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The association between muscle fiber typing obesity and race is striking. It is well-established that blacks have a higher proportion of type II skeletal muscle fibers than whites and these higher proportions of these specific types of muscle fibers lead to physiological differences between the two races which then lead to differing health outcomes between them—along with differences in athletic competition. Racial differences in health are no doubt complex, but there are certain differences between the races that we can look at and say that there is a relationship here that warrants further scrutiny.
Why is there an association between negative health outcomes and muscle phsyiology? The answer is very simple if one knows the basics of muscle physiology and how and why muscles contract (it is worth noting that out of a slew of anatomic and phsyiologic factors, movement is the only thing we can consciously control, compare to menstration and other similar physiologic processes which are beyond our control). In this article, I will describe what muscles do, how they are controlled, muscle physiology, the differences in fiber typing between the races and what it means for health outcomes between them.
Muscle anatomy and physiology
Muscle fiber number is determined by the second trimester. Bell (1980) noted that skeletal muscle fiber in 6 year olds is not different from normal adult tissue, and so, we can say that between the time in the womb and age 6, muscle fiber type is set and cannot be changed (though training can change how certain fibers respond, see below).
Muscle anatomy and physiology is interesting because it shows us how and why we move the way we do. Tendons attach muscle to bone. Attached to the tendon is the muscle belly. The muscle belly is made up of facsicles and the fascicles are made up of muscle fibers. Muscle fibers are made up of myofibrils and myofibrils are made up of myofilaments. Finally, myofilaments are made up of proteins—specifically actin and myosin, this is what makes up our muscles.
(Image from here.)
Muscle fibers are encased by sarcolemma which contains cell components such as sarcoplasm, nuclei, and mitochondria. They also have other cells called myofibrils which contain myofilaments which are then made up of actin (thin filaments) and mysoin (thick filaments). These two types of filaments form numerous repeating sections within a myofibril and each repeating section is known as a sarcomere. Sarcomeres are the “functional” unit of the muscle, like the neuron is for the nervous system. Each ‘z-line’ denotes another sarcomere across a myofibril (Franzini-Armstrong, 1973; Luther, 2009).
Other than actin and myosin, there are two more proteins important for muscle contraction: tropomyosin and troponin. Tropomyosin is found on the actin filament and it blocks myosin binding sites which are located on the actin filament, and so it keeps myosin from attaching to muscle while it is in a relaxed state. On the other hand, troponin is also located on the actin filament but troponin’s job is to provide binding sites for calcium and tropomyosin when a muscle needs to contract.
So the structure of skeletal muscle can be broken down like so: epymyseum > muscle belly > perimyseum > fascicle > endomyseum > muscle fibers > myofibrils > myofilaments > myosin and actin. Note diagram (C) from above; the sarcomere is the smallest contractile unit in the myofibril. According to sliding filament theory (see Cook, 2004 for a review), a sarcomere shortens as a result of the ‘z-lines’ moving closer together. The reason these ‘z-lines’ converge is because myosin heads attach to the actin filament which asynchronistically pulls the actin filament across the myosin, which then results in the shortening of the muscle fiber. Sarcomeres are the basic unit controlling changes in muscle length, so the faster or slower they fire depends on the majority type of fiber in that specific area.
But the skeletal muscle will not contract unless the skeletal muscles are stimulated. The nervous system and the muscular system communicate, which is called neural activiation—defined as the contraction of muscle generated by neural stimulation. We have what are called “motor neurons”—neurons located in the CNS (central nervous system) which can send impulses to muscles to move them. This is done through a special synapse called the neuromuscular junction. A motor neuron that connects with muscle fibers is called a motor unit and the point where the muscle fiber and motor unit meet is callled the neuromuscular junction. It is a small gap between the nerve and muscle fiber called a synapse. Action potentials (electrical impulses) are sent down the axon of the motor neuron from the CNS and when the action potential reaches the end of the axon, hormones called neurotransmitters are then released. Neurotransmitters transport the electrical signal from the nerve to the muscle.
Muscle fiber types
The two main categories of muscle fiber are type I and type II—‘slow’ and ‘fast’ twitch, respectively. Type I fibers contain more blood cappilaries, higher levels of mitochondria (which transforms food into ATP) and myoglobin which allows for an improved delivery of oxygen. Since myoglobin is similar to hemoglobin (the red pigment which is found in red blood cells), type I fibers are also known as ‘red fibers.’ Type I fibers are also smaller in diameter and slower to produce maximal tension, but are also the most fatigue-resistant type of fiber.
Type II fibers have two subdivisions—IIa and IIx—based on their mechanical and chemical properties. Type II fibers are in many ways the opposite of type I fibers—they contain far fewer blood cappilaries, mitochondria and myoglobin. Since they have less myoglobin, they are not red, but white, which is why they are known as ‘white fibers.’ IIx fibers have a lower oxidative capacity and thusly tire out quicker. IIa, on the other hand, have a higher oxidative capacity and fatigue slower than IIx fibers (Herbison, Jaweed, and Ditunno, 1982; Tellis et al, 2012). IIa fibers are also known as intermediate fast twitch fibers since they can use both anarobic and aerobic metabolism equally to produce energy. So IIx fibers are a combo of I and II fibers. Type II fibers are bigger, quicker to produce maximal tension, and tire out quicker.
Now, when it comes to fiber typing between the races, blacks have a higher proportion of type II fibers compared to whites who have a higher proportion of type I fibers (Ama et al, 1986; Ceaser and Hunter, 2015; see Entine, 2000 and Epstein, 2014 for reviews). Higher proportions of type I fibers are associated with lower chance of cardiovascular events, whereas type II fibers are associated with a higher risk. Thus, “Skeletal muscle fibre composition may be a mediator of the protective effects of exercise against cardiovascular disease” (Andersen et al, 2015).
Now that the basics of muscle anatomy and physiology are apparent, hopefully the hows and whys of muscle contraction and what different muscle fibers do are becoming clear, because these different fibers are distributed between the races in uneven frequencies, which then leads to differences in sporting performance but also differents in health outcomes.
Muscle fibers and health outcomes
We now know the physiology and anatomy of muscle and muscle fiber typing. We also know the differences between each type of skeletal muscle fiber. Since the two races do indeed differ in the percentage of skeletal muscle fiber possessed on average, we then should find stark differences in health outcomes, part of the reason being these differences in muscle fiber typing.
While blacks on average have a higher proportion of type II muscle fibers, whites have a higher proportion of type I muscle fibers. Noting what I wrote above about the differences between the fiber types, and knowing what we know about racial differences in disease outcomes, we can draw some inferences on how differences in muscle fiber typing between races/individuals can then affect disease seriousness/acquisition.
In their review of black-white differences in muscle fiber typing, Ceaser and Hunter (2015) write that “The longitudinal data regarding the rise in obesity indicates obesity rates have been highest among non-Hispanic Black women and Hispanic women.” And so, knowing what we know about fiber type differences between races and how these fibers act when they fire, we can see how muscle fiber typing would contribute to differences in disease acquisition between groups.
Tanner et al (2001) studied 53 women (n=28, lean women; and n=25, obese women) who were undergoing an elective abdominal surgery (either a hysterectomy or gastric bypass). Their physiologic/anatomic measures were taken and they were divided into races: blacks and whites, along with their obesity status. Tanner et al found that the lean subjects had a higher proportion of type I fibers and a lower proportion of type IIx fibers whereas those who were obese were more likely to have a higher proportion of type IIb muscle fibers.
Like other analyses on this matter, Tanner et al (2001) showed that the black subjects had a higher proportion of type II fibers in comparison to whites who had a higher proportion of type I fibers (adiposity was not taken into account). Fifty-one percent of the fiber typing from whites was type I whereas for blacks it was 43.7 pervent. Blacks had a higher proportion of type IIx fibers than whites (16.3 percent for whites and 23.4 for blacks). Lean blacks and lean whites, though, had a similar percentage of type IIx fibers (13.8 percent for whites and 15 percent for blacks). It is interesting to note that there was no difference in type I fibers between lean whites and blacks (55.1 percent for whites and 54.1 percent for blacks), though muscle fibers from obese blacks contained far fewer type I fibers compared to their white counterparts (48.6 percent for whites and 34.5 for blacks). Obese blacks’ muscle fiber had a higher proportion of type IIx fibers than obese whites’ fiber typing (19.2 percent for whites and 31 percent for blacks). Lean blacks and lean whites had a higher proportion of type I fibers than obese blacks and obese whites. Obese whites and obese blacks had more type IIx fibers than lean whites and lean blacks.
So, since type II fibers are insulin resistant (Jensen et al, 2007), then they should be related to glucose intloerance—type II diabetes—and blacks with ancestry from West Africa should be most affected. Fung (2016, 2018) shows that obesity is a disease of insulin resistance, and so, we can bring that same rationale to racial differences in obesity. Indeed, Nielsen and Christensen (2011) hypothesize that the higher prevalence of glucose intolerance in blacks is related to their lower percentage of type I fibers and their higher percentage of type II fibers.
Nielsen and Christensen (2011) hypothesize that since blacks have a lower percentage of type I fibers (the oxidative type), this explains the lower fat oxidation along with lower resting metabolic rate, sleeping metabolic rate, resting energy expenditure and Vo2 max in comparison to whites. Since type I fibers are more oxidative over the glycolitic type II fibers, the lower oxidative capacity in these fibers “may cause a higher fat storage at lower levels of energy intake than in individuals with a higher oxidative capacity” (Nielsen and Christensen, 2011: 611). Though the ratio of IIx and IIa fibers are extremely plastic and affected by lifestyle, Nielsen and Christensen do note that individuals with different fiber typings had similar oxidative capacity if they engaged in physical activity. Recall back to Caesar and Hunter (2015) who note that blacks have a lower maximal aerobic capacity and higher proportion of type II fibers. They note that lack of physical activity exacerbates the negative effects that a majority type II fibers has over majority type I. And so, some of these differences can be ameliorated between these two racial groups.
The point is, individuals/groups with a higher percentage of type II fibers who do not engage in physical activity have an even higher risk of lower oxidative capacity. Furthermore, a higher proportion of type II fibers implies a higher percentage of IIx fibers, “which are the least oxidative fibres and are positively associated with T2D and obesity” (Nielsen and Christensen, 2011: 612). They also note that this may explain the rural-urban difference in diabetes prevalance, with urban populations having a higher proportion of type II diabetics. They also note that this may explain the difference in type II diabetes in US blacks and West African natives—but the reverse is true for West Africans in the US. There is a higher rate of modernization and, with that, a higher chance to be less physically active and if the individual in question is less physically active and has a higher proportion of type II fibers then they will have a higher chance of acquiring metabolic diseases (obesity is also a metabolic disease). Since whites have a higher proportion of type I fibers, they can increase their fat intake—and with it, their fat oxidation—but this does not hold for blacks who “may not adjust well to changes in fat intake” (Nielsen and Christensen, 2011: 612).
Nielsen and Christensen end their paper writing:
Thus, Blacks of West African ancestry might be genetically predisposed to T2D because of an inherited lower amount of skeletal muscle fibre type I, whereby the oxidative capacity and fat oxidation is reduced, causing increased muscular tissue fat accumulation. This might induce skeletal muscle insulin resistance followed by an induced stress on the insulin-producing beta cells. Together with higher beta-cell dysfunction in the West African Diaspora compared to Whites, this will eventually lead to T2D (an overview of the ‘skeletal muscle distribution hypothesis’ can be seen in Figure 2).
Lambernd et al (2012) show that muscle contractions eliminated insuin resistance by blocking pro-inflammatory signalling pathways: this is the mechanism by which physical activity decreases glucose intolerance and thusly improves health outcomes—especially for those with a higher proportion of type II fibers. Thus, it is important for individuals with type II fibers to exercise, since sedentariness is associated with an age-related insulin resistance due to impaired GLUT4 utilization (Bunprajun et al, 2013).
