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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.
I say that if you are over-weight and wish to lose weight, then you should eat less. You should keep eating less until you achieve your desired weight, and then stick to that level of calorific intake.
Why only talk about calories and assume that they do the same things once ingested into the body? See Feinman and Fine (2004) to see how and why that is fallacious. This was actually studied. Contestants on the show The Biggest Loser were followed after they lost a considerable amount of weight. They followed the same old mantra: eat less, and move more. Because if you decrease what is coming in, and expend more energy then you will lose weight. Thermodynamics, energy in and out, right? That should put one into a negative energy balance and they should lose weight if they persist with the diet. And they did. However, what is going on with the metabolism of the people who lost all of this weight, and is this effect more noticeable for people who lost more weight in comparison to others?
Fothergill et al (2016) found that persistent metabolic slowdown occurred after weight loss, the average being a 600 kcal slowdown. This is what the conventional dieting advice gets you, a slowed metabolism with you having to eat fewer kcal than one who was never obese. This is what the ‘eat less, move more’ advice, the ‘CI/CO’ advice is horribly flawed and does not work!
He seems to understand that exercise does not work to induce weight loss, but it’s this supposed combo that’s supposed to be effective, a kind of one-two punch, and you only need to eat less and move more if you want to lose weight! This is horribly flawed. He then shows a few table from a paper he authored with another researcher back in 1974 (Bhanji and Thompson, 1974).
Say you take 30 people who weigh the same, have the same amount of body fat and are the same height, they eat the same exact macronutrient composition, with the same exact foods, eating at a surplus deficit with the same caloric content, and, at the end of say, 3 months, you will get a different array of weight gained/stalled/decrease in weight. Wow. Something like this would certainly disprove the CI/CO myth. Aamodt (2016: 138-139) describes a study by Bouchard and Tremblay (1997; warning: twin study), writing:
When identical twins, men in their early 20s, were fed a thousand extra calories per day for about three months, each pair showed similar weight gains. In contrast, the gains varied across twin pairs, ranging from nine to twenty-nine pound, even though the calorie imbalance esd the same for everyone. An individual’s genes also influence weight loss. When another group of identical twins burned a thousand more calories per day through exercise while maintaining a stable food intake in an inpatient facility, their losses ranged from two to eighteen pounds and were even more similar within twin pairs than weight gain.
Take a moment to think about that. Some people’s bodies resis weight loss so well that burning an extra thousand calpires a day for three months, without eating more, leads them to lose only two pounds. The “weight loss is just math” crows we met in the last chapter needs to look at what happens when their math is applied to living people. (We know what usually happens: they accuse the poor dieter of cheating, whether or not it’s true.) If cutting 3,500 calories equals one pound of weight loss, then everyone on the twuns’ exercist protocol should have lost twenty-four pounds, but not a single participant lost that much. The average weight loss was only eleven pounds, and the individual variation was huge. Such differences can result from genetic influences on resting metabolism, which varies 10 to 15 percent between people, or from differences in the gut. Because the thousand-calorie energy imbalance was the same in both the gain and loss experiments, this twin research also illustrates that it’s easier to gain weight than to lose it.
That’s weird. If a calorie were truly a calorie, then, at least in the was CI/COers word things, everyone should have had the same or similar weight loss, not with the average weight loss less than half what should have been expected from the kcal they consumed. That is a shot against the CI/CO theory. Yet more evidence against comes from the Vermont Prison Experiment (see Salans et al, 1971). In this experiment, they were given up to 10,000 kcal per day and they, like in the other study described previously, all gained differing amounts of weight. Wow, almost as if individuals are different and the simplistic caloric math of the CI/COers doesn’t size up against real-life situations.
The First Law of Thermodynamics always holds, it’s just irrelevant to human physiology. (Watch Gary Taubes take down this mythconception too; not a typo.) Think about an individual who decreases total caloric intake from 1500 kcal per day to 1200 kcal per day over a certain period of time. The body is then forced to drop its metabolism to match the caloric intake, so the metabolic system of the human body knows when to decrease when it senses it’s getting less intake, and for this reason the First Law is not violated here, it’s irrelevant. The same thing also occurred to the Biggest Loser contestants. Because the followed the CI/CO paradigm of ‘eat less and move more’.
