however, in this sample, somatotype did not explain racial differences in bone density, like other studies (Malina, 1969), Vickery, Cureton, and Collins (1988) found that blacks were also more likely to be mesomorphic (which would then express itself in racial differences in sports).
Hallinan (1994) surveyed 32 sports science, exercise physiology, biomechanics, motor development, motor learning, and measurement evaluation textbooks to see what they said racial differences in sporting performance and how they explained them. Out of these 32 textbooks, according to Wikipedia, these “textbooks found that seven [textbooks] suggested that there are biophysical differences due to race that might explain differences in sports performance, one [textbook] expressed caution with the idea, and the other 24 [textbooks] did not mention the issue.” Furthermore, Strklaj and Solyali (2010), in their paper “Human Biological Variation in Anatomy Textbooks: The Role of Ancestry” write that their “results suggest that this type of human variation is either not accounted for or approached only superficially and in an outdated manner.”
It’s patently ridiculous that most textbooks on the anatomy and physiology of the human body do not talk about the anatomic and physiologic differences between racial and ethnic groups. Hoberman (1997) also argues the same, that there is no evidence to confirm the existence of black athletic superiority. Of course, many hypotheses have been proposed to explain how and why blacks are at an inherent advantage in sport. Hoberman (1997: 269) discusses one, writing (quoting world record Olympian in the 400-meter dash, Lee Evans):
“We were bred for it [athletic dominance] … Certainly the black people who survived in the slave ships must have contained the highest proportion of the strongest. Then, on the plantations, a strong black man was mated with a strong black woman. We were simply bred for physical qualities.”
While Hoberman (1997: 270-1) also notes:
Finally, by arguing for a cultural rather than a biological interpretation of “race,” Edwards proposed that black athletic superiority results from “a complex of societal conditions” that channels a disproporitionate number of talented blacks into athletic careers.
The fact that blacks were “bred for” athletic dominance is something that gets brought up often but has little (if any) empirical support (aside from just-so stories about white slavemasters breeding their best, biggest and strongest black slaves). The notion that “a complex of societal conditions” (Edwards, 1971: 39) explains black dominance in sports, while it has some explanatory power in regard to how well blacks do in sporting competition, it, of course, does not tell the whole story. Edwards (1978: 39) argues that these complex societal conditions “instill a heightened motivation among black male youths to achieve success in sports; thus, they channel a proportionately greater number of talented black people than whites into sports participation.” While this may, in fact, be true, this does nothing to rebut the point that differences in anatomic and physiologic factors are a driving force in racial differences in sporting performance. However, while these types of environmental/sociological arguments do show us why blacks are over-represented in some sports (because of course motivation to do well in the sport of choice does matter), they do not even discuss differences in anatomy or physiology which would also be affecting the relationship.
For example, one can have all of the athletic gifts in the world, one can be endowed with the best body type and physiology to do well in any type of sport you can imagine. However, if he does not have a strong mind, he will not succeed in the sport. Lippi, Favaloro, and Guidi (2008) write:
An advantageous physical genotype is not enough to build a top-class athlete, a champion capable of breaking Olympic records, if endurance elite performances (maximal rate of oxygen uptake, economy of movement, lactate/ventilatory threshold and, potentially, oxygen uptake kinetics) (Williams & Folland, 2008) are not supported by a strong mental background.
Any athlete—no matter their race—needs a strong mental background, for if they don’t, they can have all of the physical gifts in the world, they will not become top-tier athletes in the sport of their choice; advantageous physical factors are imperative for success in differing sports, though myriad variables work in concert to produce the desired effect so you cannot have one without the other. On the other side, one can have a strong mental background and not have the requisite anatomy or physiology needed to succeed in the sport in question, but if he has a stronger mind than the individual with the requisite morphology, then he probably will win in a head-to-head competition. Either way, a strong mind is needed for strong performance in anything we do in life, and sport is no different.
Echoing what Hoberman (1997) writes, that “racist” thoughts of black superiority in part cause their success in sport, Sheldon, Jayaratne, and Petty (2007) predicted that white Americans’ beliefs in black athletic superiority would coincide with prejudice and negative stereotyping of black’s “intelligence” and work ethic. They studied 600 white men and women to ascertain their beliefs on black athletic superiority and the causes for it. Sheldon, Jayaratne, and Petty (2007: 45) discuss how it was believed by many, that there is a “ perceived inverse relationship between athleticism and intelligence (and hard work).” (JP Rushton was a big proponent of this hypothesis; see Rushton, 1997. It should also be noted that both Rushton, 1997 and Entine, 2000 believe that blacks’ higher rate of testosterone—3 to 15 percent— [Ross et al, 1986; Ellis and Nyborg, 1992; see rebuttal of both papers] causes their superior athletic performance, I have convincingly shown that they do not have higher levels of testosterone than other races, and if they do the difference is negligible.) However, in his book The Sports Gene: Inside the Science of Extraordinary Athletic Performance, Epstein (2014) writes:
With that stigma in mind [that there is an inverse relationship between “intelligence” and athletic performance], perhaps the most important writing Cooper did in Black Superman was his methodological evisceration of any supposed inverse link between physical and mental prowess. “The concept that physical superiority could somehow be a symptom of intellectual superiority became associated with African Americans … That association did not begin until about 1936.”
What Cooper (2004) implied is that there was no “inverse relationship” with intelligence and athletic ability until Jesse Owens blew away the competition at the 1936 Olympics in Berlin, Germany. In fact, the relationship between “intelligence” and athletic ability is positive (Heppe et al, 2016). Cooper is also a co-author of a paper Some Bio-Medical Mechanisms in Athletic Prowess with Morrison (Morrison and Cooper, 2006) where they argue—convincingly—that the “mutation appears to have triggered a series of physiological adjustments, which have had favourable athletic consequences.”
Thus, the hypothesis claims that differences in glucose conversion rates between West African blacks and her descendants began, but did not end with the sickling of the hemoglobin molecule, where valine is substituted for glutamic acid, which is the sixth amino acid of the beta chain of the hemoglobin molecule. Marlin et al (2007: 624) showed that male athletes who were inflicted with the sickle cell trait (SCT) “are able to perform sprints and brief exercises at the highest levels.” This is more evidence for Morrison and Cooper’s (2006) hypothesis on the evolution of muscle fiber typing in West African blacks.
Bejan, Jones, and Charles (2010) explain that the phenomenon of whites being faster swimmers in comparison to blacks being faster runners can be accounted for by physics. Since locomotion is a “falling-forward cycle“, body mass falls forward and then rises again, so mass that falls from a higher altitude falls faster and forward. The altitude is set by the position of center of mass above the ground for running, while for swimming it is set by the body rising out of the water. Blacks have a center of gravity that is about 3 percent higher than whites, which implies that blacks have a 1.5 percent speed advantage in running whereas whites have a 1.5 percent speed advantage in swimming. In the case of Asians, when all races were matched for height, Asians fared even better, than whites in swimming, but they do not set world records because they are not as tall as whites (Bejan, Jones, and Charles, 2010).
It has been proposed that stereotype threat is part of the reasons for East African running success (Baker and Horton, 2003). They state that many theories have been proposed to explain black African running success—from genetic theories to environmental determinism (the notion that physiologic adaptations to climate, too, drive differences in sporting competition). Baker and Horton (2003) note that “that young athletes have internalised these stereotypes and are choosing sport participation accordingly. He speculates that this is the reason why white running times in certain events have actually decreased over the past few years; whites are opting out of some sports based on perceived genetic inferiority.” While this may be true, this wouldn’t matter, as people gravitate toward what they are naturally good at—and what dictates that is their mind, anatomy, and physiology. They pretty much argue that stereotype threat is a cause of East African running performance on the basis of two assertions: (1) that East African runners are so good that it’s pointless to attempt to win if you are not East African and (2) since East Africans are so good, fewer people will try out and will continue the illusion that East Africans would dominate in middle- and long-distance running. However, while this view is plausible, there is little data to back the arguments.