(Also see Morrison and Cooper’s (2006) hypothesis that “reduced oxygen-carrying capacity induced a shift to more explosive muscle properties” (Epstein, 2014: 179). Epstein notes that the only science there is on this hypothesis is one mouse and rat study showing that low hemoglobin can “induce a switch to more explosive muscle fibers” (Epstein, 2014: 178), but this has not been tested on humans to see if it would hold. If this is tested on humans and if it does hold, then that would lend credence to Morrison’s and Cooper’s (2006) hypothesis.)
Knowing what we know about muscle anatomy and physiology and how muscles act we can understand the influence the different muscle types have on disease and how they contribute to disease variation between race, sex and the individual level. Especially knowing how type II fibers act when the individual in question is insulin resistant is extremely important—though it has been noted that individuals who participate in aerobic exercise decrease their risk for cardiometabolic diseases and can change the fiber distribution difference between IIx and IIa fibers, lowering their risk for acquiring cardiometabolic diseases (Ceaser and Hunter, 2015).
Thinking back to sarcomeres (the smallest contractile unit in the muscle) and how they would act in type II fibers: they would obviously contract much faster in type II muscles over type I muscles; they would then obviously tear faster than type I muscles; since type II muscles are more likely to be insulin resistant, then those with a higher proportion of type II fibers need to focus more on aerobic activity to “balance out” type IIx and IIa fibers and decrease the risk of cardiometabolic disease due to more muscle contractions (Lambernd et al, 2012). Since blacks have a higher proportion of type II fibers and are more likely to be sedentary than whites, and since those who have a higher proportion of type II fibers are more likely to be obese, then it is clear that exercise can and will ameliorate some of the disparity in cardiometabolic diseases between blacks and whites.
Racial differences in body fat are clear to the naked eye: black women are more likely to carry more body fat than white women; Mexican American women are more likely to carry more body fat than white women, too. Different races/ethnies/genders of these races/ethnies have different formulas to assess body fat through the use of skin-folds. The sites to grasp the skin is different based on gender and race.
Body mass index (BMI) and waist circumference is overestimated in blacks, which means that they need different formulas to assess their BMI and adiposity/lean mass. Race-specific formulas/methods are needed to assess body fat and, along with it, disease risk, since blacks are more likely to be obese (black women, at least, it’s different with black American men with more African ancestry, see below). The fact of the matter is, when matched on a slew of variables, blacks had lower total and abdominal fat mass than whites.
This is even noted in Asian, black and white prepubertal children. He et al (2002) show that sex differences in body fat distribution are present in children who have yet to reach puberty and the differences in body fat in Asians is different than that from blacks and whites which also varies by sex. Asian girls had greater gynoid fat by DXA scan only, with girls having greater gynoid fat than boys. Asian girls had lower adjusted extremity fat and gynoid fat compared to white and black girls. Though, Asian boys had a lower adjusted extremity by fat as shown by DXA (a gold standard in body fat measurement) when compared to whites, but greater gynoid fat than whites and blacks.
Vickery, Cureton, and Collins, (1988), Wagner and Heyward (2000), and Robson, Bazin, and Soderstrom (1971) show that there are considerable body composition differences between blacks and whites. These differences in body composition come down to diet, of course, but there is also a genetic/physiologic component there as well. Combining the known fact that skin-fold testing is not conducive to a good estimate, black American men with more African ancestry are less likely to be obese.
Vickery, Cureton, and Collins (1988) argue that, if accurate estimates of body fat percentages are to be obtained, race-specific formulas need to be developed and used as independent variables to assess racial differences in body fat percentage. Differences in muscularity don’t seem to account for these skinfold differences, nor does greater mesomorphy. One possible explanation for differences in skinfold thickness is that blacks may store most of their body fat subcutaneously. (See Wagner and Heyward, 2000 for a review on fat patterning and body composition in blacks and whites.)
The often-used Durnin-Womersley formula which is used to predict body fat just from skin folds. However, “The 1974 DW equations did not predict %BF(DXA) uniformly in all races or ethnicities” (Davidson et al, 2011). Truesdale et al (2016) even show that numerous formulas used to estimate percent body fat are flawed, even some formulas used on different races. Most of the equations tested showed starkly different conclusions. But, this is based on NHANES data and the only data they provide regarding skin-folds is the tricep and subscapular skinfold so there may still be more problems with all of the equations used to assess body fat percentage between races. (Also see Cooper, 2010.)
Klimentidis et al (2016) show that black men—but not black women—seem to be protected against obesity and central adiposity (fat gain around the midsection) and that race negatively correlated with adiposity. The combo of male gender and West African ancestry predicted low levels of adiposity compared to black Americans with less African ancestry. Furthermore, since black men and women have—theoretically—the same SES, then cultural/social factors would not play as large a role as genetic factors in explaining the differences in adiposity between black men and black women. Black men with more African ancestry had a lower WHR and less central adiposity than black men with less African ancestry. If we assume that they had similar levels of SES and lived in similar neighborhoods, there is only one reason why this would be the case.
Klimentidis et al (2016) write:
One interpretation is that AAs are exposed to environmental and/or cultural factors that predispose them to greater obesity than EAs. Possibly, some of the genes that are inherited as part of their West-African ancestry are protective against obesity, thereby “canceling out” the obesifying effects of environment/culture, but only in men. Another interpretation is that genetic protection is afforded to all individuals of African descent, but this protection is overwhelmed by cultural and/or other factors in women.
Black men do, as is popularly believed, prefer bigger women over smaller women. For example, Freedman et al (2004) showed that black American men were more likely to prefer bigger women. Black American men “are more willing to idealize a woman
of a heavier body size, with more curves, than do their White American counterparts” (Freedman et al, 2004: 197). It is then hypothesized that black American men find these figures attractive (figures with “more curves” (Freedman et al, 2004: 197)) to protect against eating pathologies, such as anorexia and bulimia. So, it has been established that black men have thinner skin folds than whites which leads to skewed lean mass/body fat readings and black men with more African ancestry are less likely to be obese. These average differences between races, of course, contribute to differing disease acquisition.
I have covered differences in body fat in a few Asian ethnies and have come to the obvious conclusion: Asians, at the same height, weight etc as whites and blacks, will have more adipose tissue on their bodies. They, too, like blacks and whites, have different areas that need to be assessed for skin folds to estimate body fat.
Henriques (2016: 29) has a table on the equations for calculating estimated body density from skin fold measures from various populations. Of interest are the ones on blacks or ‘Hispanics‘, blacks or athletes and blacks and whites. (The table is provided from NSCA, 2008 so the references are not in the back of the text.)
For black and ‘Hispanic’ women aged 18-55 years, the sites to use for skin-folds are the chest, abdomen, triceps, subscapular, suprailiac, midaxillary, and the thigh. For blacks or athletes aged 18-61 years, the sites to use are the same as before (but a different equation is used for body fat estimation). For white women or anorexic women aged 18-55, the sites used are just triceps, suprailiac and the thigh. For black and white boys aged 6-17, only the triceps and the calf is used. It is the same for black and white girls, but, again, a different formula is used to assess body fat (Henriques, 2016: 29).
Morrison et al (2012) showed that white girls had a higher percent body fat when compared to black girls at ages 9-12 but every age after, black girls had higher percent body fat (which is related to earlier menarche in black girls since they have higher levels of body fat which means earlier puberty; Kaplowitz, 2008). Black girls, though, had higher levels of fat in their subscapular skin folds than white girls at all ages.
So, it seems, there are population-/race-specific formulas that need to be created to better assess body fat percentage in different races/ethnies and not assume that one formula/way of assessing body fat should be used for all racial/ethnic groups. According to the literature (some reviewed here and in Wagner and Heyward, 2000), these types of formulas are sorely needed to better assess health markers in certain populations. These differences in body fat percentage and distribution then have real health consequences for the races/ethnies in question.
Leading behavior geneticist Robert Plomin is publishing “Blueprint: How DNA Makes Us Who We Are” in October of 2018. I, of course, have not read the book yet. But if the main thesis of the book is that DNA is a “code”, “recipe”, or “blueprint”, then that is already wrong. This is because presuming that DNA is any of the three aforementioned things marries one to certain ideas, even if they themselves do not explicitly state them. Nevertheless, Robert Plomin is what one would term a “hereditarian”, meaning that he believes that genes—more than environment—shape an individual’s psychological and other traits. (That’s a false dichotomy, though.) In the preview for the book at MIT Press, they write:
In Blueprint, behavioral geneticist Robert Plomin describes how the DNA revolution has made DNA personal by giving us the power to predict our psychological strengths and weaknesses from birth. A century of genetic research shows that DNA differences inherited from our parents are the consistent life-long sources of our psychological individuality—the blueprint that makes us who we are. This, says Plomin, is a game-changer. It calls for a radical rethinking of what makes us who were are.
Genetics accounts for fifty percent of psychological differences—not just mental health and school achievement, but all psychological traits, from personality to intellectual abilities. Nature defeats nurture by a landslide.
Plomin explores the implications of this, drawing some provocative conclusions—among them that parenting styles don’t really affect children’s outcomes once genetics is taken into effect. Neither tiger mothers nor attachment parenting affects children’s ability to get into Harvard. After describing why DNA matters, Plomin explains what DNA does, offering readers a unique insider’s view of the exciting synergies that came from combining genetics and psychology.
I won’t get into most of these things today (I will wait until I read the book for that), but this will be just an article showing that DNA is, in fact, not a blueprint, and DNA is not a “code” or “recipe” for the organism.
It’s funny that the little blurb says that “Nature defeats nurture by a landslide“, because, as I have argued at length, nature vs nurture is a false dichotomy (See Oyama, 1985, 2000, 1999; Moore, 2002; Schneider, 2007; Moore, 2017). Nature vs nurture is the battleground that the false dichotomy of genes vs environment is fought on. However, it makes no sense to partition heritability estimates if it is indeed true that genes interact with environment—that is, if nature interacts with nurture.
DNA is also called “the book of life”. For example, in her book The Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease, and Inheritance, Nessa Carey writes that “There’s no debate that the DNA blueprint is a starting point” (pg 16). This, though, can be contested. “But the promise of a peep into the ‘book of life’ leading to a cure for all diseases was a mistake” (Noble, 2017: 161).
Developmental psychologist and cognitive scientist David S. Moore concurs. In his book The Developing Genome: An Introduction to Behavioral Epigenetics, he writes (pg 45):
So, although I will talk about genes repeatedly in this book, it is only because there is no other convenient way to communicate about contemporary ideas in molecular biology. And when I refer to gebe, I will be talking about a segment or segments of DNA containing sequence information that is used to help construct a protein (or some other product that performs a biological function). But it is worth remembering that contemporary biologists do not mean any one thing when they talk about “genes”; the gene remains a fundementally hypothetical concept to this day. The common belief that there are things inside of us that constitute a set of instructions for building bodies and minds—things that are analogous to “blueprings” or “recipes”—is undoubedtly false. Instead, DNA segements often contain information that is ambiguous, and that must be edited or arranged in context-dependent ways before it can be used.
Still, other may use terms like “genes for” trait T. This, too, is incorrect. In his outstanding book Making Sense of Genes, Kostas Kamporakis writes (pg 19):
I also explain why the notion of “genes for,” in the vernacular sense, is not only misleading but also entirely inaccurate and scientifcally illegitamate.
First, I show that genes “operate” in the context of development only. This means that genes are impllicated in the development of characters but do not determine them. Second, I explain why single genes do not alone produce characters or disease but contribute to their variation. This means that genes can account for variation in characters but cannot alone explain their origin. Third, I show that genes are not the masters of the game but are subject to complex regulatory processes.