Processed food is not bad in itself, but it is hard to monitor what is in it, and it is probably best avoided if you wish to lose weight, that is, it should not be a large part of your habitual intake.
If you’re trying to lose weight you should most definitely avoid processed foods and carbohydrates.
In general, all foods are good for you, in moderation. There are circumstances when you may have to eat what is available, even if it is not the best basis for a permanent sustained diet.
I only contest the ‘all foods are good for you’ part. Moderation, yes. But in our hedonistic world we live in today with a constant bombardment of advertisements there is no such thing as ‘moderation’. Finally, again, willpower is irrelevant to obesity.
I’d like to know the individual weight gains in Thompson’s study. I bet it’d follow both what occurred in the study described by Aamodt and the study by Sims et al. The point is, human physiological systems are more complicated than to attempt to break down weight loss to only the number of calories you eat, when not thinking of what and how you eat it. What is lost in all of this is WHEN is a good time to eat? People continuously speak about what to eat, where to eat, how to eat, who to eat with but no one ever seriously discusses WHEN to eat. What I mean by this is that people are constantly stuffing their faces all day, constantly spiking their insulin which then causes obesity.
The fatal blow for the CI/CO theory is that people do not gain or lose weight at the same rate (I’d add matched for height, overall weight, muscle mass and body fat, too) as seen above in the papers cited. Why people still think that the human body and its physiology is so simple is beyond me.
Hedonism along with an overconsumption of calories consumed (from processed carbohydrates) is why we’re so fat right now in the third world and the only way to reverse the trend is to tell the truth about human weight loss and how and why we get fat. CI/CO clearly does not work and is based on false premises, no matter how much people attempt to save it. It’s highly flawed and assumed that the human body is so ‘simple’ as to not ‘care’ about the quality of the macro nor where it came from.
An opinion piece by sociologist Roslyn Kerr, senior lecturer in sociology of sport, from Lincoln University wrote an article on January 18th for The Conversation titled Why it might be time to eradicate sex segregation in sports where she argues against sex segregation in sports. She does publish articles on sports history, leisure studies and sports management and used to be a gymnast so she should have good knowledge—perhaps better than the general public—on anatomy and physiology and how they interact during elite sporting performances. Though is there anything to the argument she provides in her article? Maybe.
The paper is pretty good, though it, of course, uses sociological terms and cites feminist theorists talking about gender binaries in sports and how they’re not ‘fair’. One thing continously brought up in the paper is how there is no way to discern sex regarding sporting competitions (Simpson et al, 1993; Dickinson et al, 2002; Heggie, 2010), with even chromosome-based testing being thrown out (Elsas et al, 2000). which can be seen with the Olympics “still struggling to define gender“. They state that women are put through humiliating tests to discern their sex.
They use this to buttress their own arguments which are based off of what bodies of disables athletes did: whether or not one competed in a particular sport was not on their disability, per se, but the functionality of their own bodies. As an example, sporting bodies used to group people with, say, a similar spinal injury even though they had different physical abilities. Call me crazy, but I most definitely see the logic that these authors are getting at, and not only because I ruminated on something similar back in the summer in an article on transgendered athletes in sports, writing:
This then brings up some interesting implications. Should we segregate competitions by race since the races have strength and weaknesses due to biology and anatomy, such as somatype? It’s an interesting question to consider, but I think we can all agree on one thing: Women should compete with women, and men should compete with men. Thus, transgenders should compete with transgenders.