To explain African running success, we must do it through a systems view—not one of reductionism (i.e., gene-finding). We need to see how the systems in question interact with every part. So while Jamaicans, Kenyans, and Ethiopians (and American blacks) do dominate in running competitions, attempting to “find genes” that account for success n these sports seems like a moot point—since the whole system is what matters, not what we can reduce the system in question to.
However, there are some competitions that blacks do not do so well in, and it is hardly discussed—if at all—by any author that I have read on this matter. Blacks are highly under-represented in strength sports and strongman competitions. Why? My explanation is simple: the causes for their superiority in sprinting and distance running (along with what makes them successful at baseball, football, and basketball) impedes them from doing well in strength and strongman competitions. It’s worth noting that no black man has ever won the World’s Strongest Man competition (indeed the only African country to even place—Rhodesia—was won by a white man) and the causes for these disparities come down to racial differences in anatomy and physiology.
I discussed racial differences in the big four lifts and how racial differences in anatomy and physiology would contribute to how well said race performed on the lift in question. I concluded that Europeans and Asians had more of an advantage over blacks in these lifts, and the reasons were due to inherent differences in anatomy and physiology. One major cause is also the differing muscle fiber typing distribution between the races (Alma et al, 1986; Tanner et al, 2002; Caesar and Henry, 2015 while blacks’ fiber typing helps them in short-distance sprinting (Zierath and Hawley, 2003). Muscle fiber typing is a huge cause of black athletic dominance (and non-dominance). Blacks are not stronger than whites, contrary to popular belief.
I also argued that Neanderthals were stronger than Homo sapiens, which then had implications for racial differences in strength (and sports). Neanderthals had a wider pelvis than our species since they evolved in colder climes (at the time) (Gruss and Schmidt, 2016). With a wider pelvis and shorter body than Homo sapiens, they were able to generate more power. I then implied that the current differences in strength and running we see between blacks and whites can be used for Neanderthals and Homo sapiens, thusly, evolution in differing climates lead to differences in somatotype, which eventually then lead to differences in sporting competition (what Baker and Horton, 2003 term “environmental determinism” which I will discuss in the context of racial differences in sports in the future).
Finally, blacks dominate the sport of bodybuilding, with Phil Heath dominating the competition for the past 7 years. Blacks dominate bodybuilding because, as noted above, blacks have thinner skin folds than whites, so their striations in their muscles would be more prevalent, on average, at the same exact %BF. Bodybuilders and weightlifters were similar in mesomorphy, but the bodybuilders showed more musculature than the bodybuilders whereas the weightlifters showed higher levels of body fat with a significant difference observed between bodybuilders and weightlifters in regard to endomorphy and ectomorphy (weightlifters skewing endo, bodybuilders skewing ecto, as I have argued in the past; Imran et al, 2011).
To conclude, blacks do dominate American sporting competition, and while much ink has been spilled arguing that cultural and social—not genetic or biologic—factors can explain black athletic superiority, they clearly work in concert with a strong mind to produce the athletic phenotype, no one factor has prominence over the other; though, above all, if one does not have the right mindset for the sport in question, they will not succeed. A complex array of factors is the cause of black athletic dominance, including muscle fibers, the type of mindset, anatomy, overall physiology and fat mass (among other variables) explain the hows and whys of black athletic superiority. Cultural and social explanations—on their own—do not tell the whole story, just as genetic/biologic explanations on their own would not either. Every aspect—including the historical—needs to be looked at when discussing the dominance (or lack thereof) in certain sports along with genetic and nongenetic factors to see how and why certain races and ethnies excel in certain sports.
Explaining African Running Success Through a Systems View
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Last year I bought The Genius in All of Us: New Insights Into Genetics, Talent, and IQ (Shenk, 2010) and while the book is interesting and I agree with a few things he says, he gets it horribly wrong on athleticism and ethnicity. Some of it I may be able to forgive since the book was written in 2010, but he does make some glaring errors. Chapter 6—pages 100-111—is titled Can White Men Jump? Ethnicity, Genes, Culture, and Success.
In the beginning of the chapter, Shenk writes that after the 2008 Beijing Summer Olympics, many articles were written about the Jamaican women who took the top three spots in the 100 and 200m races, with the emergence of Usain Bolt and his record-setting performance. Shenk (2010: 101) writes:
The powerful protein [alpha-actinin-3] is produced by a special gene variant called ACTN3, at least one copy of which is found in 98 percent of Jamaicans—far higher than in many other ethnic populations.
An impressive fact, but no one stopped to do the math. Eighty percent of Americans also had at least one copy of ACTN3—that amounts to 240 million people. Eighty-two percent of Europeans have it as well—that tacks on another 597 million potential sprinters. “There’s simply no clear relationship between the frequency of this variant in a population and its capacity to produce sprinting superstars,” concluded geneticist Daniel MacArthur.
I have written about MacArthur’s thoughts on the ACTN3 variant—that he helped discover, no less—in an article on Jamaicans, Kenyans, and Ethiopians and the explanatory factors in regard to their success in running competitions. Though, the article from MacArthur was written in 2008 and Shenk’s book was written in 2010, considerable advances have been made in this field. It was found that “combined effects of morphological and contractile properties of individual fast muscle fibers attribute to the enhanced performance observed in RR genotypes during explosive contractions” (Broos et al, 2016). Of course when talking about sprinting and morphology, you must think of the somatype. The somatype that is conducive to running success is a tall, lanky body with long limbs, as longer limbs can cover more distance. So European runners don’t have the right somatype, nor are the XX genotype for the ACTN3 variant high in Jamaicans (this genotype is present in ~2 percent of the Jamaican population; Scott et al, 2010). This—among other reasons I have laid out in the past—are why Jamaicans excel in sprinting competitions compared to other ethnic groups.
Shenk (2014: 10) further writes that sports success seem to come in ‘geographic clusters’, and the field of sports geography has been developed to understand it. “What they’ve discovered is that there’s never a single cause for a single cluster,” Shenk writes. “Rather, the success comes from many contributions of climate, media, demographics, politics, training, spirituality, education, economics and folklore. In short, athletic clusters are not genetic, but systemic.” Shenk then discusses the fact that these explanations are not good enough and that some ‘sports geographers’ have transformed themselves into ‘sports geneticists’ and then cites Jon Entine’s 2002 book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It where Shenk quotes Entine who quotes geneticist and physiologist Claude Bouchard who says that “these biological characteristics are not unique to West or East African blacks. These populations are seen in all populations, including whites” (Shenk, 2010: 102). Of course they’re not unique to one population and I don’t think that anyone has ever claimed that. Though the frequencies of these biological, morphological and physiological characteristics are not distributed evenly amongst populations and this explains how and why certain populations excel in certain sports when compared to others.
Shenk (2010: 102) also quotes Entine (2002), writing: “Entine also acknowledges that we haven’t actually found the actual genes he’s alluding to. “These genes will likely be identified early in the [twenty-first century],” he predicts.” We have ‘found some genes’ that aid in athletic performance, the ACTN3 genotype combined with type II fibers and the right morphology, as mentioned above for one. (Though a systems view—one of holism—makes much more sense here than a reducionist view. You must look at the whole system, not reduce things down, but that’s for another day.) That, in my opnion, is a large driver for ethnic differences in sports like this, because you need certain traits if you want to excel in these types of competitions.