Genes can only be seen as passive templates, not ultimate causes (Noble, 2011), and they cannot explain the origin of different characters but can account for variation in physical characters. Genes only “do” something in the context of development; they are inert molecules and thusly cannot “cause” anything on their own.
Genes are not ‘for’ traits, but they are difference-makers for traits. Sterelny and Griffiths (1999: 102), in their book Sex and Death: An Introduction to Philosophy of Biology write:
Sterelny and Griffiths (1988) responded to the idea that genes are invisible to selection by treating genes as difference makers, and as visible to selection by virtue of the differences they make. In doing so, they provided a formal reconstruction of the “gene for” locution. The details are complex, but the basic intent of the reconstruction is simple. A certain allele in humans is an “allele for brown eyes” because, in standard environments, having that allele rather than alternatives typically available in the population means that your eyes will be brown rather than blue. This is the concpet of a gene as a difference maker. It is very important to note, however, that genes are context-sensitive difference makers. Their effects depend on the genetic, cellular, and other features of their environment.
(Genes can be difference makers for physical traits, but not for psychological traits because no psychophysical laws exist, but I’ll get to that in the future.)
Note how the terms “context-sensitive” and “context-dependent” continue to appear. The DNA-as-blueprint statement presumes that DNA is context-independent, but we cannot divorce genes—whatever they are—from their context, since genes and environment, nature and nurture, are intertwined. (And it is even questioned if ‘genes’ are truly units of inheritance, see Fogle, 1990. Fogle, 2000 also argues to dispense with the concept of “gene” and that biologists should be using terms like intron, promoter region, and exon. Nevertheless, there is a huge disconnect with the term “gene” in molecular biology and classical genetics. Keller 2000 argues that there are still uses for the term “gene” and that we should not dispense with the term. I believe we should dispense with it.)
Susan Oyama (2000: 77) writes in her book The Ontogeny of Information:
“Though a plan implies action, it does not itself act, so if the genes are a blueprint, something else is the constructor-construction worker. Though blueprints are usually contrasted with building materials, the genes are quite easily conceptualized as templates for building tools and materials; once so utilized, of course, they enter the developmental process and influence its course. The point of the blueprint analogy, though, does not seem to be to illuminate developmental processes, but rather to assume them and, in celebrating their regularity, to impute cognitive functions to genes. How these functions are exercised is left unclear in this type of metaphor, except that the genetic plan is seen in some peculiar way to carry itself out, generating all the necessary steps in the necessary sequence. No light is shed on multiple developmental possibilities, species-typical or atypical.“
The Modern Synthesis is one of the causes for the genes-as-blueprints thinking; the Modern Synthesis has causation in biology wrong. Genes are not active causes, but they are passive templates, as argued by many authors. They, thus, cannot “cause” anything on their own.
In his 2017 book Dance to the Tune of Life: Biological Relativity, Denis Noble writes (pg 157):
As we saw earlier in this chapter, these triplet sequences are formed from any combination of the four bases U, C, A and G in RNA and T, C, A and G in DNA. They are often described as a genetic ‘code’, but it is important to understand that this usage of the word ‘code’ carries overtones that can be confusing.
A code was originally an intentional encryption used by humans to communicate. The genetic ‘code’ is not intentional in that sense. The word ‘code’ has unfortunately reinforced the idea that genes are active and even complete causes, in much the same was as a computer is caused to follow the instructions of a computer program. The more nuetral word ‘template’ would be better. Templates are used only when required (activated); they are not themselves active causes. The active causes lie within the cells themselves since they determine the expression patterns for the different cell types and states. These patterns are comminicated to the DNA by transcrption factors, by methylation patterns and by binding to the tails of histones, all of which influence the pattern and speed of transcription of different parts of the genome. If the word ‘instruction’ is useful here at all, it is rather that the cell instructs the genome. As Barbara McClintock wrote in 1984 after receiving her Nobel Prize, the genome is an ‘organ of the cell’, not the other way around.
Realising that DNA is under the control of the system has been reinforced by the discovery that cells use different start, stop and splice sites for producing different messenger RNAs from a single DNA sequence. This enables the same sequence to code different proteins in different cell types and under different conditions [here’s where context-dependency comes into play again].
Representing the direction of causality in biology the wrong way round is therefore confusing and has far-reaching conseqeunces. The causality is circular, acting both ways: passive causality by DNA sequences acting as otherwise inert templates, and active causality by the functional networks of interactions that determine how the genome is activated.
This takes care of the idea that DNA is a ‘code’. But what about DNA being a ‘blueprint’, that all of the information is contained in the DNA of the organism before conception? DNA is clearly not a ‘program’, in the sense that all of the information to construct the organism exists already in DNA. The complete cell is also needed, and its “complex structures are inherited by self-templating” (Noble, 2017: 161). Thus, the “blueprint” is the whole cell, not just the genome itself (remember that the genome is an organ of the cell).
Lastly, GWA studies have been all the rage recently. However, there is only so much we can learn just from association studies, before we need to turn to the physiological sciences for functional analyses. Indeed, Denis Noble (2018) writes in a new editorial:
As with the results of GWAS (genome-wide association studies) generally, the associations at the genome sequence level are remarkably weak and, with the exception of certain rare genetic diseases, may even be meaningless (13, 21). The reason is that if you gather a sufficiently large data set, it is a mathematical necessity that you will find correlations, even if the data set was generated randomly so that the correlations must be spurious. The bigger the data set, the more spurious correlations will be found (3).
The results of GWAS do not reveal the secrets of life, nor have they delivered the many cures for complex diseases that society badly needs. The reason is that association studies do not reveal biological mechanisms. Physiology does. Worse still, “the more data, the more arbitrary, meaningless and useless (for future action) correlations will be found in them” is a necessary mathematical statement (3).
Nor does applying a highly restricted DNA sequence-based interpretation of evolutionary biology, and its latest manifestation in GWAS, to the social sciences augur well for society.
It is further worth noting that there is no privileged level of causation in biological systems (Noble, 2012)—a priori, there is no justification to privilege one system over another in regard to causation, so saying that one level of the organism is “higher” than another (for instance, saying that genes are, and should be, privileged over the environment or any other system in the organism regarding causation) is clearly false, since there is upwards and downwards causation, influencing all levels of the system.
In sum, it is highly misleading to refer to DNA as “blueprints”, a “code”, or a “recipe.” Referring to DNA in this way means that one presumes that DNA can be divorced from its context—that it does not work together with the environment. As I have argued in the past, association studies will not elucidate genetic mechanisms, nor will heritability estimates (Richardson, 2012). We need physiological testing for these functional analyses, and association studies like GWAS and even heritability estimates don’t tell us this type of information (Panofsky, 2014). So, it seems, that what Plomin et al are looking for that they assume are “in the genes”, are not there, because they use a false model of the gene (Burt, 2015; Richardson, 2017). Genes are resources—templates to be used by and for the system—not causes of traits and development. They can account for differences in variation, but cannot be said to be the origin of trait differences. Genes can be said to be difference makers, but knowing whether or not they are difference makers for behavior, in my opinion, cannot be known.
(For further information on genes and what they do, reach Chapters Four and Five of Ken Richardson’s book Genes, Brains, and Human Potential: The Science and Ideology of Intelligence. Plomin himself seems to be a reductionist, and Richardson took care of that paradigm in his book. Lickliter (2018) has a good review of the book, along with critiques of the reductionist paradigm that Plomin et al follow.)
Everyone wants to know the keys to athletic success, however, as I have argued in the past, to understand elite athletic performance, we must understand how the system works in concert with everything—especially in the environments the biological system finds itself in. To reduce factors down to genes, or training, or X or Y does not make sense; to look at what makes an elite athlete, the method of reductionism, while it does allow us to identify certain differences between athletes, it does not allow us to appreciate the full-range of how and why elite athletes differ in their sport of choice. One large meta-analysis has been done on the effects of a few genotypes on elite athletic performance, and it shows us what we already know (blacks are more likely to have the genotype associated with power performance—so why are there no black Strongmen or any competitors in the World’s Strongest Man?). A few studies and one meta-analysis exist, attempting to get to the bottom of the genetics of elite athletic performance and, while it of course plays a factor, as I have argued in the past, we must take a systems view of the matter.
One 2013 study found that a functional polymorphism in the angiotensinogen (ATG) region was 2 to 3 times more common in elite power athletes than in (non-athlete) controls and elite endurance athletes (Zarebska et al, 2013). This sample tested was Polish, n = 223, 156 males, 67 females, and then they further broke down their athletic sample into tiers. They tested 100 power athletes (29 100-400 m runners; 22 powerlifters; 20 weightlifters; 14 throwers and 15 jumpers) and 123 endurance athletes (4 tri-athletes; 6 race walkers; 14 road cyclists; 6 15 to 50 m cross-country skiers; 12 marathon runners; 53 rowers; 17 3 to 10 km runners; and 11 800 to 1500 m swimmers).
Zarebska et al (2013) attempted to replicate previous associations found in other studies (Buxens et al, 2009) most notably the association with the M235T polymorphism in the AGT (angiotensinogen) gene. Zarebska et al’s (2013) main finding was that there was a higher representation of elite power athletes with the CC and C alleles of the M235T polymorphism compared with endurance athletes and controls, which suggests that the C allele of the M235T gene “may be associated with a predisposition to power-oriented
events” (Zarebska et al, 2013: 2901).
Elite power athletes were more likely to possess the CC genotype; 40 percent of power athletes had the genotype whereas 13 percent of endurance had it and 18 percent of non-athletes had it. So power athletes were more than three times as likely to have the CC genotype, compared to endurance athletes and twice as likely to have it compared to non-athletes. On the other hand, one copy of the C allele was found in 55 percent of the power athletes whereas, for the endurance athletes and non-athletes, the C allele was found in about 40 percent of individuals. (Further, in the elite anaerobic athlete, explosive power was consistently found to be a difference maker in predicting elite sporting performance; Lorenz et al, 2013.)
Now we come to the more interesting parts: ethnic differences in the M235T polymorphism. Zarebska et al (2013: 2901-2902) write:
The M235T allele distribution varies widely according to the subject’s ethnic origin: the T235 allele is by far the most frequent in Africans (;0.90) and in African-Americans (;0.80). It is also high in the Japanese population (0.65–0.75). The T235 (C4027) allele distribution of the control participants in our study was lower (0.40) but was similar to that reported among Spanish Caucasians (0.41), as were the sports specialties of both the power athletes (throwers, sprinters, and jumpers) and endurance athletes (marathon runners, 3- to 10-km runners, and road cyclists), thus mirroring the aforementioned studies.
Zarebska et al (2013: 2902) conclude that their study—along with the study they replicated—supports the hypothesis that the C allele of the M235T polymorphism in the AGT gene may confer a competitive advantage in power-oriented sports, which is partly mediated through ANGII production in the skeletal muscles. Mechanisms can explain the mediation of ANGII production in skeletal muscles, such as a direct skeletal muscle hypertrophic effect, along with the redistribution of between muscle blood flow between type I (slow twitch) and II fibers (fast twitch), which would then augment power and speed. However, it is interesting to note that Zarebska et al (2013) did not find any differences between “top-elite” level athletes who had won medals in international competitions compared to elite-level athletes who were not medalists.
The big deal about this gene is that the AGT gene is part of the renin-angiotensin system which is partly responsible for blood pressure and body salt regulation (Hall, 1991; Schweda, 2014). There seems to be an ethnic difference in this polymorphism, and, according to Zarebska et al (2013), African Americans and Africans are more likely to have the polymorphisms that are associated with elite power performance.