Of course I posed the question regarding different races since they have different strengths and weaknesses on average due to evolution in different environments. Kerr and Obel (2017) conclude (pg 13):
Numerous authors have noted that the current two-sex classification system is problematic. They argued that it does not include all bodies, such as intersex bodies, and more importantly, does not work to produce fair competition. Instead, some argued that other traits that we know influence sporting success should be used to classify bodies. In this article, we extended this idea through using the ANT concepts of assemblage and black box. Specifically, we interpreted the current understanding of the body that sex segregation is based on as a black box that assumes the constant superiority of the male body over the female. But we argued that with the body understood as an assemblage, this classification could be reassembled so that this black box is no longer given. Instead we argued that by identifying the multiple traits that make up the assemblage of sporting success, sex classification becomes irrelevant and that it is these traits that we should use to classify athletes rather than sex. Drawing on the example of disability sport we noted that the black box of a medical label was undone and replaced with an emphasis on functionality with different effects for each sport. This change had the effect of undoing rigid medical disability label and enabling athletes’ bodies to be viewed as assemblages consisting of various functional and potentially changing physical abilities. We used this discussion to propose a model of classified that eliminated the need for sex segregation and instead used physical measures such as LBM and VO2 capabilities to determine an athlete’s competitive class.
All of their other arguments aside that I disagree with in their paper (their use of ‘feminist theory’, gendered divisions, short discussions and quotes from other authors on the ‘power structure’ of males), I definitely see the logic here and, in my opinion, it makes sense. Anyway, those shortcomings aside, the actual argument of using anatomy and physiology and seeing which different parts work in concert to produce elite athletic performance in certain sports then having some kind of test, say, the Heath-Carter method for somatype (Wilmore, 1970) to a test of Vo2 max (Cureton et al, 1986) to even lean body mass (LBM).
Healy et al (2014) studied 693 elite athletes in a post-competition setting. They assesed testosterone, among other variables such as aerobic performance. They observed a difference of 10 of between men and women’s LBM and that it exclusively accounts for the “observed diffences in strength and aerobic performance seen between the sexes” while they conclude:
We have shown that despite differences in mean testosterone level between genders, there is complete overlap of the range of concentrations seen. This shows that the recent decision of the IOC and IAAF to limit participation in elite events to women with ‘normal’ serum testosterone is unsustainable.
Yes, this testosterone-influences-sports-performance is still ongoing. I’ve covered it a bit last year, and while I believe there is a link between testosterone and athletic ability and have provided some data and a few anecdotes from David Epstein, I do admit that the actual literature is scant with conclusive evidence that testosterone positively influences sport performance. Either way, if testosterone truly does infer an advantage then, of course, the model (which Kerr and Obel admit is simple at the moment) will need to be slightly revised. Arguments and citations can be found in this article written back in the summer on whether or not transgender MtFs should compete with women. This is also directly related to the MtF who dominated women a few months back.
Either way, the argument that once we better identify anatomic and physiologic causes for differences in certain sporting competition, this could, in theory, be used instead of sex segregation. I think it’s a good idea personally and to see how effective it could be there should be a trial run on it. Kerr and Obel state that it would make competition more ‘fair’. However, Sanchez et al, 2014 cite Murray (2010) who writes “fair sports competition does not require that athletes be equal in every imaginable respect.”
At the end of the day, what a lot of this rests on is whether or not testosterone infers athletic advantage at the elite level and there is considerable data for both sides. It’ll be interesting to see how the major sporting bodies handle the question of testosterone in sports and transgenders and hyperandrogenic females.
Personally, I think there may be something to Kerr and Obel’s arguments in their paper (feminist/patriarchy garbage aside) since it’s based on anatomy and physiology which is what we see on the field. However, it can also be argued that sex/gender is manifested in the brain which then infers other advantages/disadvantages in sports. Nonetheless, I think the argument in the paper is sound (the anatomy and physiology arguments only). For instance, we can look at one sport, say, 100 m dash, and we can say “OK, we know that sprinters have meso-ecto somatypes and that combined with the RR ACTN3 genotype, that confers elite athletic performance (Broos et al, 2016).” We could use those two variables along with leg length, foot length etc and then we can test—both in the lab and on the field—which variables infer advantages in certain sports. Another sport we can think of is swimming. Higher levels of body fat with wide clavicles and chest cavity are more conducive to swimming success. We could use those types of variables for swimming and so on.
Of course, this method may not work or it may only work in theory but not work in practice. Using lean body mass, Vo2 max etc etc based on which sport is in question may be better than using the ‘sex binary’, since some women (trust me, I’ve trained hundreds) would be able to compete head-to-head with men and, if for nothing else, it’d be good entertainment.