He then discusses the success of the Kenyans in distance running—stating that 90 percent of Kenyan runners come from a small subset of Kenyans called the Kalenjin. He cites a few stories of some Kalenjin who talk about their experiences with no running water in their homes and that they had to “run to the river, to take your shower, run home, change, [run] to school . . . Everything is running” (Keino, a Kalenjin boy, quoted from Shenk, 2010: 104). Of course this is attributed to a multitude of factors, all of which have to work in concert to get the desired effect. For instance, sports psychologists have found that strong cultural achievement and the ability to work hard, compete, outdo others and seek new challenges drives their running dominance.
Shenk (2010: 106-107) then writes:
1.DESPITE APPEARANCES TO THE CONTRARY, RACIAL AND ETHNIC GROUPS ARE NOT GENETICALLY DISCRETE.
Skin color is a great deceiver; actual genetic differences between ethnic and geographic groups are very, very limited. All human beings are descended from the same African ancestors … [blah blah blah] … By no stretch of the imagination, then, does any ethnicity or region have an exclusive lock on a particular body type or secret high-performance gene. Body shapes, muscle fiber types, etc., are actually quite varied and scattered, and true athletic potential is widespread and plentiful.
Of course, I don’t think I have ever read anyone who denies this. However, as I’ve noted too many times to count, certain body types and muscle fiber distributions are more likely to be found in certain populations due to where their ancestors evolved recently, and so the fact that ‘actual genetic differences between ethnic and geographic groups are very, very, limited’ does not mean much when talking about dominance by a few populations in elite sporting competition. It just so happens to be the case that the somatypes and muscle fiber distributions that are conducive to running success are more likely to be found in populations of West and East African descent. This is an undeniable fact. (Also note how these ‘appearances to the contrary’ show how race is real.)
2.GENES DON’T DIRECTLY CAUSE TRAITS; THEY ONLY INFLUENCE THE SYSTEM.
Consistent with other lessons of GxE [Genes x Environment], the surprising finding of the $3 billion Human Genome Project is that only in rare instances do specific gene variants directly cause specific traits or diseases. …
As the search for athletic genes continues, therefore, the overwhelming evidence suggests that researchers will instead locate genes prone to certain types of interactions: gene variant A in combination with gene variant B, provoked into expression by X amount of training + Y altitude + Z will to win + a hundred other life variables (coaching, injuries, etc.), will produce some specific result R. What this means, of course, What this means, of course, is that we need to dispense rhetorically with thick firewall between biology (nature) and training (nurture). The reality of GxE assures that each persons genes interacts with his climate, altitude, culture, meals, language, customs and spirituality—everything—to produce unique lifestyle trajectories. Genes play a critical role, but as dynamic instruments, not a fixed blueprint. A seven- or fourteen- or twenty-eight-year-old is not that way merely because of genetic instruction. (Shenk, 2010: 107)
Nothing really wrong here. He is correct, which is why you need to look at the whole biological system, which also includes the culture, climate, environment and so on that the biological, developmental system finds itself in. However, Shenk then gets it wrong again writing that Jamaicans are a ‘quite heterogenous genetic group’ due to being a transport between North and South America. He states—correctly—that Jamaicans ancestry is about equal to that of African-Americans, but the individual variation in ancestry varies by “46.8 to 97.0 percent” (Shenk, 2010: 108).
Shenk gets a lot wrong here. For example. African-American and Jamaicans—despite both being descended from slave populations—have differing maternal ancestry which somehow influences athletic success. Deason (2017) found that 1) modern Jamaicans are descended from slaves and, who had considerable selective pressure on the population; 2) maternal ancestry could either influence sports success or be a false positive; 3) maternal lineages were different in Jamaicans and African-Americans, implying that the same maternal lineage is not distributed evenly between both sprinting populations; 4) some evidence exists that the genetic histories of Jamaicans and African-Americans are different based on their maternal haplotypes; 5) low SES and low access to healthcare—classic indicators of high African ancestry—were not directly linked to elite athletic success; 6) comparisons of the genomes of African-Americans and Jamaicans did not significantly differ since the estimated number of generations since admixture occurred, which implies that controls were not more likely to have more recent European ancestry than athletes; and 7) the regions of the genome that influence sprinting performance may be different in both populations. This is the best evidence to date against Shenk’s simplistic notions of the genetics between Jamaicans and African-Americans.
Differences in fast twitch fibers between Europeans and West Africans explain a large amount of the variance between Europeans and West African descendants in regard to sprinting success, while those with more symmetrical knees and ankles tend to run faster in the 100m dash (Trivers et al, 2014). This would also imply that Jamaicans have more symmetry in their knees and ankles than Europeans, though I am not aware of data that makes this comparison.
Shenk finally discusses the psycho-social-cultural aspects behind the phenomenon, stating that Roger Bannister, the first person to break the four minute mile, stated that while “biology sets limits to performance, it is the mind that plainly determines how close individuals come to those absolute limits” (Shenk, 2010: 110-111). Numerous psychological factors do, indeed, need to combine in order for the individual in question to excel in sports—along with the requisite anatomical/physiological/morphological traits too. Sasaki and Sekiya note that “changes in physiological arousal and movement velocuty induced by mild psychological pressure played a significant role in the sprint performance.” (See also Bali, 2015.)
Lippi, Favaloro, and Guidi, (2008) note how “An advantageous physical genotype is not enough to build a top-class athlete, a champion capable of breaking Olympic records, if endurance elite performances (maximal rate of oxygen uptake, economy of movement, lactate/ventilatory threshold and, potentially, oxygen uptake kinetics) (Williams & Folland, 2008) are not supported by a strong mental background.” I have argued this for months, even if the beneficial somatype is there in the athlete in question, if he/she does not have the will to win they will not succeed in their goals. Psychosocial factors, of course, matter just as much as the physical but all of these factors work in concert to get the outcomes that occur in these sports.
Attempting to pinpoint one or a few traits—while it may help us to understand better physilogic and anatomic processes—tells us nothing about the entire system. This is why, for instance, the whole athletes system needs to be looked at—call it the ‘systems view of the athlete’, where all of these aforementioned variables work in concert to express elite athletic performance, with no one variable being higher than another as an explanatory factor in sports success. Though Shenk gets a few things right (like his point on genes not causing traits on their own, they just influence the system, and I’d take it a step further to note that genes are passive in their relationship to the physiological system as a whole and are only activated by the system as needed, not being ’causes’ on their own; Noble, 2008), he’s largely misguided on how certain aspects of Jamaican ancestry and morphology help propel them to running success in comparison to other ethnies.
When explaining elite athletic performance in certain areas of sports, you must take a view of the whole system, with each known variable influencing the next in the chain, if you want to explain why certain ethnies or racial groups do better in a given sport than other groups. A systems view is the only view to take when comparing populations in different athletic competitions. So the influence of culture, psychology, social effects, morphology, ancestry, anatomy, physiology, muscle fibers, etc all work in concert to produce elite athletic phenotypes that then excel in these sports, and reducing this down to certain variables—while it may help us understand some of the inner mechanics—it does nothing to help advance the hows and whys of elite success in sports competition when comparing different populations.
Blood Pressure, Stress, and the Social Environment: On Black-White Differences in Blood Pressure
1800 words
Blood pressure (BP) is a physiological variable. Therefore since it is a physiological variable then it can be affected by environmental and social changes. How do racial differences come into play here, for instance? Since blacks face more (perceived) discrimination, then they should, on average, have higher BP levels than whites. This is what we find—but the effect is mostly seen in low-income blacks. How do psychosocial factors come into play here in the black-white BP gap?