There is also a meta-analysis on genotyping and elite power athlete performance (Weyerstrab et al, 2017). Weyerstrab et al (2017) meta-analyzed 36 studies which attempted to find associations between genotype and athletic ability. One of the polymorphisms studied was the famous ACTN3. It has been noted that, when conditions are right (i.e., the right morphology), the combined effects of morphology along with the contractile properties of the individual muscle fibers contribute to the enhanced performance of those with the RR ACTN3 genotype (Broos et al, 2016), while Ma et al (2013) also lend credence to the idea that genetics influences sporting performance. This is, in fact, the most-replicated association in regard to elite sporting performance: we know the mechanism behind how muscle fibers contract; we know how the fibers contract and the morphology needed to maximize the effectiveness of said fast twitch fibers (type II fibers). (Blacks have a higher proportion of type II fibers [see Caeser and Henry, 2015 for a review].)
Weyerstrab et al (2017) meta-analyzed 35 articles, finding significant associations with genotype and elite power performance. They found that ten polymorphisms were significantly associated with power athlete states. Their most interesting findings, though, were on race. Weyerstrab et al (2017: 6) write:
Results of this meta-analysis show that US African American carriers of the ACE AG genotype (rs4363) were more than two times more likely to become a power athlete compared to carriers of the ACE preferential genotype for power athlete status (AA) in this population.
“Power athlete” does not necessarily have to mean “strength athlete” as in powerlifters or weightlifters (more on weightlifters below).
Lastly, the AGT M235T polymorphism, while associated with other power movements, was not associated with elite weightlifting performance (Ben-Zaken et al, 2018). As noted above, this polymorphism was observed in other power athletes, and since these movements are largely similar (short, explosive movements), one would rightly reason that this association should hold for weightlifters, too. However, this is not what we find.
Weightlifting, compared to other explosive, power sports, is different. The beginning of the lifts take explosive power, but during the ascent of the lift, the lifter moves the weight slower, which is due to biomechanics and a heavy load. Ben-Zaken et al (2018) studied 47 weightlifters (38 male, 9 female) and 86 controls. Every athlete that was studied competed in national and international meets on a regular basis. Thirty of the weightlifters were also classified as “elite”, which entails participating in and winning national and international competitions such as the Olympics and the European and World Championships).
Ben-Zaken et al (2018) did find that weightlifters had a higher prevalence of the AGT 235T polymorphism when compared to controls, though there was no difference in the prevalence of this polymorphism when elite and national-level competitors were compared, which “[suggests] that this polymorphism cannot determine or predict elite competitive weightlifting performance” (Ben-Zaken et al, 2018: 38). Of course, a favorable genetic profile is important for sporting success, though, despite the higher prevalence of AGT in weightlifters compared to controls, this could not explain the difference between national and elite-level competitors. Other polymorphisms could, of course, contribute to weightlifting success, variables “such as training experience, superior equipment and facilities, adequate nutrition, greater familial support, and motivational factors, are crucial for top-level sports development as well” (Ben-Zaken et al, 2018: 39).
I should also comment on Anatoly Karlin’s new article The (Physical) Strength of Nations. I don’t disagree with his main overall point; I only disagree that grip strength is a good measure of overall strength—even though it does follow the expected patterns. Racial differences in grip strength exist, as I have covered in the past. Furthermore, there are associations between muscle strength and longevity, with stronger men being more likely to live longer, fuller lives (Ruiz et al, 2008; Volkalis, Haille, and Meisinger, 2015; Garcia-Hermosa, et al, 2018) so, of course, strength training can only be seen as a net positive, especially in regard to living a longer and fuller life. Hand grip strength does have a high correlation with overall strength (Wind et al, 2010; Trosclair et al, 2011). While handgrip strength can tell you a whole lot about your overall health (Lee et al, 2016), of course, there is no better proxy than actually doing the lifts/exercises to ascertain one’s level of strength.
There are replicated genetic associations between explosive, powerful athletic performance, along with even the understanding of the causal mechanisms behind the polymorphisms and their carry-over to power sports. We know that if morphology is right and the individual has the RR ACTN3 genotype, that they will exceed in explosive sports. We know the causal pathways of ACTN3 and how it leads to differences in sprinting competitions. It should be worth noting that, while we do know a lot more about the genomics of sports than we did 20, even 10 years ago, current genetic testing has zero predictive power in regard to talent identification (Pitsladis et al, 2013).
So, of course, for parents and coaches who wonder about the athletic potential of their children and students, the best way to gauge whether or not they will excel in athletics is…to have them compete and compare them to other kids. Even if the genetics aspect of elite power performance is fully unlocked one day (which I doubt it will be), the best way to ascertain whether or not one will excel in a sport is to put them to the test and see what happens. We are in our infancy in understanding the genomics of sporting performance, but when we do understand which genotypes are more prevalent in regard to certain sports (and of course the interactions of the genotype with the environment and genes), then we can better understand how and why others are better in certain sports.
The genomics of elite sporting performance is very interesting; however, the answer that reductionists want to see will not appear: genes are difference makers (Sterelny and Griffith, 1999), not causes, and along with a whole slew of other environmental and mental factors (Lippi, Favaloro, and Guidi 2008), along with a favorable genetic profile with sufficient training (and everything else that comes along with it) are needed for the athlete to reach their maximum athletic potential (see Guth and Roth, 2013). Genetic and environmental differences between individuals and groups most definitely explain differences in elite sporting performance, though elucidating what causes what and the mechanisms that cause the studied trait in question will be tough.
Just because group A has gene or gene networks G and they compete in competition C does not mean that gene or gene networks G contribute in full—or in part—to sporting success. The correlations could be coincidental and non-functional in regard to the sport in question. Athletes should be studied in isolation, meaning just studying a specific athlete in a specific discipline to ascertain how, what, and why works for the specific athlete along with taking anthropomorphic measures, seeing how bad they want “it”, and other environmental factors such as nutrition and training. Looking at the body as a system will take us away from privileging one part over another—while we also do understand that they do play a role but not the role that reductionists believe.
These studies, while they attempt to show us how genetic factors cause differences at the elite level in power sports, they will not tell the whole story, because we must look at the whole system, not reduce it down to the sum of its parts (Shenk, 2011: chapter 5). While blacks are more likely to have these polymorphisms that are associated with elite power athlete performance, this does not obviously carry over to strongman and powerlifting competition.
In the 1940s, psychologist William Sheldon created a system of body measures known as “somatotyping”, then took his somatotypes and attempted to classify each soma (endomorph, ectomorph, or mesomorph) to differing personality types. It was even said that “constitutional psychology can guide a eugenics program and save the modern world from itself.”
Sheldon attempted to correlate different personality dimensions to different somas. But his somas fell out of favor before being revived by two of his disciples—without the “we-can-guess-your-personality-from-your-body-type” canard that Sheldon used. Somatotyping, while of course being put to use in a different way today compared to what it was originally created for, it gives us reliable dimensions for human appendages and from there we can ascertain what a given individual would excel at in regard to sporting events (obviously this is just on the basis of physical measures and does not measure the mind one needs to excel in sports).
The somatotyping system is straightforward: You have three values, say at 1-1-7; the first refers to endomorphy, the second refers to mesomorphy and the third refers to ectomorphy, therefore a 1-1-7 would be an extreme ectomorph. However, few people are at the extreme end of each soma, and most people have a combination of two or even all three of the somas.
According to Carter (2002): “The somatotype is defined as the quantification of the present shape and composition of the human body.” So, obviously, somas can change over time. However, it should be noted that the somatotype is, largely, based on one’s musculoskeletal system. This is where the appendages come in, along with body fat, wide and narrow clavicles and chest etc. This is why the typing system, although it began as a now-discredited method, should still be used today since we do not use the pseudoscientific personality measures with somatotyping.
Ectomorphs are long and lean, lanky, you could say. They have a smaller, narrower chest and shoulders, along with longer arms and legs, and have a hard time gaining weight, and a short upper body (I’d say they have a harder time gaining weight due to a slightly faster metabolism, in the variation of the normal range of metabolism, of course). Put simply, ectomorphs are just skinny and lanky with less body fat than mesos and endos. Human races that fit this soma are East Africans and South Asians (see Dutton and Lynn, 2015; one of my favorite papers from Lynn for obvious reasons).
Endomorphs are stockier, shorter and have wider hips, along with short limbs, a wider trunk, more body fat and can gain muscular strength easier than the other somas. Thus, endos, being shorter than ectos and mesos, have a lower center of gravity, along with shorter arms. Thus, we should see that these somas dominate strongman competitions and this is what we see. Pure strength competitions are perfect for this type, such as Strongman competitions and powerlifting. Races that generally conform to this type are East Asians, Europeans, and Pacific Islanders (see Dutton and Lynn, 2015).
Finally, we have mesomorphs (the “king” of all of the types). Mesos are more muscular on average than the two others, they have less body fat than endos but more body fat than ectos; they have wider shoulders, chest and hips, a short trunk and long limbs. The most mesomorphic races are West Africans (Malina, 1969), and due to their somatotype they can dominate sprinting competitions; they also have thinner skin folds (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000), and so they would have an easier time excelling at running competitions but not at weightlifting, powerlifting, or Strongman (see Dutton and Lynn, 2015).
These anatomic differences between the races of man are due to climatic adaptations. The somatypic differences Neanderthals and Homo sapiens mirror the somatotype difference between blacks and whites; since Neanderthals were cold-adapted, they were shorter, had wider pelves and could thusly generate more power than the heat-adapted Homo sapiens who had long limbs and narrow pelvis to better dissipate heat. Either way, we can look at the differences in somatotype between races that evolved in Europe and Africa to ascertain the somatotype of Neanderthals—and we also have fossil evidence for these claims, too (see e.g., Weaver and Hublin, 2009; Gruss and Schmitt, 2016)
Now, just because somatotyping, during its conception, was mixed with pseudoscientific views about differing somas having differing psychological types, does not mean that these differences in body type do not have any bearing on sporting performance. We can chuck the “constitutional psychology” aspect of somatotyping and just keep the anthropometric measures, and, along with the knowledge of human biomechanics, we can then discuss, in a scientific manner, why one soma would excel in sport X or why one soma would not excel in sport X. Attempting to argue that since somatotyping began as some crank psuedoscience does not mean that it is not useful today, since we do not ascribe inherent psychological differences to these somas (I’d claim that saying that this soma has a harder time gaining weight compared to that soma is not ascribing a psychological difference to the soma; it is taking physiologically and on average we can see that different somas have different propensities for weight gain).
In her book Straightening the Bell Curve: How Stereotypes about Black Masculinity Drive Research about Race and Intelligence, Hilliard (2012: 21) discusses the pitfalls of somatotyping and how Sheldon attempted to correlate personality measures with his newfound somatotypes:
As a young graduate student, he [Richard Herrnstein] had fallen under the spell of Harvard professor S. S. Stevens, who had coauthored with William Sheldon a book called The Varieties of Temperament: A Psychology of Constitutional Differences, which popularized the concept of “somatotyping,” first articulated by William Sheldon. This theory sought, through the precise measurement and analysis of human body types, to establish correlations comparing intelligence, temperament, sexual proclivities, and the moral worth of individuals. Thus, criminals were perceived to be shorter and heavier and more muscular than morally upstanding citizens. Black males were reported to rank higher on the “masculine component” scale than white males did, but lower in intelligence. Somatotyping lured the impressionable young Herrnstein into a world promising precision and human predictability based on the measuring of body parts.
Though constitutional psychology is now discredited, there may have been something to some of Sheldon’s theories. Ikeda et al (2018: 3) conclude in their paper, Re-evaluating classical body type theories: genetic correlation between psychiatric disorders and body mass index, that “a trans-ancestry meta-analysis of the genetic correlation between psychiatric disorders and BMI indicated that the negative correlation with SCZ supported classical body type theories proposed in the last century, but found a negative correlation between BD and BMI, opposite to what would have been predicted.” (Though it should be noted that SCZ is a, largely if not fully, environmentally-induced disorder, see Joseph, 2017.)