However, in my opinion, the logic on using anatomy and physiology instead of sex to segregate in sports is intriguing and, if nothing else, would finally give feminists (and non-feminists) the ‘equality’ they ask for.
I’ve had a few discussions with Grey Enlightenment on this blog, regarding construct validity. He has now published a response piece on his blog to the arguments put forth in my article, though unfortunately it’s kind of sophomoric.
He calls himself a ‘race realist’yet echoes the same arguments used by those who oppose such realism.
1) One doesn’t have to believe in racial differences in mental traits to be a race realist as I have argued twice before in my articles You Don’t Need Genes to Delineate Race and Differing Race Concepts and the Existence of Race: Biologically Scientific Definitions of Race. It’s perfectly possible to be a race realist—believe in the reality of race—without believing there are differences in mental traits—‘intelligence’, for instance (whatever that is).
2) That I strongly question the usefulness and utility of IQ due to its construction doesn’t mean that I’m not a race realist.
3) I’ve even put forth an analogous argument on an ‘athletic abilities test’ where I gave a hypothetical argument where a test was constructed that wasn’t a true test of athletic ability and that it was constructed on the basis of who is or is not athletic, per the constructors’ presuppositions. In this hypothetical scenario, am I really denying that athletic differences exist between races and individuals? No. I’d just be pointing out flaws in a shitty test.
Just because I question the usefulness and (nonexistent) validity of IQ doesn’t mean that I’m not a race realist, nor that I believe groups or individuals are ‘the same’ in ‘intelligence’ (whatever that may be; which seems to be a common strawman for those who don’t bow to the alter of IQ).
Blood alcohol concentration is very specific and simple; human intelligence by comparison is not . Intelligence is polygenic (as opposed to just a single compound) and is not as easy to delineate, as, say, the concentration of ethanol in the blood.
It’s irrelevant how ‘simple’ blood alcohol concentration is. The point of bringing it up is that it’s a construct valid measure which is then calibrated against an accepted and theoretical biological model. The additive gene assumption is false, that is, genes being independent of the environment giving ‘positive charges’ as Robert Plomin believes.
He says IQ tests are biased because they require some implicit understanding if social constructs, like what 1+1 equals or how to read a word problem, but how is a test that is as simple as digit recall or pattern recognition possibly a social construct.
What is it that allows individuals to be better than others on digit recall or pattern recognition (what kind of pattern recognition?)? The point of my 1+1 statement is that it is construct valid regarding one’s knowledge of that math problem whereas for the word problem, it was a quoted example showing how if the answer isn’t worded correctly it could be indirectly testing something else.
He’s invoking a postmodernist argument that IQ tests do not measure an innate, intrinsic intelligence, but rather a subjective one that is construct of the test creators and society.
I could do without the buzzword (postmodernist) though he is correct. IQ tests test what their constructors assume is ‘intelligence’ and through item analysis they get the results they want, as I’ve shown previously.
If IQ tests are biased, how is then [sic] that Asians and Jews are able to score better than Whiles [sic] on such tests; surely, they should be at a disadvantage due to implicit biases of a test that is created by Whites.
If I had a dollar for every time I’ve heard this ‘argument’… We can just go back to the test construction argument and we can construct a test that, say, blacks and women score higher than whites and men respectively. How well would that ‘predict’ anything then, if the test constructors had a different set of assumptions?
IQ tests aren’t ‘biased’, as much as lower class people aren’t as prepared to take these tests as people in higher classes (which East Asians and Jews are in). IQ tests score enculturation to the middle class, even the Flynn effect can be explained by the rise in the middle class, lending credence to the aforementioned hypothesis (Richardson, 2002).
Regarding the common objection by the left that IQ tests don’t measures [sic] anything useful or that IQ isn’t correlated with success at life, on a practical level, how else can one explain obvious differences in learning speed, income or educational attainment among otherwise homogeneous groups? Why is it in class some kids learn so much faster than others, and many of these fast-learners go to university and get good-paying jobs, while those who learn slowly tend to not go to college, or if they do, drop out and are either permanently unemployed or stuck in low-paying, low-status jobs? In a family with many siblings, is it not evident that some children are smarter than others (and because it’s a shared environment, environmental differences cannot be blamed).