BP is regulated by cardiac output, vascular resistance of blood flow, blood volume, arterial stiffness, and, of course, the individual’s emotional state which can decrease or increase BP. Neural mechanisms also exist which regulate BP (Chopra, Baby, and Jacob, 2011). Knowing how and why BP increases or decreases will have us better understand the social contexts of increased BP in low SES blacks.
BP is a complex physiological trait. It can go up and down due to what occurs in the immediate environment. Values of 120/80 mmHg are cited as ‘average’ values, but we have no idea what an ‘average’ BP is. Nevertheless—like most/all physiological variables—there is a wide range of what is considered ‘normal’. Due to the variance in human physiological systems, what is ‘normal’ for one individual is not ‘normal’ for another. Variation in BP (like, say, 120 SBP (systolic blood pressure) to 140 SBP) is ‘normal’. I believe even around 110 for SBP is within that range. For DPB (diastolic blood pressure) between 75 and 90 is within normal diurnal fluctuations due to activity/eating/etc (Taylor, Wilt, and Welch, 2011). BP, like testosterone, is one of those tricky variables to measure and so must be measured upon waking to see if there are any problems. So even for a trait like BP, there seems to be a ‘normal range’.
About 33 percent of blacks have hypertension (HTN) (Peters, Arojan, and Flack, 2006). Urban blacks are more likely to have higher BP levels than whites, but “At present, there is no complete explanation for these differences and further research is required” (Lindhorst et al, 2007). Low SES is correlated with higher levels of BP in black Americans—especially those with darker skin—but not Africans in Africa (Fuchs, 2011), suggesting that this is an American phenomenon that needs to be addressed. One good explanation, in my view, is the social environment. Physiological traits are extremely malleable due to the need to be able to ‘change gears’ in an instant, for instance to either fight or flight. Though, in our modernized world, these responses—mostly—have no need and so (due to our supposed civilized behavior), one’s BP rises due to social stress and other environmental factors and it is due to the urban environment.
What is the cause of high BP in blacks?
One explanation that has been given to explain higher rates of BP in blacks when compared to whites is discrimination. However, studies show mixed evidence on whether or not so-called discrimination raises BP (Couto, Goto, and Bastos, 2012). The same American effect (American blacks having higher BP than American whites) is seen even in the UK London area (Agyemang and Bhopal, 2003). This, yet again, is more evidence that the social environment drives these differences—again, regardless of whether or not any of the discrimination is real or imagined. Say most of it were imagined: it’d be irrelevant because the imagined discrimination leads to very real physiological outcomes in BP.
The country of birth also has an effect on BP. In one study, it was noted that Africans had significantly higher BP when compared to Asians (which is identical/lower) and native French living in France (Bahous et al, 2015). Ethnic differences in BP increase due to similar sodium intake is lower than what is usually cited (Graudal and Jurgens, 2015). However, other authors have pointed out that basing conclusions off of observational studies have problems, like the estimation of sodium intake being inaccurate since it’s a one-time measure; (Gunn et al, 2013; Cobb et al, 2014)
There is also evidence—along with pathways—that show how certain social activities work to lower stress and BP, including participation at church (Livingstone, Devine, and Moore, 1991). Black Americans can make other lifestyle changes in order to decrease BP, such as exercise and other lifestyle interventions. Redman, Baer, and Hicks state that “gene-environment interactions, job-related stress, racism, and other psychosocial factors to racial/ethnic disparities” need to be explored as causes for higher rates of HTN in blacks compared to whites. And with the knowledge of how all physiological systems work in terms of stress and other factors, should be explored as causes for this disparity.
Grim et al (1990) state that factors that influence high BP in blacks compared to whites are inherited and that is the major source of variation between these populations. However, the other mounting social/physiological evidence deserves an explanation; that is not inherited, and what we know about how our physiology responds to stress and discrimination—whether real or imagined—are extremely important and lead to extremely real, and important, outcomes in these populations. It is also argued that since blacks en route to America during the slave trade died from salt-depletive diseases, that blacks with a higher genetic propensity to absorb salt survived and this is why blacks have a higher propensity to absorb salt and are more ‘salt-sensitive’, which also could explain higher rates of HTN in American blacks compared to their cousins in Africa (Wilson and Grim, 1991). However, Curtin (1992) disputes this because “There is no evidence that diet or the resulting patterns of disease and demography among slaves in the American South were significantly different from those of other poor southerners”.
However, in regards to the social environment, Williams (1992) drives one of the best arguments I have encountered in this literature so far, stating that while genetic factors play a small part in regards to the BP gap between blacks and whites, social factors are arguably more important than genetic ones (and with our homeodynamic physiology, this does make sense). Dressler (1990) for instance, argues that skin color is a proxy for both social class and discrimination and these factors explain a large amount of the variation. Psychosocial variables can also explain heightened BP (Marmot, 1985; Cuffee et al, 2014). Yan et al (2003) also note how “time urgency/impatience” and “hostility” “were associated with a dose-response increase in the long-term risk of hypertension.” Henry (1988) also argues that calcium, obesity and genetic factors cannot be the aetiology of HTN in blacks, while also proposing that high sodium intakes are due to psychosocial stress (Williams, 1992: 136).
Obesity also leads to hypertension (Re, 2009) while blacks are more likely to be obese than whites, however, black American men with more African ancestry are less likely to be obese (Klimentidis et al, 2016). This would imply that the greater amount of African ancestry in American blacks both protects against obesity and along with it HTN. Williams (1992) makes a convincing argument that environmental and social factors are the cause for the black-white BP gap. And while genetic factors are important, no doubt, environmental and social factors are arguably more important to this debate.
Kulkarni et al (1998) show that increased stress leads to subsequent BP elevations which, over time, will lead to HTN. In a 2009 meta-analysis, Gasparin et al show how “individuals who had stronger responses to stressor tasks were 21% more likely to develop blood pressure increase when compared to those with less strong responses.”
Further, in support for the ‘perceived stress’ hypothesis in regards to blacks ‘perceiving’ stress and discrimination, “stress denial in combination with abdominal obesity, alcohol consumption, and smoking may be proxy for a high stress level” (Suter et al, 1997). Carroll et al (2001) also show how there are is “modest support for the hypothesis that heightened blood pressure reactions to mental stress contribute to the development of high blood pressure.” Sparrenberger et al (2009) also did a systematic review of observational studies, finding that “Acute stress is probably not a risk factor for hypertension. Chronic stress and particularly the non-adaptive response to stress are more likely causes of sustained elevation of blood pressure.”
Lastly, Langford (1981) shows that when SES is controlled for, the black-white BP disparity vanishes, implying that social and environmental—not genetic—factors are the cause for elevated HTN levels in black Americans. Sweet et al (2007) showed that for lighter-skinned blacks, as SES rose BP decreased while for darker-skinned blacks BP increased as SES did while implicating factors like ‘racism’ as the ultimate causes. This is solid evidence that both skin color and SES are predictors of higher prevalence of BP in black populations, and since other studies show that this is not noticed in higher class blacks, nor is this noticed in blacks in Africa, then the main causes of this disparity are social and environmental in nature.
(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 a very convincing argument that education and not genetic ancestry cause disparities in BP between blacks and whites.
WebMD states that, of course, both environmental and genetic factors are at play in regards to black’s increased propensity for acquiring HTN. Fuchs (2011) also states that “They [environmental and behavioral factors] could act directly or by triggering mechanisms of blood pressure increase that are dormant in blacks living in Africa” and explain why black Americans have higher rates of BP than Africans in Africa. Further, race and ethnicity are independent predictors of HTN (Holmes et al, 2013).