These different types (i.e., the differing limb lengths/body proportions) have implications for sporting performance. Asfaw and A (2018) found that Ethiopian women high jumpers had the highest ectomorph values whereas long and triple jumpers were found to be more mesomorphic. Sports good for ectos are distance running due to their light frame, tennis etc—anything that the individual can use their light frame as an advantage. Since they have longer limbs and a lighter frame, they can gain more speed in the run up to the jump, compared to endos and mesos (who are heavier). This shows why ectos have a biomechanical advantage when it comes to high jumping.
As for mesomorphs, the sports they excel at are weightlifting, powerlifting, strongman, football, rugby etc. Any sport where the individual can use their power and heavier bone mass will they excel in. Gutnik et al (2017) even concluded that “These results suggest with high probability that there is a developmental tendency of change in different aspects of morphometric phenotypes of selected kinds of sport athletes. These phenomena may be explained by the effects of continuous intensive training and achievement of highly sport-defined shapes.” While also writing that mesomorphy could be used to predict sporting ability.
Finally, for endomorphs, they too would excel in weightlifting, powerlifting, and strongman, but do on average better since they have different levers (i.e., shorter appendages so they can more weight and a shorter amount of time in comparison to those with longer limbs like ectos).
Thus, different somatotypes excel in different sports. Different races and ethnies have differing somatotypes (Dutton and Lynn, 2015), so these different bodies that the races have, on average, is part of the cause for differences in sporting ability. That somatotyping began as a pseudoscientific endeavor 70 years ago does not mean that it does not have a use in today’s world—because it clearly does due to the sheer amount of papers on the usefulness of somatotyping and relating differences in sporting performance due to somatotyping. For example, blacks have thinner skin folds (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000) which is due to their somatotype, which is then due to the climate their ancestors evolved in.
Somatotyping can show us the anthropometric reasons for how and why certain individuals, ethnies, and races far-and-away dominate certain sporting events. It is completely irrelevant that somatotyping began as a psychological pseudoscience (what isn’t in psychology, am I right?). Understanding anthropometric differences between individuals and groups will help us better understand the evolution of these somas along with how and why these somas lead to increased sporting performance in certain domains. Somatotyping has absolutely nothing to do with “intelligence” nor how morally upstanding one is. I would claim that somatotyping does have an effect on one’s perception of masculinity, and thus more masculine people/races would tend to be more mesomorphic, which would explain what Hilliard (2012) discussed when talking about somatotyping and the attempts to correlate differing psychological tendencies to each type.
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.
|Data from Malina, (1969: 438)||n||Mesomorph||Ectomorph||Endomorph|
|Data from Malina (1969: 438)||Blacks||Whites|
|Thin-build body type||8.93||5.90|
|Submedium fatty development||48.31||29.39|
|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.
I’ve been chronicling the VDH recently since it has great explanatory—and predictive—power. Light skin is a clear adaptation to low UVR, while dark skin is a clear adaptation to high UVR. Dark, highly melanized skin confers advantages in high UVR environments, such as protection against DNA damage, and also absorbs sufficient UV for vitamin D production while also protecting against folate depletion. However, when our ancestors migrated out of Africa, dark skin would not cut it in temperate environments with highly variable UV rays. This is where our highly adaptive physiology came into play, ensuring that we survived in highly variable environments. Light skin was important in low UVR environments in order to synthesize ample vitamin D, however, that synthesized vitamin D then conferred numerous other physiological advantages to the cold.
Eighty to ninety percent of the vitamin D required for humans comes from the sun, whereas ten to twenty percent comes from the diet, such as fatty fish, eggs, and dairy products (fortified with vitamin D, of course) (Ajabshir, Asif, and Nayer, 2014). Humans need to rely on high amounts of UV rays for vitamin D synthesis (Carlberg, 2014) other than Arctic peoples. Since dark skin does not synthesize vitamin D as well as light skin, skin gradually lightened as our ancestors migrated out of Africa (Juzeniene et al, 2009). This was then imperative to the physiologic adaptations that then occurred as our physiology had to adapt to novel, colder environments with fewer UV rays.
Sufficient amounts of vitamin D are highly important for the human musculoskeletal system (Wintermeyer et al, 2016), which is extremely important for birthing mothers. Along with the increased vitamin D synthesis in low UV environments, the heightened production of vitamin D conferred numerous other physiologic benefits which then helped humans adapt to colder environments with more varying UVR.
Vasoconstriction occurs when the blood vessels constrict which leads to heightened blood pressure, whereas vasodilation is the dilation of blood vessels which decreases blood pressure. So evolutionarily speaking, we had to have adaptive physiology in order to be able to “switch” back and forth between vasoconstriction and vasodilation, depending on what the current environment needed. Vasodilation, though, most likely had no advantage in high UV environments, and thus must have been an advantage in low UV environments, where it was more likely to be colder and so, when the blood vessels constrict, blood pressure increases and thus, heat loss could be considerably slowed in these environments due to these physiologic adaptations.
The races also differ, along with many other physiologic abilities, in nitric oxide-mediated vasodilation. Vasodilation is the dilation of blood vessels, which increases blood pressure. Mata-Greenwood and Chen (2008) reviewed the relevant literature regarding black/white differences in nitric oxide-dependent vasorelaxation and concluded that nitric oxide vasodilation is reduced in darker-skinned populations. Thus, we can infer that in lighter-skinned populations nitric oxide vasodilation is increased in lighter-skinned populations, which would have conferred a great physiological advantage when it came to colonizing environments with lower UV rays.
VDR and vitamin D metabolizing enzymes are present in adipose tissue. Tetrahydrobiopterin; which acts as a cofactor in the synthesis of nitric oxide and its primary function is as a vasodilator in the blood vessels (meaning that blood pressure is increased, to keep more heat in the cold) (Chalupsky and Cai, 2005). Since vasodilation is the body’s primary response to heat stress, blood flow increases which allows heat to leave the body. Therefore, the human body’s ability regarding vasodilation and vasoconstriction mechanisms were important in surviving areas with varying UVR.
One function of our adipose tissue is the storage of vitamin D, while vitamin D metabolizing enzymes and VDR are also expressed in the adipocyte (Abbas, 2017). With these known actions of vitamin D on adipose tissue, we can speculate that since vitamin D and the VDR are expressed in adipose tissue, it may have exerted a role in the adipose tissue which may have been important for surviving in cold, low UV environments (see below).
Furthermore, since these mechanisms are brought on by short-term changes, we can infer that it would hardly be of any use in high UVR environments and would be critical in temperate environments. So, vasodilation and vasoconstriction have little to no benefit in high UVR environments but seem to be imperative in temperate environments where UVR varies. It’s also likely that vitamin D influences vasodilation by influential nitric oxide synthesis (see Andrukhova et al, 2014) and vasoconstriction by influencing the renin-angiotensin system (Ajabshir, Asig, and Nayer, 2014).
This would have conferred great benefit to our ancestors as they migrated into more temperate and colder climates. You can read this for information on how adaptive our physiology is and why it’s like that. Because we went into numerous new environments and natural selection couldn’t act quickly enough, therefore the human body’s physiology is extremely adaptive.
What this suggests is that as skin lightened and adapted to low UV, the increased synthesis in vitamin D influenced vasodilation by a strong influence on nitric oxide synthase, along with vasoconstriction, implies that it would have been easier to survive in novel environments due to adaptive physiology and skin color, along with body fat reserves and the physiologic effects of vitamin D on adipose tissue. These physiologic adaptations would have been of no to little use in Africa. Thus, they must have been useful after we migrated out of Africa and experienced wildly varying environments—the whole reason why our physiology evolved (Richardson, 2017: chapter 5).
When the human body is exposed to cold, a few things occur: cutaneous vasoconstriction, shivering (Castellani and Young, 2016), “behavioral thermoregulation” (Young, Sawka, and Pandolf, 1996), while the human body can adapt physiologically to the cold (Young, 1994). The physiologic functions that vitamin D and folate in regard to vasodilation and vasoconstriction, there is a great chance that these effects were important in maintaining energy homeostasis in colder climates.
In sum, the evolution of light skin conferred a great survival advantage to our ancestors. This then upped the production of vitamin D synthesis in the body, which where then of utmost importance in regard to the adaptation of the human physiology to colder, lower-UV environments. Without our adaptive physiological systems, we would not have been able to leave Africa into novel environments. We need both behavioral thermoregulation as well as adaptive physiology to be able to survive in novel environments. Thus, the importance of skin lightening in our evolution becomes clearer:
As humans migrated out of Africa, lighter skin was needed to synthesize vitamin D. This was especially important to women, who needed higher amounts of vitamin D, in order to produce enough calcium for lactation and pregnancy—so the babe had enough calcium to grow its skeleton in the womb. With the uptake in vitamin D synthesis, this then allowed more adaptive physiologic changes that occurred due to the cold, and along with vasodilation and vasoconstriction, along with shivering and adapting behaviorally to the new environments, were our ancestors able to survive. Dark skin cannot synthesize vitamin D as well as light skin in low UV environments; this also can be seen with the lowered production of nitric oxide-dependent vasodilation in dark-skinned populations. Thus, vasoconstriction conferred no physiologic benefit in high UV environments, but almost certainly conferred a physiologic benefit in low UV environments.
Extremists exist in every ideology (there are too many to name but take the books March of the Titans (Kemp, 1999) to Testosterone Rex (Fine, 2017) as examples), but some are (in my opinion) more extreme (and funnier and more delusional) than others (even if they’re almost neck and neck). Afrocentrists veer toward the extreme side (as Nordicists veer to the extreme side on the opposite end). But certain beliefs these ideologies have may “sound right” to the uneducated ear, especially when they begin to weave fantastical stories with physiological terminology in order to woo the listener. You see things like “Melanin affects the idea of white supremacy“, but what does this really mean (you will see what it means near the end of this article)? The one saying it may believe it themselves, though it all doesn’t make sense. The extremist views that are more interesting are the Afrocentric ones, though, especially the melanin theory that gets thrown around in Afrocentric circles.
Melanin is produced by melanocytes. Melanin is synthesized from L-tyrosine, with the help of tyrosinase, which is one of the main enzymes for melanin production (Solano, 2014; D’Mello et al, 2016). (See Cone, 2006 for a review of the melanocortin system.) Melanin absorbs energy from UV rays which then dissipate in the body as heat (de Monteallano, 1993). There are three types of melanin: eumelanin (there are two types of eumelanin: brown eumelanin and black eumelanin), pheomelanin (these two are present in the human epidermis; Thody et al, 1991; Solano, 2014) and neuromelanin. Pheomelanin and eumelanin are found in the hair and skin.
Races that live closer to the equator have higher concentrations of melanin in their skin (not neuromelanin, which will be discussed later) which then causes dark skin pigmentation. But everyone on earth has around the same number of melanocytes; skin pigmentation differences come down to differences in UV exposure (for which melanin is useful; and produced due to UV radiation Brenner and Hearing, 2008), disease (albinism and vitiligo), size of melanocytes (see below) and genetic make up.
Europeans and Chinese have about half as much melanin as African and Indian skin types, whereas Africans had the largest melanosomes, followed by the Indians, Mexicans, Chinese, and Europeans, therefore variation in melanosome size may also account for skin variation between races. It’s also interesting to note that people, no matter the skin color, who are born in high UV areas—regardless of ethnicity—have twice as much epidermal melanin compared to people born in low UV areas (Alaluf et al, 2002).