Conclusion
Blacks and whites do differ in BP, and its aetiology is both complex and hard to untangle Genetic factors probably don’t account for a lot of this variance since Africans in Africa have low levels of BP compared to their black American cousins. Numerous lines of evidence shows that social and environmental factors are the cause, and so to change this, all people—especially blacks—should be educated on how to change these problems in our society. Whether discrimination is real or imagined, the effects of it lead to real physiological outcomes that then lead to increased health disparities between these populations.
Sex Differences in Aggressive Behavior and Testosterone
1700 words
Many long-time readers may know of the numerous tirades of been on in regards to the “testosterone causes crime and aggression” myth. It’s a fun subject to talk about because the intelligent human physiological system is an amazing system. However, people who are not privy to the literature on testosterone in regards to race, aggression, crime, sex differences etc are only aware of whatever they read in pop science articles. So since they never read the actual papers themselves, they get a clouded view of a subject.
In my last article, I wrote about how there are no “testosterone genes”. In previous articles on the hormone, I have proven that there is no causal link between testosterone and aggression. But when comparing the sexes, how do the results look? Do they look the same with men being more violent while women—who have substantially less testosterone than men—do not have any higher levels of aggression or crime? The most recent study I’m aware of is by Assari, Caldwell, and Zimmerman (2014) titled: Sex Differences in the Association Between Testosterone and Violent Behaviors.
To make a long story short, there was no relationship between testosterone and aggression in men, but a significant relationship between testosterone and aggression in women. This data comes from the Flint Adolescent Study, a longitudinal study conducted between the years of 1994 to 2012. In regards to testosterone collection, saliva was used which has a perfect correlation with circulating testosterone. The eligibility to be included in the testosterone assay was “provided consent for the procedure, not being pregnant, not having anything to eat, drinking nothing except water, and not using tobacco, 1 hour prior to collection” (Assari, Caldwell, and Zimmerman, 2014).
The adolescent who contributed saliva gave a whole slew of demographic factors including SES, demographics, psychological factors, family relations, religion, social relations, behavior, and health. They were aged 14 to 17 years of age. They collected data during face-to-face interviews,
Age and SES were used as control variables in their multivariate analysis. For violent behaviors, the authors write:
Youths were asked how often they had engaged in the following behaviors; ‘had a fight in school’, ‘taken part in a rumble where a group of your friends were against another group’, injured someone badly enough to need bandages or a doctor’, ‘hit a teacher or supervisor at work (work supervisor)’, used a knife or gun or other object (like a club) to get something romantic a person’, ‘carried a knife or razor’, or ‘carried a gun’. All items used a Likert response, ranging from 1 (0 times) to 5 (4 or more times). Responses to each item were averages to calculate the behavior during the last year. Total score was calculated as the average of all items. Higher scores indicated more violent behaviors (a = 0.79). This measure has shown high reliability and validity and it has been used previously in several published reports.
This is a great questionnaire. The only thing I can think of that’s missing is fighting/arguing with parents.
In regards to testosterone assaying, they were assayed after 11 am to “control for changes due to diurnal rhythm” (Assari, Caldwell, and Zimmerman, 2014). I’m iffy on that since testosterone levels are highest at 8 am but whatever. This analysis is robust. Saliva was not taken if the subject had smoked or ingested something other than water or if a subject was pregnant. Assays should be taken as close to 8 am, as that’s when levels are highest. However one study does argue to extend the range to 8 am to 2 pm (Crawford et al, 2015) while other studies show that this only should be the case for older males (Long, Nguyen, and Stevermer, 2015). Even then assays were done at the higher end of the range as stated by Crawford et al (2015), so differences shouldn’t be too much.
86.4 percent of the sample was black whereas 13.4 percent were white. 41.2 percent of the subjects had some college education whereas 58.2 percent of the subjects lived with a partner or relative. 21.4 percent of the subjects were unemployed.
The mean age was 20.5 for both men and women, however, which will be a surprise to some, testosterone did not predict aggressive behavior in men but did in women. Testosterone and aggressive behavior were positively correlated, whereas there was a negative correlation between education and testosterone and aggressive behavior. Though education was associated with aggressive behavior in men but not women. So sex and education was associated with aggressive behavior (the sex link being women more privy to aggressive behavior while men are more privy to aggressive behavior due to lack of education). Females who had high levels of education had lower levels of aggressive behavior. Again: testosterone wasn’t associated with violent behavior in men, but it was in women. This is a very important point to note.
This was a community sample, so, of course, there were different results when compared to a laboratory setting, which is not surprising. Laboratory settings are obviously unnatural settings whereas the environment you live in every day obviously is more realistic.
This study does contradict others, in that it shows that there is no association between testosterone and aggression in men. However, still other research shows that testosterone is not linked to aggression or impulsivity, but to sensation-seeking, sexual experience or sociality (Daitzman and Zuckerman, 1980; Zuckerman, 1984). Clearly, testosterone is a beneficial hormone and due to the low correlation of testosterone with aggression (between .08 and .14; Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005). This paper, yet again, buttresses my arguments in regards to testosterone and aggressive behavior.
In regards to the contrast in the literature the authors describe, they write:
One of the many factors that may explain the inconsistency in these findings is the community versus clinical setting, which has been shown to be a determinant of these associations. Literature has previously shown that many of the findings that can be found in clinical samples may not be easily replicated in a community setting (36).
This is like the (in)famous, unreplicable stereotype threat (see Stroessner and Good). It can only be replicated in a lab, not in an actual educational setting. And it also seems that this is the case for testosterone and aggressive behavior.
Just because women have lower testosterone and are less likely to engage in aggressive behavior, that doesn’t mean that a relationship does not exist between females. “It is also plausible to attribute sex differences in the above studies to differential variations in the amount of testosterone among men and women” (Assari, Caldwell, and Zimmerman, 2014). This view supports the case that testosterone is linked to aggression in females, even though their range of testosterone is significantly lower than men’s, while it may also be easier to assay women for testosterone due to less diurnal variation in comparison to men (Book, Starzyk, and Quinsey, 2001).
Assari, Caldwell, and Zimmerman, (2014) also write (which, again, buttresses my arguments):
Age may explain some of the conflicting results across the studies. A meta-analysis of community and selected samples suggested that there might be only low to modest association between testosterone and aggression, with mean weighted correlations ranging from 0.08 to 0.14, in males. Overall, these meta-analyses suggest that the testosterone-aggression association is equally strong in 12 to 21-year-olds, as it is in 22 to 35-year-olds, but that it may be less strong in age groups younger than 12, than in those who are older.
So, testosterone may be associated with aggressive behavior and violence in women but not in men. In men, the significant moderator was education. It’s interesting to note that Mazur (2016) noted that young black males with little education had higher levels of testosterone than age-matched samples of other blacks. This, along with the evidence provided here, may be a clue that if the social environment changes, then so will higher levels of testosterone (as I have argued here).
They, perhaps taking too large of a leap here, argue that “aggressive behaviors may be more social and less biologically based among men” (Assari, Caldwell, and Zimmerman, 2014). Obviously social factors are easier to change than biological ones (in theory), so, they argue, preventative measures may be easier for men than women. More studies need to be done on the complex interactions between sex, testosterone, aggression, biology and the social environment which then shapes the aggressive behaviors of those who live there.
Testosterone and aggression studies are interesting. However, you must know a good amount of the literature to be able to ascertain good studies from the bad, what researchers should and should not have controlled for, time of assay, etc because these variables (some not in the author’s hands, however) can and do lead to false readings if certain variables are not controlled for. All in all, the literature is clearly points to, though other studies contest this at times, the fact that testosterone does not cause aggressive behavior in men. The myth needs to die; the data is piling up for this point of view and those who believe that testosterone causes aggressive behavior and crime (which I have shown it does not, at least for men) will soon be left in the dust as we get a better understanding of this pivotal hormone.
(In case anyone was going to use this as evidence that black women have higher levels of testosterone than white women, don’t do it because it’s not true. You’ll only embarrass yourself like this guy did. Read the comments and see him say that you don’t need scientific measurements, you only need to ‘observe it’ and through ‘observation’ we can deduce that black women have higher levels of testosterone than white women. This is not true. Quoting Mazur, 2016:
The pattern [high testosterone] is not seen among teenage boys or among females.
…
There is no indication of inordinately high T among young black women with low education.
Whoever still pushes that myth is an idealogue; I have retracted my article ‘Black Women and Testosterone‘, but idealogues just gloss over it and read what they think will bolster their views when I have provided the evidence to the contrary. It pisses me off that people selectively read things then cite my article because they think it will confirm their pre-conceived notions. Well too bad, things don’t work like that.)
Black-White Differences in Physiology
2050 words
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).
Blood pressure
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.
Conclusion
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.
No, Black Women Do Not Have Higher Testosterone than White Women (And More On Hereditarian Claims on Racial Testosterone Differences)
1850 words
It has been over a year since I wrote the article Black Women and Testosterone, and I really regret it. Yes, I did believe that black women had higher levels of testosterone than white women due to one flimsy study and another article on pregnant black women. I then wised up to the truth about testosterone and aggression/crime/race/sex and revised the articles (like I have done with r/K selection theory). However, after I revised my views on the supposed differences in testosterone between black men/white men and black women/white women, people still cite the article, disregarding the disclaimer at the top of the article. I quoted Mazur (2016), who writes (emphasis mine):
The pattern [high testosterone] is not seen among teenage boys or among females.
…
There is no indication of inordinately high T among young black women with low education.
…
Honor cultures are cast as male affairs, but with T data in hand for both sexes, it is worth exploring whether or not a similar pattern exists among women. Mean T was calculated as a function of age for the four combinations of race and education used in Table 1 but now for women. All plots show T declining with age, from about 35 ng/dL in the 20–29 age group to about 20 ng/dL among women 60 years and older. The four plots essentially overlap without discernible differences among them. Given the high skew of T among adult females, both raw and ln-transformed values were analyzed with similar results. There is no indication of inordinately high T among young black women with low education.
…
In the present study, at least, the sexes differ because the very high T seen among young black men with low education does not occur among young black women with low education.
This is very clear… Mazur (2016) analyzed the NHANES 2011-2012 data and this is what he found. I understand that most HBD bloggers do believe this, well, like a lot of their strong assertions (which I have rebutted myself), they’re wrong. They don’t get it. They do not understand the hormone.
The reason why I’m finally writing this (which is long overdue) is that I saw a referral from this website today: https://www.minds.com/RedPillTV who writes about the aforementioned black women and testosterone article:
It is known that blacks have the highest levels of testosterone out of the major races of humanity. However, what’s not known is that black women have higher rates than white women. The same evolutionary factors that make it possible for black men to have high testosterone make it possible for women as well.
https://notpoliticallycorrect.me/2016/09/06/black-women-and-testosterone/
…..No. It seems that people just scroll on by the disclaimer at the top that is bolded and italicized and just go to the (now defunct) article and attempt to prove their assertion that black women have higher testosterone than white women with an article that I have stated myself I no longer believe and have provided the rationale/data for the position. This shows that people have their own biases and no matter what the author writes about their views that have changed due to good arguments/data, they will still attempt to use the article to prove their assertion.
I’ve written at length that testosterone does not cause 1) aggression, 2) crime and 3) prostate cancer. People are scared of testosterone mostly due to the media fervor of any story that may have a hint of ‘toxic masculinity’. They (most alt-righters) are scared of it because of Lynn/Rushton/Templer/Kanazawa bullshit on the hormone. Richard Lynn doesn’t know what he’s talking about on testosterone. No, Europeans did not need lower levels of aggression in the cold; Africans didn’t need higher levels of aggression (relative to Europeans) to survive in the tropics. The theory that supposed differential testosterone differences between the races are “the physiological basis in males of the racial differences in sexual drive which form the core of the different r/K reproduction strategies documented by J.P. Rushton” (Lynn, 1990: 1203). The races, on average, do not differ in testosterone as I have extensively documented. So hereditarians like Lynn and others need to look for other reasons to explain blacks’ higher rate of sexual activity.
Rushton’s views on the testosterone and supposed r/K continuum have been summarily rebutted by me. These psychologists’ views on the hormone (that they don’t understand the production of nor do they understand the true reality of the differences between the races) are why people are afraid of testosterone. No, testosterone is not some ‘master switch’ as Rushton (1999) asserts. Rushton asserts that racial differences in temperament are mediated by the hormone testosterone. He further dives into this assertion stating “Testosterone level correlates with temperament, self-concept, aggression, altruism, crime, and sexuality, in women as well as in men (Harris, Rushton, Hampson, & Jackson, 1996). It may ‘correlate’ with aggression and crime, but as I have documented, they do not cause either.
The aggression/testosterone correlation is only .08 (Archer, Graham-Kevan, and Davies, 2005). Furthermore, the diurnal variation in testosterone does not directly correlate to when testosterone levels are highest in the day (at 8 am and drop thereafter), with adults peaking in crime at 10 pm and kids at 3 pm, with rises at 8 pm and 12 pm (not surprisingly, kids go in to school around 8 am, go to recess at 12 and leave at 3).
(Source: The Office of Juvenile Justice and Delinquency Prevention (OJJDP))
If you’ve read as much Rushton as I have, you’ll notice that he begins to sound like a broken record when talking about certain things. One of the most telling is Rushton’s repeated assertions that blacks average 3-19 percent higher testosterone than whites. The 3 percent number comes from Ellis and Nyborg (1992) and the 19 percent number comes from Ross et al (1986) (which Rushton should know that after adjustments for confounding, it decreased to 13 percent). These are the only studies that hereditarians ever cite for these claims that blacks average higher testosterone than whites. That seems a bit fishy to me. Cite a 30-year-old study along with a 25-year-old study (with such huge variation from Rushton and those who cite him for this matter—3-19 percent!!) as ‘proof’ that blacks average such higher levels of testosterone in comparison to whites.
Ross et al (1986) is one of the most important studies to rebut for this hereditarian claim that testosterone causes all of these maladies in black American populations. Ross et al (1986) propose that higher levels of the hormone lead to the higher rates of prostate cancer in black American populations. However, meta-analyses do not show this (Zagars et al, 1998; Sridhar et al, 2010).
Rushton et al’s assertions—largely—lie on this supposed testosterone difference between the races and how it supposedly leads to higher rates of crime, prostate cancer, aggression, and violence. However, the truth of the matter is, this is all just hereditarian bullshit. Larger analyses—as I have extensively documented—do not show this trend. And even accepting the claim that blacks have, say, 19 percent higher levels of testosterone than whites, it still would not explain the supposed prostate cancer rates between the races (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even if blacks had 19 percent higher testosterone than whites, it would not explain higher levels of crime nor aggression due to such a hilariously low correlation of .08 (Archer, Graham-Kevan, and Davies, 2005).
Finally, I have a few words for Michael Hart and his (albeit sparse) claims on testosterone in his 2007 book Understanding Human History.
Hart (2007) writes:
(Many of these differences in sexual behavior may be a consequence of the fact that
blacks, on average, have higher levels of testosterone than whites.7) (pg. 127)
And….. footnote number 7 is…. surprisingly (not): 7) Ross, R., et al. (1986). Not going to waste my time on this one, again. I’ve pointed out numerous flaws in the study. (I will eventually review the whole thing.)