Melanin and pseudoscience
Rushton and Templer (2012) wrongly hypothesized that the melanocortin system modulated sexuality and aggression and humans as they do in animals. The claims made here are may “sound good” to one who isn’t well-versed in the physiology of aggression and sexuality, but to those people, Rushton and Templer’s hypothesis “sounds good enough” and so they believe it without question. On the opposite side, you have black “academics” who believe that melanin gives blacks some type of “greatness” and is the reason for their “natural moves.’ In the book Darwin’s Athletes: How Sport Has Damaged Black America and Preserved the Myth of Race, Hoberman (1997: 89) shortly discusses Afrocentric melanin theorists:
Finally, there are the melanin theorists. a motley collection of pseudo-scientific cranks and better-known members of the black academic demimonde who attended the Fourth Annual World Melanin Conference in Dallas in April 1989—Leonard Jeffries, John Henrik Clarke, Ivan Van Sertima, and others. For these racial biologists, the pigment that makes skin dark is “the Chemical Key to Black Greatness” and accounts for an entire range of superior black aptitudes: “The reason why Black athletes do so well and have these ‘natural moves’ is these melanic tracks in the brainstem tie into the cerrebellum . . . a part of us that controls motor movement (Dr. Richard King). The real signifigance of the melanin theory is that it is the reductio ad absurdum of black racial seperatism, putting its adherents in a de facto alliance with white racists, who have their own reasons to establish separate racial physiologies. Afrocentric science curricula that promote melanin theory have been introduced in a nimber of urban school districts in the United States, thereby doing educational damage to those children who can least afford it.
Note how there are similarities to Rushton and Templer’s (2012) hypothesis on the melanocortin system in darker-pigmented races (mainly blacks since that’s the race they theorized on). But what I find the funniest about melanin theory, as that some Afrocentrists use higher levels of melanin as “physiologic” proof that blacks are “superior athletes” (this can be explained without appealing to melanin). Though do note how the Afrocentric view of melanin and Rushton and Templer’s (2012) view of the melanocortin system and melanin are stark opposites of each other—and they’re both horribly wrong.
Now let’s look at some quotes from some Afrocentric websites.
These quotes are from Suzar’s (1999) book Blacked Out Through Whitewash: Exposing the Quantum Deception/Rediscovering and Recovering Suppressed Melanated (the author cites another book, Melanin: The Chemical Key to Black Greatness by Carol Barnes (1988):
“…your mental processes (brain power) are controlled by the same chemical that gives Black humans their superior physical (athletics, rhythmic dancing) abilities. This chemical…is Melanin!”
The abundance of melanin in Black humans produces a superior organism both mentally and physically. Black infants sit, stand, crawl and walk sooner than whites, and demonstrate more advanced cognitive skills than their white counterparts because of their abundance of melanin. Melanin is the neuro-chemical basis foe what is called “SOUL” in Black people. Melanin refines the nervous system in such a way that messages from the brain reach other areas of the body more rapidly in Black people than in the other. In the same way Blacks excel in athletics, Blacks can excel in all other areas as well (like they did in the past!) once the road blocks are removed.
Notice how this uses Rushton-like data similar to his ‘life history/r/K’ theory of human racial differences. People can have any kind of data they want, but when they start discussing the data then they are leaving the realm of science and are entering the realm of philosophy. They then interpret the data wrong, as evidence for ‘superiority’ in certain traits, and those who are less informed will buy it without question. Do note the similarities to Rushton and Templer’s (2012) hypothesis on the causes for sexual behavior and aggression differences in human races: melanin and the melanocortin system is partly a cause for these racial disparities. You only need a ‘good story’ (a just-so story) that seems like it is a plausible explanation in order to lure someone who’s unsuspecting to pseudo-science. (I would liken melanin to ‘g’ here. Both melanin and ‘g’ are given ‘powers’ that do not exist; but in the case of ‘g’, it doesn’t exist so at least Afrocentrists are discussing an actual hormone, though they are horribly misrepresenting what the actual data on melanin says.)
The most in-depth take-down of Afrocentric melanist theories is from de Mantellano (1993). Afrocentric theory states that black people—and Egyptians because they were black too (they weren’t)—since they have higher levels of melanin in their skin, then this gives them physical and mental superiority over those with less melanin in their skin. They misinterpret (willingly or not) many papers in order to push their pseudo-scientific theories to the ignorant masses (which already is occurring in inner-city schools, widening the already wide science gaps; see de Manteallno, 1992). What Afrocentrists do not understand is that all humans have similar anounts of neuromelanin (which they wrongly conflate with skin melanin), while neuromelanin levels in the brain are also independent of melanin levels in the skin. So the fantastic claims of melanin causing physical and mental ‘superiority’ (whatever that is) for darker-skinned individuals is unfounded.
Further claims from Afrocentrists are that since blacks have more skin melanin then this also means they have more melatonin and beta-melanocyte-stimulating hormone. Melatonin in humans also has no physiological relationship to skin color (de Mantellano, 1993). Lastly, Afrocentric melanists also state, as I have covered before, that Europeans are African albino mutants.
In fact, the claim that whites are just African albino mutants is ridiculous. Whites can produce eumelanin, while albinos can’t. Albinos are also homozygous recessive—since albinism is a Mendelian disorder, one must be homozygous recessive for “the albinism gene” (de Mantellano, 1993: 42). They can mate forever and they will never create offspring with the ability to synthesize melanin. Therefore it is impossible for whites to have been African albinos.
De Mantellano (1993) concludes that the theory is not to be taken seriously (of course) but states that “The idea that there are distinct races and that one is superior to the others is as racist and erroneous when it refers to high melanin levels as it was when it described low melanin levels (the Aryan “master race”)” (pg 54). Of course, no ‘master race’ exists, and the concept of ‘superiority’ has no basis in evolutionary biology, but race exists and is a biological reality. Though that doesn’t mean that any of the Afrocentric claims covered here have any basis—that’s because they conflate neuromelanin and melanin in the skin, even if they didn’t conflate the two they still would not be correct.
The fatal flaw in this type of Afrocentric “reasoning” is that neuromelanin differs in structure, location, and biosynthesis from skin melanin. Afrocentrists assert that neuromelanin and skin melanin are correlated. Though what falsifies this assertion is that albinos have the same amount of neuromelanin in their brains as non-albinos. So all of the purported ‘mental and physical superiority’ that was ’caused by melanin’ makes no sense, because neuromelanin and skin melanin were conflated. Neuromelanin does not even have the physiologic effects that most Afrocentrists believe.
Most Afrocentric melanists also cite individuals who cite…. rat studies and then extrapolate those results to humans. This is dumb. Yes I know the tired old “Humans are animals too!” but just because we’re animals too doesn’t mean that hormones work the same way in all species; it’s just some sort of bland appeal.
Perhaps one of the most amusing parts of de Mantellano (1993) is where he quotes a few prominent Afrocentrists who ‘argue’ that white men are afraid of black men because “Africans have very dominant genes”:
The conspiracy to destroy black youth. . . . It has to do with the fact that in terms of genetics and genes that because Africans have dominant genes that it is very possible for Africans to annihilate the European population. And the best way to prevent the annihilation is to get to the root of the perpetrator who could do that.
And that, of course, would be African men. Because it is men, specifically African men, that start the reproductive process off. For example, in looking at the four possibilities of sexual relationships. Of looking at those four there is only one possibility to produce a European child. If you have an African man with an African woman you will produce a child of color. If you have an African man with a European woman you will also produce a child of color. If you have a European man with an African woman that will also produce a child of color. European men can only produce a child that looks like them when they connect with a European woman. As the result of that, then, European men are very much afraid of African men and the conspiracy is directly centered at them. . . . And that’s that conspiracy is synonymous with the word genocide, and genocide not only is gradual, it is collective (Kunjufu, 1989).
The reason that the Black male . . . is and always has been central to the issue of white supremacy is clarified by the definition of racism as white genetic survival. In the collective white psyche, Black males represent the greatest threat to white genetic survival because only males (of any color) can impose sexual intercourse, and Black males have the greatest genetic potential (of all non-white males) to cause white genetic annihilation. Thus, Black males must be attacked and destroyed in a power system designed to assure white genetic survival. . . . The prevention of white genetic annihilation is pursued through all means, including chemical and biological warfare. Today, the white genetic survival imperative, instead of using chemicals in gas chambers, is using chemicals in the streets-crack, cocaine, ecstasy, PCP, heroin and methadon [sic] (all “designer chemicals”). [Welsing, 1991a: 4]
Other more outlandish ideas are quoted by de Mantellano (1993) too, and all of the claims made about the physiology of melanin, neuromelanin bringing supernatural, physical and mental powers are horribly flawed. These people have no understanding of the physiology of the hormone, nor what they’re really speaking about. These attempted physiological theories to attempt to show racial ‘superiority’ make absolutely no sense if one has a basic understanding of the physiological system.
Claims made by Afrocentrists regarding melanin and neuromelanin range from blacks having more melanin in their muscle cells which is the cause for black athleticism; darker-eyed people having quicker reaction times which was thought to be caused by melanin; melanin centers in the brain being important for controlling and coordination of the body and brain power; to being critical for control of memory, motivation, mental maturation etc; causing altered states of consciousness which then causes black people who attend Church to speak in toungues; helps in the processing of memory; melanin and the pineal gland is at highest functionality in humans; and they conflate skin melanin with neuromelanin, when they are two different hormones (references for these claims can be found in de Montenallo, 1993).
Psuedo-science about melanin is rampant, no matter which side one is on. Both sides make ridiculous assertions and leaps of logic regarding melanin, and I find it very amusing that each group is talking about the same thing while attempting to argue the polar opposite of what the other is arguing. These misconceptions come from no understanding of physiology, to ideological biases, to delusions of ‘superiority’ to just plain ignorance overall. Afrocentrist fairy tales most probably are widening and already-wide science gap between blacks and whites. Of course, race doesn’t really have any bearing on whether or not you’ll believe something, though of course, black kids are more susceptible to believing the fantastical stories and non-understandings of physiology that come from their inner-city teachers who will then indoctrinate them to their ideology.
Correlations between skin pigmentation and neuromelanin are nonexistent. Further, there is no known physiological relationship between melatonin and skin color in humans. Therefore, the assertion that blacks have more melatonin due to their skin color and they then have this physical and mental superiority due to melanin has absolutely no scientific basis (even though those who push these types of theories have absolutely no understanding of the physiology of the hormone they are discussing). Racial pride ‘stories’ are harmful to science education; I don’t see March of the Titans being taught at schools (if I am in error let me know), but Afrocentric melanist theories are?
The most important thing to take note of here is the similarities between Rushton and Templer (2012) and melanists. They mirror each other so well, they are talking about the same exact hormone, but both groups have wildly different conclusions. Rushton and Templer (2012) were driven by the (wrong) hypothesis that testosterone caused aggression and crime and that since a whole slew of animals that had dark pigmentation were aggressive, therefore this should apply to humans too because “Evolution doesn’t stop at the neck”, as most people say. On the other side, we have melanists making wild, almost sci-fi like claims about the power and magic of this one hormone in black bodies and only black bodies. To believe something like that you’d have to be either ignorant or highly biased.
Melanism is clearly untenable, and Afrocentrists who push this ‘theory’ should take a few physiology classes and learn what this hormone does in the human body because they are woefully misinformed, reading books of pseudo-science.
Racial differences in sporting success are undeniable. The races are somewhat stratified in different sports and we can trace the cause of this to differences in genes and where one’s ancestors were born. We can then say that there is a relationship between them since, they have certain traits which their ancestors also had, which then correlate with geographic ancestry, and we can explain how and why certain populations dominate (or would have the capacity to based on body type and physiology) certain sporting events. Critiques of Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It are few and far between, and the few that I am aware of are alright, but this one I will discuss today is not particularly good, because the author makes a lot of claims he could have easily verified himself.
In 2010, Ian Kerr published The Myth of Racial Superiority in Sports, who states that there is a “dark side” to sports, and specifically sets his sights on Jon Entine’s (2000) book Taboo. In this article, Kerr (2010) makes a lot of, in my opinion, giant claims which provide a lot of evidence and arguments in order to show their validity. I will discuss Kerr’s views on race, biology, the “environment”, “genetic determinism”, and racial dominance in sports (which will have a focus on sprinting/distance running in this article).
Since establishing the reality and validity of the concept of race is central to proving Entine’s (2002) argument on racial differences in sports, then I must prove the reality of race (and rebut what Kerr 2010 writes about race). Kerr (2010: 20) writes:
First, it is important to note that Entine is not working in a vacuum; his assertions about race and sports are part of a larger ongoing argument about folk notions of race. Folk notions of race founded on the idea that deep, mutually exclusive biological categories dividing groups of people have scientific and cultural merit. This type of thinking is rooted in the notion that there are underlying, essential differences among people and that those observable physical differences among people are rooted in biology, in genetics (Ossorio, Duster, 2005: 2).
Dividing groups of people does have scientific, cultural and philosophical merit. The concept of “essences” has long been discarded by philosophers. Though there are differences in both anatomy and physiology in people that differ by geographic location, and this then, at the extreme end, would be enough to cause the differences in elite sporting competition that is seen.
Either way, the argument for the existence of race is simple: 1) populations differ in physical attributes (facial, morphological) which then 2) correlate with geographic ancestry. Therefore, race has a biological basis since the physical differences between these populations are biological in nature. Now that we have established that race exists using only physical features, it should be extremely simple to show how Kerr (2010) is in error with his strong claims regarding race and the so-called “mythology” of racial superiority in sports. Race is biological; the biological argument for race is sound (read here and here, and also see Hardimon, 2017).
True genetic determinism—as is commonly thought—does not have any sound, logical basis (Resnick and Vorhaus, 2006). So Kerr’s (2010) claims in this section need to be dissected here. This next quote, though, is pretty much imperative to the soundness and validity of his whole article, and let’s just say that it’s easy to rebut and invalidates his whole entire argument:
Vinay Harpalani is one of the most outspoken critics of using genetic determinism to validate notions of inferiority or the superiority of certain groups (in this case Black athletes). He argues that in order for any of Entine’s claims to be valid he must prove that: 1) there is a systematic way to define Black and White populations; 2) consistent and plausible genetic differences between the populations can be demonstrated; 3) a link between those genetic differences and athletic performance can be clearly shown (2004).
This is too easy to prove.
1) While I do agree that the terminology of ‘white’ and ‘black’ are extremely broad, as can be seen by looking at Rosenberg et al (2002), population clusters that cluster with what we call ‘white’ and ‘black’ exist (and are a part of continental-level minimalist races). So is there a systematic way to define ‘Black’ and ‘White’ populations? Yes, there is; genetic testing will show where one’s ancestors came from recently, thereby proving point 1.
2) Consistent and plausible genetic differences between populations can be demonstrated. Sure, there is more variation within races than between them (Lewontin, 1972; Rosenberg et al, 2002; Witherspoon et al, 2007; Hunley, Cabana, and Long, 2016). Even these small between-continent/group differences would have huge effects on the tail end of said distribution.
3) I have compiled numerous data on genetic differences between African ethnies and European ethnies and how these genetic differences then cause differences in elite athletic performance. I have shown that Jamaicans, West Africans, Kenyans and Ethiopians (certain subgroups of the two aforementioned countries) have genetic/somatypic differences that then lead to differences in these sporting competitions. So we can say that race can predict traits important for certain athletic competitions.
1) The terminology of ‘White’ and ‘Black’ are broad; but we can still classify individuals along these lines; 2) consistent and plausible genetic differences between races and ethnies do exist; 3) a link between these genetic differences between genes/athletic differences between groups can be found. Therefore Entine’s (2002) arguments—and the validity thereof—are sound.
Kerr (2010) then makes a few comments on the West’s “obsession with superficial physical features such as skin color”, but using Hardimon’s minimalist race concept, skin color is a part of the argument to prove the existence and biological reality of race, therefore skin color is not ‘superficial’, since it is also a tell of where one’s ancestors evolved in the recent past. Kerr (2010: 21) then writes:
Marks writes that Entine is saying one of three things: that the very best Black athletes have an inherent genetic advantage over the very best White athletes; that the average Black athlete has a genetic advantage over the average White athlete; that all Blacks have the genetic potential to be better athletes than all Whites. Clearly these three propositions are both unknowable and scientifically untenable. Marks writes that “the first statement is trivial, the secondly statistically intractable, and the third ridiculous for its racial essentialism” (Marks, 2000: 1077).
The first two, in my opinion (the very best black athletes have an inherent genetic advantage over the very best white athletes and the average black athlete has a genetic advantage over the average white athlete), are true, and I don’t know how you can deny this; especially if you’re talking about AVERAGES. The third statement is ridiculous, because it doesn’t work like that. Kerr (2010), of course, states that race is not a biological reality, but I’ve proven that it is so that statement is a non-factor.
Kerr (2010) then states that “ demonstrating across the board genetic variations between
populations — has in recent years been roundly debunked“, and also says “ Differences in height, skin color, and hair texture are simply the result of climate-related variation.” This is one of the craziest things I’ve read all year! Differences in height would cause differences in elite sporting competition; differences in skin color can be conceptualized as one’s ancestors’ multi-generational adaptation to the climate they evolved in as can hair texture. If only Kerr (2010) knew that this statement here was the beginning of the end of his shitty argument on Entine’s book. Race is a social construct of a biological reality, and there are genetic differences between races—however small (Risch et al, 2002; Tang et al, 2005) but these small differences can mean big differences at the elite level.
The “environment” and biological variability
Kerr (2010) then shifts his focus over to, not genetic differences, but biological differences. He specifically discusses the Kenyans—Kalenjin—stating that “height or weight, which play an instrumental role in helping define an individual’s athletic prowess, have not been proven to be exclusively rooted in biology or genetics.” While estimates of BMI and height are high (both around .8), I think we can disregard the numbers since they came from highly flawed twin studies, since molecular genetic evidence shows lower heritabilities. Either way, surely height is strongly influenced by ‘genes’. Another important caveat is that Kenya has one of the lowest BMIs in the world, 20.7 for Kenyan men, which also is part of the cause of why certain African ethnies dominate running competitions.
I don’t disagree with Kerr (2010) here too much; many papers show that SES/cultural/social factors are very important to Kenyan runners (Onywera et al, 2006; Wilbur and Pistiladis, 2012; Tucker, Onywera, and Santos-Concejero, 2015). You can have all of the ‘physical gifts’ in the world, if it’s not combined with the will to want to do your best, along with cultural and social factors you won’t succeed. But having an advantageous genotype and physique are useless without a strong mind (Lippi, Favaloro, and Guidi, 2008):
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.”
Dissecting this, though, is tougher. Because being born at certain altitudes will cause certain advantageous traits, such as a larger lung capacity (and you will have an advantage in lung capacity when competing at lower altitudes), but certain subpopulations live in these high-altitude areas, so what is it? Genetic? Cultural? Environmental? All three? Nature vs nurture is a false dichotomy; so it is a mixture of the three.
How does one explain, then, the athlete who trains countless hours a day fine-tuning a jump shot, like LeBron James or shaving seconds off sub-four minute miles like Robert Kipkoech Cheruiyot, a four time Boston Marathon winner?
Literally no one denies that elite athletes put in insane amounts of practice; but if everyone has the same amount of practice they won’t have similar abilities.
He also briefly brings up muscle fibers, stating:
These include studies on African fast twitch muscle fibers and development of motor skills. Entine includes these studies to demonstrate irrevocable proof of embedded genetic differences between populations but refuses to accept the fact that any differences may be due to environmental factors or training.
This, again, shows ignorance of the literature. An individual’s muscle fibers are formed during development from the fusion of several myoblasts, with differentiation being completed before birth. Muscle fiber typoing is also set at age 6, no difference in skeletal muscle tissue was found when comparing 6-year-olds and adults, therefore we can state that muscle fiber typing is set by age 6 (Bell et al, 1980). You can, of course, train type II fibers to have similar aerobic capacity to type I fibers, but they’ll never be fully similar. This is something that Kerr (2010) obviously is ignorant to because he’s not well-read on the literature which causes him to make dumb statements like “any differences [in muscle fiber typing] may be due to environmental factors or training“.
Black domination in sports
Finally, Kerr (2010) discusses the fact that whites dominated certain running competitions in the Olympics and that before the 1960s, a majority of distance-running gold medals went to white athletes. He then states that the 2008 Boston Marathon winner was Kenyan; but the next 4 behind him were not. Now, let’s check out the 2017 Marathon winners: Kenya, USA, Japan for the top 3; while 5 Kenyans/Ethiopians are in the top 15 while the same is also true of women; a Kenyan winner, with Kenyans/Ethiopians taking 5 of the top 15 spots. The fact that whites used to do well in running sports is a non-factor; Jesse Owens blew away the competition in the Games in Germany, which showed how blacks would begin to dominate in the US decades later.
Kerr (2010) then ends the article with a ton of wild claims; the wildest one, in my opinion, being that “Kenyans are no more genetically different from any other African or European population on average“, does anyone believe this? Because I have data to the contrary. They have a higher Vo2 max, which of course is trainable but with a ‘genetic’ component (Larsen, 2003), while other authors argue that genetic differences between populations account for differences in success in running competition between populations (Vancini et al, 2014), while male and female Kenyan and Ethiopian runners are the fastest in the half and full marathon (Knechtle et al, 2016). There is a large amount of data out there that speaks about Kenyan/Ethiopian and others’ dominance in running; it seems Kerr (2010) just ignored the data. I agree with Kerr that Kenyanholos show that humans can adapt to their environment; but his conclusion here:
The fact that runners coming from Kenya do so well in running events attests to the fact the combination of intense high altitude training, consumption of a low-fat, high protein diet, and a social and cultural expectation to succeed have created in recent decades an environment which is highly conducive to producing excellent long-distance runners.
is very strong, and while I don’t disagree at all with anything here, he’s disregarding how somatype and genes differ between Kenyans and other populations that compete in these sports that then lead to differences in elite sporting competitions.
Elite sporting performance is influenced by myriad factors, including psychology, ‘environment’, and genetic factors. Something that Kerr (2010) doesn’t understand—because he’s not well-read on this literature—is that many genetic factors that influence sporting performance are known. The ability to become elite depends on one’s capacity for endurance, muscle performance, the ability of the tendons and ligaments to withstand stress and injury, and the attitude to train and push above and beyond what normal people can do (Lippi, Longo, and Maffulli, 2010). We can then extend this to human races; some are better-equipped to excel in running competitions than others.
On its face, Kerr’s (2010) claim that there are no inherent differences between races is wrong. Races differ in somatype, which is due to evolution in different geographic locations for tens of thousands of years. The human body is perfectly adapted to for long distance running (Murray and Costa, 2012), and since our capabilities for endurance running evolved in Africa and they, theoretically, have a musculoskeletal structure similar to the Homo sapiens that left Africa around 70 kya, then it’s only logical to state that African’s, on average, have an inherent ability in running competitions (West and East Africans, while North Africans fare very well in middle distance running, which, again, comes down to living in higher altitudes like Kenyans and Ethiopians).
Wagner and Heyward (2000) reviewed many studies on the physiological differences between blacks and whites. Blacks skew towards mesomorphy; black youths had smaller billiac and bitrochanteric width (the widest measure of the pelvis at the outer edges and the flat process on the femur, respectively), and black infants had longer extremities than white infants (Wagner and Heyward, 2000). We have anatomic evidence that blacks are superior runners (in an American context). Mesomorphic athletes are more likely to be sprinters (Sands et al, 2005; which is also seen in prepubescent children: Marta et al, 2013) Kenyans are ecto-dominant (Vernillo et al, 2013) which helps to explain their success at long-distance running. So just on only looking at the phenotype (a marker for race with geographic ancestry, proving the biological existence of race) we can confidently state, on average just by looking at an individual or a population, how they will fare in certain competitions.