It seems unlikely, though, that the higher testosterone level in blacks — which is largely genetic in origin — has no effect on their sexual behavior (pg. 128; emphasis mine)
This is bullshit. People see the moderately high heritability of testosterone (.60; Harris, Vernon, and Boomsma, 1998) and jump right to the “It’s genetics!!!” canard without even understanding its production in the body (it is a cholesterol-based hormone which is indirectly controlled by DNA, there are no ‘genes for’ testosterone). Here are the steps: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone
I have documented numerous lines of evidence showing that testosterone is extremely sensitive to environmental factors (Mazur and Booth, 1998; Mazur, 2016), and due to the homeodynamic physiology we have acquired due to ever-changing environments (Richardson, 2017), this allows our hormones to up- or down-regulate depending on what occurs in the environment. The quote from Hart is bullshit; he doesn’t know what he’s talking about.
For females in Siberia, the disadvantages of failing to find a man who would
provide for her and her children during their childhood were much greater than they were in tropical climates, and females who were not careful to do so were much less likely to pass on their genes. Furthermore, because females in harsh climates were so demanding on this point, males who seemed unlikely to provide the needed assistance found it hard to find mates. In other words, there was a marked sexual selection against such males. Such selection could result, for example, in the peoples living in northerly climates gradually evolving lower levels of testosterone than the peoples living in subSaharan Africa. (pg. 131)
This is a bullshit just-so story. Africans in Africa have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006).
Note also that a difference in testosterone level frequently affects not
only the sexual behavior of a young male, but also his aggressiveness.
No it does not (Archer, Graham-Kevan, and Davies, 2005).
Thankfully, that’s all he wrote about testosterone. There is so much bullshit out there. Though, people who like and seek out the truth will learn that there are no racial differences and that testosterone does not cause crime/aggression/prostate cancer and that it’s just hereditarian bullshit.
The evidence I have amassed and the arguments I have given point to a few things: 1) the races do not differ in testosterone/there is a small negligible difference; 2) testosterone does not cause crime; 3) testosterone does not cause aggression; 4) black women do not have higher levels of testosterone than white women; 5) high levels of testosterone do not cause prostate cancer; and 6) even allowing a 19 percent black/white difference will not have hereditarian claims hold true.
So for anyone who comes across my old articles on testosterone and sex/race, do a bit more reading of my newer material here to see my new viewpoints/arguments. DO NOT cite these articles as proof for your claims of higher levels of black men/women. DO cite the old articles ALONG WITH the new ones to show how and why my views changed along with the studies I have cited that changed my view. (Actually understanding the production of testosterone in the body was a huge factor too, which I talk about in Why Testosterone Does Not Cause Crime.)
Why Testosterone Does Not Cause Crime
1900 words
Edit: (The correlation between aggression and testosterone isn’t .14 as Book et al (2001) state; the true correlation is .08 (Archer, Graham-Kevan and Davies, 2005) So it’s even lower than I thought. This is one of the many reasons why testosterone does not cause crime. It’s just feminist bullshit and fear mongering from people who do not understand the hormone and what it does in the body. The misconceptions come from Rushton’s r/K selection bullshit which has been summarily refuted.)
Recently, I’ve written at length on racial differences in testosterone and how the correlation between testosterone and physical aggression is .14. Pitifully low to account for the cause of crime and any overall differences in racial crime (that will be touched on at length in the future). Tonight I will show, yet again, why testosterone does not cause crime by looking at what times most crimes are committed by both adults and children under the age of 18. This will definitively put the ‘testosterone causes crime’ myth to bed for good.
Before I get into the time of day that most crimes are committed, I must talk about the production of testosterone in the body. There are no ‘genes for’ testosterone (although men who had three certain alleles had a 6.5 fold higher risk of having low testosterone; Ohlsson et al, 2011, I am unaware of there being a variation by race; over 10,000 Caucasian men were studied). There is, however, an indirect control of testosterone synthesis by DNA. DNA regulates the production of testosterone by coding for enzymes that convert cholesterol to testosterone (testosterone is a cholesterol-based hormone).
There are five simple steps to the production of testosterone: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone). That’s how testosterone is produced in the body. It is indirectly controlled by DNA.
Above is a graph from the Office of Juvenile Justice and Delinquency Prevention which shows the time of day that most crimes are committed. Notice how crime goes up as the time of day goes on and since kids are at school, they’re more likely to fight. This then peaks at 3 pm when kids are getting out of school.
Now look at rates of crime for adults. At its peak of 10 pm, it’s vastly lower than that of people under the age of 18, which is important to keep in mind. You can see how at 8 am that rates of crime are low for adults and high for kids, right when they would be entering school so there would be a lot of other kids around and the chance for violence goes up. Keep the times of 8 am (kids when they enter school), 12 pm (when most kids go on lunch) and 3 pm (when most kids get out of school) along with the hours of 12 pm to 8 pm for adults (when 74 percent of crimes are committed by adults).
- In general, the number of violent crimes committed by adults increases hourly from 6 a.m. through the afternoon and evening hours, peaks at 10 p.m., and then drops to a low point at 6 a.m. In contrast, violent crimes by juveniles peak in the afternoon between 3 p.m. and 4 p.m., the hour at the end of the school day.
- Nearly one-third (29%) of all violent crime committed by juvenile offenders occurs between 3 p.m. and 7 p.m. In comparison, 26% of all violent committed by adult offenders occurs between 8 p.m. and 12 p.m.
So since testosterone varies by day and levels are highest at 8 am and lowest at 8 pm (Brambilla et al, 2009; however testing men aged 45 years of age and older is fine before 2 pm due to a blunted circadian rhythm; Long, Nguyen, and Stevermer, 2015), then how could testosterone account for why men commit most of their crimes at night and why the crime that children commit spikes when they go to school, go to lunch and get out of school? The answer is that it doesn’t because testosterone does not cause crime. What testosterone does cause, however, are feelings of confidence and dominance, which does not—surprisingly—lead to increased aggression and assault on others (Booth et al, 2006).
What testosterone does cause, however, is social dominance and success, not physical aggression and maladjustment (Shcaal et al, 1996). The effects of environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Furthermore, aggressive behavior is first noticed in infancy and reaches its peak before school age (Tremblay et al, 2004; Cote et al, 2006). Though testosterone does seem to have an effect on aggression in preschool boys, however genetic and environmental causality has not been established (Sanchez-Martin et al, 2000).
Nevertheless, the meta-analyses I cited last week show that testosterone has an extremely low correlation of .14, so other factors must be at play. However, Sanchez-Martin et al (2000:778-779) also note that “Tremblay et al (1998) suggested that associations between testosterone titer and physical aggression are likely to be observed in contexts where such attack leads to social dominance. This may be true of the preschool boys in the present study. The data generated in the present study generally support Scerbo and Kolko (1994), who studied older children (7 to 14 years of age). They found a significant relationship between testosterone levels and aggression (as assessed by clinical staff).”
It’s interesting to note that in the case of Scerbo and Kolko (1994) that after controlling for age and size, testosterone correlated with aggression when rated by staff but not parents or teachers. ‘Staff’ refers to clinic staff at a facility where the children were assessed for hyperactivity disorders. Of course, the staff would rate higher levels of aggression compared to parents of teachers—people who are around the children every day—since they would want a higher chance for diagnosis for certain drugs to ‘cure’ the hyperactivity, but I digress. Testosterone does not induce aggression in children, but it does induce social dominance and confidence which does not lead to aggression (Rowe et al, 2004; Booth et al, 2006).