Kerr’s (2010) arguments leave a ton to be desired. Race exists and is a biological reality. I don’t know why this paper got published since it was so full of errors; his arguments were not sound and much of the literature contradicts his claims. What he states at the end about Kenyans is not wrong at all, but to not even bring up genetic/biologic differences as a factor influencing their performance is dishonest.
Of course, a whole slew of factors, be they biological, cultural, psychological, genetic, socioeconomic, anatomic, physiologic etc influence sporting performance, but certain traits are more likely to be found in certain populations, and in the year 2018 we have a good idea of what influences elite sporting performance and what does not. It just so happens that these traits are unevenly distributed between populations, and the cause is evolution in differing climates in differing geographic locations.
Race exists and is a biological reality. Biological anatomic/physiological differences between these races then manifest themselves in elite sporting competition. The races differ, on average, in traits important for success in certain competitions. Therefore, race explains some of the variance in elite sporting competition.
Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals? A Response to Rushton and Templer (2012)
Rushton et al have kept me pretty busy over the last year or so. I’ve debunked many of their claims that rest on biology—such as testosterone causing crime and aggression. The last paper that Rushton published before he died in October of 2012 was an article with Donald Templer—another psychologist—titled Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals? (Rushton and Templer, 2012) and they make a surfeit of bold claims that do not follow. They review animal studies on skin and fur pigmentation and show that the darker an animal’s skin or fur, the more likely they are to be aggressive and violent. They then conclude that, of course (it wouldn’t be a Rushton article without it), that the long-debunked r/K ‘continuum’ explains the co-variation between human populations in birth rate, longevity, violent crime, infant mortality and rate and acquisition of AIDS/HIV.
In one of the very first articles I wrote on this site, I cited Rushton and Templer (2012) favorably (back when I had way less knowledge of biology and hormones). I was caught by biases and not knowing anything about what was discussed. After I learned more about biology and hormones over the years, I came to find out that the claims in the paper are wrong and that they make huge, sweeping conclusions based on a few correlations. Either way, I have seen the error of my ways and the biases that lead me to the beliefs I held, and when I learned more about hormones and biology I saw how ridiculous some of the papers I have cited in the past truly were.
Rushton and Templer (2012) start off the paper by discussing Ducrest et al (2008) who state that within each species studied, darker-pigmented individuals of said species exhibited higher rates of aggression, sexuality and social dominance (which is caused by testosterone) than lighter-pigmented individuals in that same species. They state that this is due to pleiotropy—when a single gene has to or more phenotypic effects. They then refer to Rushton and Jensen (2005) to reference the claim that low IQ is correlated with skin color (skin color doesn’t cause IQ, obviously).
They then state that in 40 vertebrate species that within each that the darker-pigmented members had higher levels of aggression and sexual activity along with a larger body size, better stress resistance, and are more physically active while grooming (Ducrest, Keller, and Roulin, 2008). Rushton and Templer (2012) then state that this relationship was ‘robust’ across numerous species, specifically 36 species of birds, 4 species of fish, 3 species of mammals, and 4 species of reptiles.
Rushton and Templer (2012) then discuss the “Validation of the pigmentation system as causal to the naturalistic observations was demonstrated by experimentally manipulating pharmacological dosages and by studies of cross-fostering“, citing Ducrest, Keller, and Roulin (2008). They even state that ‘Placing darker versus lighter pigmented individuals with adoptive parents of the opposite pigmentation did not modify offspring behavior.” Seems legit. Must mean that their pigmentation caused these differences. They then state something patently ridiculous: “The genes that control that balance occupy a high level in the hierarchical system of the genome.” Though, unfortunately for their hypothesis, there is no privileged level of causation (Noble, 2016; also see Noble, 2008), so this is a nonsense claim. Genes are not ‘blueprints’ or ‘recipes’ (Oyama, 1985; Schneider, 2007).
They then refer to Ducrest, Keller and Roulin (2008: 507) who write:
In this respect, it is important to note that variation in melanin-based coloration between human populations is primarily due to mutations at, for example, MC1R, TYR, MATP and SLC24A5 [29,30] and that human populations are therefore not expected to consistently exhibit the associations between melaninbased coloration and the physiological and behavioural traits reported in our study.
This quote, however, seems to be ignored by Rushton and Templer (2012) throughout the rest of their article, and so even though they did a brief mentioning of the paper and how one should be ‘cautious’ in interpreting the data in their study, it seems like they just brush it under the rug to not have to contend with it. Rushton and Templer (2012) then cite the famous silver fox study, where tame foxes were bred. They lost their dark fur and became lighter and, apparently, were less aggressive than their darker-pigmented kin. These animal studies are, in my useless when attempting to correlate skin color and the melanocortin system in the modulation of aggressive behavior, so let’s see what they write about human studies.
It’s funny, because Rushton and Templer (2012) cite Ducrest, Keller, and Roulin (2008: 507) to show that caution should be made when assessing any so-called differences in the melanocortin system between human races. They then disregard that by writing “A first examination of whether melanin based pigmentation plays a role in human aggression and sexuality (as seen in non-human animals), is to compare people of African descent with those of European descent and observe whether darker skinned individuals average higher levels of aggression and sexuality (with violent crime the main indicator of aggression).” This is a dumb comparison. Yes, African nations commit more crime than European nations, but does this mean that the skin color (or whatever modulates skin color/melanocortin system) is the cause for this? No. Not at all.
There really isn’t anything to discuss here, though, because they just run through how different African nations have higher levels of crime than European and East Asian nations, how blacks report having more sex and feel less guilty about it. Rushton and Templer (2012) then state that one study “asked married couples how often they had sex each week. Pacific Islanders and Native Americans said from 1 to 4 times, US Whites answered 2–4 times, while Africans said 3 to over 10 times.” They then switch over to their ‘replication’ of this finding, using the data from Alfred Kinsey (Rushton and Bogaert, 1988). Though, unfortunately for Rushton and Bogaert, there are massive problems with this data.
Though, the Kinsey data can hardly be seen as representative (Zuckerman and Brody, 1988), and it is also based on outdated, non-representative, non-random samples (Lynn, 1989). Rushton and Templer (2012) also discuss so-called differences in penis size between races, too. But I have written two response articles on the matter and shown that Rushton used shoddy sources like ‘French Army Surgeon who contradicts himself: “Similarly, while the French Army surgeon announces on p. 56 that he once discovered a 12-inch penis, an organ of that size becomes “far from rare” on p. 243. As one might presume from such a work, there is no indication of the statistical procedures used to compute averages, what terms such as “often” mean, how subjects were selected, how measurements were made, what the sample sizes were, etc” (Weizmann et al, 1990: 8).
Rushton and Templer (2012) invoke, of course, Rushton’s (1985; 1995) r/K selection theory as applied to human races. I have written numerous articles on r/K selection and attempts at reviving it, but it is long dead, especially as a way to describe human populations (Anderson, 1991; Graves, 2002). The theory was refuted in the late 70s (Graves, 2002), and replaced with age-specific mortality (Reznick et al, 2002). Some of his larger claims I will cover in the future (like how r/K relates to criminal activity), but he just goes through all of the same old motions he’s been going through for years, bringing nothing new to the table. In all honesty, testosterone is one of the pillars of Rushton’s r/K selection theory (e.g., Lynn, 1990; Rushton, 1997; Rushton, 1999; Hart, 2007; Ellis, 2017; extensive arguments against Ellis, 2017 can be found here). If testosterone doesn’t do what he believes it does and the levels of testosterone between the races are not as high as believed/non-existent (Gapstur et al, 2002; read my discussion of Gapstur et al 2002; Rohrmann et al, 2007; Richard et al, 2014. Though see Mazur, 2016 and read my interpretation of the paper) then we can safely disregard their claims.
Another is that Blacks have the most testosterone (Ellis & Nyborg, 1992), which
helps to explain their higher levels of athletic ability (Entine, 2000).
As I have said many times in the past, Ellis and Nyborg (1992) found a 3 percent difference in testosterone levels between white and black ex-military men. This is irrelavent. He also, then cites John Entine’s (2002) book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It, but this doesn’t make sense. Because he literally cites Rushton who cites Ellis and Nyborg (1992) and Ross et al (1986) (stating that blacks have 3-19 percent higher levels of testosterone than whites, citing Ross et al’s 1986 uncorrected numbers)—and I have specifically pointed out numerous flaws in their analysis and so, Ross et al (1986) cannot seriously be used as evidence for high testosterone differences between the races. Though I cited Fish (2013), who wrote about Ellis and Nyborg (1992):
“These uncorrected figures are, of course, not consistent with their racial r- and K-continuum.”
Rushton and Templer (2012) then state that testosterone acts like a ‘master switch’ (Rushton, 1999), implicating testosterone as a cause for aggression, though I’ve shown that this is not true, and that aggression causes testosterone production, testosterone doesn’t cause aggression. Testosterone does control muscle mass, of course. But Rushton’s claim that blacks have deeper voices due to higher levels of testosterone, but this claim does not hold in newer studies.
Rushton and Templer (2012) then shift gears to discuss Templer and Arikawa’s (2006) study on the correlation between skin color and ‘IQ’. However, there is something important to note here from Razib:
we know the genetic architecture of pigmentation. that is, we know all the genes (~10, usually less than 6 in pairwise between population comparisons). skin color varies via a small number of large effect trait loci. in contrast, I.Q. varies by a huge number of small effect loci. so logically the correlation is obviously just a correlation. to give you an example, SLC45A2 explains 25-40% of the variance between africans and europeans.
long story short: it’s stupid to keep repeating the correlation between skin color and I.Q. as if it’s a novel genetic story. it’s not. i hope don’t have to keep repeating this for too many years.
Rushton and Templer (2012: 7) conclude:
The melanocortin system is a physiological coordinator of pigmentation and life history traits. Skin color provides an important marker placing hormonal mediators such as testosterone in broader perspective.
I don’t have a problem with the claim that the melanocortin system is a physiological coordinator of pigmentation, because it’s true and we have a great understanding of the physiology behind the melanocortin system (see Cone, 2006 for a review). EvolutionistX also has a great article, reviewing some studies (mouse studies and some others) showing that increasing melatonin appears to decreases melanin.
Rushton and Templer’s (2012) make huge assumptions not warranted by any data. For instance, Rushton states in his VDare article on the subject, J. Phillipe Rushton Says Color May Be More Than Skin Deep, “But what about humans? Despite all the evidence on color, aggression, and sexuality in animals, there has been little or no discussion of the relationship in people. Ducrest & Co. even warned that genetic mutations may make human populations not exhibit coloration effects as consistently as other species. But they provided no evidence.” All Rushton and Templer (2012) do in their article is just restating known relationships with crime and race, and then attempting to implicate the melanocortin system as a factor driving this relationship, literally off of a slew of animal studies. Even then, the claim that Ducrest, Keller, and Roulin (2008: 507) provide no evidence for their warning is incorrect, because before they stated that, they wrote “In this respect, it is important to note that variation in melanin-based coloration between human populations is primarily due to mutations at, for example, MC1R, TYR, MATP and SLC24A5 [29,30]. . .” Melanin does not cause aggression, it does not cause crime. Rushton and Templer just assume too many things based on no evidence in humans, while their whole hypothesis is structured around a bunch of animal studies.
In conclusion, it seems like Rushton and Templer don’t know anything about the physiology of the melanocortin system if they believe that pigmentation and the melanocortin system modulates aggression and sexual behavior in humans. I know of no evidence (studies, not Rushton and Templer’s 2012 relationships with crime and then asserting that, because these relationships are seen in animals, that it must mean that the melanocortin system in humans modulates the relationships too) for these assertions by Rushton and Templer (2012). The fact that they think that restating relationships between crime and race, country of origin and race, supposed correlations with testosterone and crime and blacks supposedly having higher testosterone than whites, among other things, is caused by the melanocortin system and pigmentation has no basis in reality.