There was also little difference in testosterone between socially dominant prisoners and aggressive prisoners (Ehrenkraz, Bliss, and Sheard, 1974). Furthermore, the testosterone increase leading to pubertal development in boys is not associated with increased aggression (Tremblay et al, 1998; Booth et al, 2006: 171). Indeed, increased body size is a marker for physical aggression in children, and I doubt these children have high muscle mass so, I assume, they have high levels of body fat and thusly lower levels of testosterone than they would have if they were leaner. Yet another strike against the ‘testosterone causes crime/physical aggression’ hypothesis.
Indeed, this has some implications for the honor culture hypothesis of why low-income blacks have higher levels of testosterone than similarly aged blacks with some college (Mazur, 2016). The patterns for crime as shown by the OOJDP shows that crime rises as the day progresses from the morning until its peak at 3 pm for children and then sharply declines while for adults it peaks at 10 pm.
Testosterone does increase when a challenge is issued; when one man feels his reputation is threatened, the propensity for violence is increased, but this was most notably seen in Southern men (Cohen et al, 1996). So the same would be said for this ‘culture of honor’ found in low-income black neighborhoods, the so-called ‘code of the street’ as stated by Anderson (1994: 88): “Moreover, if a person is assaulted, it is important, not only in the eyes of his opponent but in the eyes of his “running buddies,” for him to avenge himself. Otherwise, he risks being “tried” (challenged) or “moved on” by any number of others. To maintain his honor, he must show he is not someone to be “messed with” or “dissed.””
This culture of honor is found all over the world, including Brazil where homicide can be explained by the need to maintain honor and can be understood by taking into account cultural factors; biological, psychological and socioeconomic factors do not explain murder in Northeast Brazil as well as honor and culture (de Souza et al, 2015). People in honor cultures also have a higher chance of self-harm (Osterman and Brown, 2011) as well as a higher chance of committing violence in school (Brown, Osterman, and Barnes, 2009).
Testosterone does not cause crime; it does not cause aggression. Increases in testosterone before, during and after events are a physiologic process to prime the body for competition. As cited above, dominant behavior does not necessarily lead to violence in most cases, which may be surprising for some. Indeed, honor and culture may explain a nice amount of the homicide and violence rate in the South. Since testosterone is highest at 8 am and lowest at 8 pm and the rates of crime committed by adults and children are vastly different than the diurnal variance in the day, then testosterone does not cause crime and its increase is not associated with crime, but social dominance and confidence which does not lead to crime.
Hopefully—if anyone still believes testosterone to be the boogeyman its made out to be—I’ve put those misconceptions to rest. Racial differences in testosterone cannot be the cause of racial differences in crime—because there is either no statistical difference in testosterone between the races or the difference is non-existent. Testosterone is clearly a beneficial hormone—as I have extensively documented. Misunderstandings of the hormone are abound—especially in the HBD sphere—only due to literally a few paragraphs in a book (Rushton, 1997) and one study that showed blacks have higher testosterone than whites which was the cause of their higher rates of prostate cancer (Ross et al, 1986). The study is hard to find so I had to buy access to it. I will cover this in the future, but I discovered that they assayed the subjects when it was convenient for them—between the hours of 10 am and 3 pm—which is unacceptable. You cannot gauge racial differences in testosterone from a small study (n=50) and a non-representative sample (college students). For these reasons, the study should be thrown in the trash—especially when formulating evolutionary hypotheses.
Testosterone is one of the most important hormones for vital functioning. By knowing how it is processed in the body and that there are no ‘genes for’ testosterone (‘low testosterone genes’ notwithstanding) along with how testosterone has a low relationship with physical aggression one should not be scared of having high levels, on the contrary, one should be scared of having low levels. I have once again proven my case that testosterone is not related to violence in showing the diurnal variation in testosterone levels in adults, as well as the time of day that crimes are committed by both adults and children. High testosterone means high confidence and high dominance—and those two traits have a lot to do with masculinity—which do not lead to violence.
I know why testosterone does not cause crime—because I have an understanding of the hormone, how its produced in the body and what its effects on the body are. The most important thing to note here, is that even if blacks had 15 percent higher testosterone than whites, it still wouldn’t explain higher rates of crime or disease such as prostate cancer. So those who try so hard to prove that blacks have higher levels of the hormone do so in vain, because even if they did it wouldn’t mean anything for any theories they may have. The myth of testosterone causing aggression and crime need to be put to bed for good.
Chewing the Cud
by Scott Jameson
RaceRealist and I have been ruminating on a lot of stuff lately. Here’s a fun one: what economic system works best relative to what we know about human health? In my mind there are two approaches: the libertarian approach, and quasi-fascism.
In the libertarian approach, there’s no regulation of sugar placed in our food. That’s already the case. But here’s an improvement: you don’t have to pay for anyone’s gastric bypass after they overeat that sugar.
In the fascist approach, there is regulation of sugar, because a fascist state does not allow people to poison each other for profit. You still have to pay for others’ medical expenses, but those expenses will be lower.
Here’s an advantage to the libertarian approach. In that society, the people who stuff their faces and refuse to get off the couch- who are dumber and lazier on average, probably- will have a higher mortality rate on average. Eugenics need not cost a dime.
But you run into a snag, sand in the gears of your hands-off system, when Big Food kicks out a whole bunch of crappy dietary advice, at which point a minority of reasonably intelligent people will be led astray, perhaps to the grave. How could a libertarian society stop that from taking place? Would it even bother? Could the system broadly work in spite of this snag?
A libertarian society doesn’t pay for idiots to have children. That’s good, but half of your population (women) are unlikely to ever support it. Women don’t do libertarianism; observe Rand Paul’s demographic Achilles Heel on page 25. When women asked men what to do about so-and-so’s eighth unpaid for child, we’d have to look them in the eyes and give a deadpan “let’s hope private charity can handle it.” There was a time, before FDR, when women would’ve accepted that answer. They were still in the kitchen back then, and I don’t know how to put them back there.
A fascist society has more hands-on eugenics, possibly genome editing or embryo selection. Also good. Expensive, but obviously worth it.
We welcome your input on these issues.
*****
As an aside, White men are well-known as the most conservative, small government, nationalist group out there in our current political atmosphere. I always hear people spewing the schmaltziest nonsense about the values of the Founding Fathers. They were, relative to our political compass, nationalist libertarians. Accordingly, modern nationalists and libertarians do best with the exact same demographics that used to vote on candidates back then: property-owning White men. The sole reason that Ron and Rand Paul couldn’t get elected is that they are too similar to the Founding Fathers. Any other candidate who blathers on about the Founding values is simply a liar, and their obvious lies show a disrespect of your intelligence.
If you’re a libertarian, but not an ethno-nationalistic and patriarchal thinker, then you simply haven’t gotten the memo: women and minorities do not want to create the same world that you do, nor will they ever. Evolution gave us women who want social safety nets and other races which are better off if they parasitize off of your tax dollars. All of the most libertarian societies that ever existed (early US, ancient Athens, Roman Republic) were entirely run by White men, and adding women to the electorate gave us the welfare state. Aristophanes was right.
*****
We’re also ruminating on the difference between IQ and expertise. I know of no mentally complicated task of which one can be a master without being intelligent. Take the IQs of chess grandmasters and you will find no morons.
Contrast that with purely physical activities. I bet you there are some really stupid people out there who are great at dancing for example. A prodigiously capable cerebellum may not predict an equally capable frontal lobe.
Discounting tasks which exclusively require things like simple physical coordination, muscle memory, etc, I ought to think that IQ is the biggest component of expertise.
NotPoliticallyCorrect 