1) I’m not a leftist.
2) I never stated that IQ tests don’t correlate with success in life. They correlate with success in life since achievement tests and IQ tests are different versions of the same test. This, of course, goes back to our good friend test construction. IQ is correlated with income at .4, meaning 16 percent of the variance is explained by IQ and since you shouldn’t attribute causation to correlations (lest you commit the cum hoc, ergo propter hoc fallacy), we cannot even truthfully say that 16 percent of the variation between individuals is due to IQ.
3) Pupils who do well in school tend to not be high-achieving adults whereas children who were not good pupils ended up having good success in life (see the paper Natural Learning in Higher Education by Armstrong, 2011). Furthermore, the role of test motivation could account for low-paying, low-status jobs (Duckworth et al, 2011; though I disagree with their consulting that IQ tests test ‘intelligence’ [whatever that is] they show good evidence that in low scorers, incentives can raise scores, implying that they weren’t as motivated as the high scorers). Lastly, do individuals within the same family experience the same environment the same or differently?
As teachers can attest, some students are just ‘slow’ and cannot grasp the material despite many repetitions; others learn much more quickly.
This is evidence of the uselessness of IQ tests, for if teachers can accurately predict student success then why should we waste time and money to give a kid some test that supposedly ‘predicts’ his success in life (which as I’ve argued is self-fulfilling)? Richardson (1998: 117) quotes Layzer (1973: 238) who writes:
Admirers of IQ tests usually lay great stress on their predictive power. They marvel that a one-hour test administered to a child at the age of eight can predict with considerable accuracy whether he will finish college. But as Burt and his associates have clearly demonstrated, teachers’ subjective assessments afford even more reliable predictors. This is almost a truism.
Because IQ tests test for the skills that are required for learning, such as short term memory, someone who has a low IQ would find learning difficult and be unable to make correct inferences from existing knowledge.
Right, IQ tests test for skills that are required for learning. Though a lot of IQ test questions are general knowledge questions, so how is that testing anything innate if you’ve first got to learn the material, and if you have not you’ll score lower? Richardson (2002) discusses how people in lower classes are differentially prepared for IQ tests which then affects scores, along with psycho-social factors that do so as well. It’s more complicated than ‘low IQ > X’.
All of these sub-tests are positively correlated due to an underlying factor –called g–that accounts for 40-50% of the variation between IQ scores. This suggests that IQ tests measure a certain factor that every individual is endowed with, rather than just being a haphazard collection of questions that have nothing to do with each other. Race realists’ objection is that g is meaningless, but the literature disagrees “… The practical validity of g as a predictor of educational, economic, and social outcomes is more far-ranging and universal than that of any other known psychological variable. The validity of g is greater the complexity of the task.”
I’ve covered this before. It correlates with the aforementioned variables due to test construction. It’s really that easy. If the test constructors have a different set of presuppositions before the test is constructed then completely different outcomes can be had just by constricting a different test.
Then what about ‘g’? What would one say then? Nevertheless, I’ve heavily criticized ‘g’ and its supposed physiology, and if physiologists did study this ‘variable’ and if it truly did exist, 1) it would not be rank ordered because physiologists don’t rank order traits, 2) they don’t assume normal variations, they don’t estimate heritability and attempt to untangle genes from environment, 3) they don’t assume that normal variation is related to genetic variation (except in rare cases, like down syndrome, for instance), and 4) nor do they assume within the normal range of physiological differences that a higher level is ‘better’ than a lower. My go-to example here is BMR (basal metabolic rate). It has a similar heritability range as IQ (.4 to .8; which is most likely overestimated due to the use of the flawed twin method, just like the heritability of IQ), so is one with a higher BMR somehow ‘better’ than one with a lower BMR? This is what logically follows from assuming that ‘g’ is physiological and all of the assumptions that come along with it. It doesn’t make logical, physiological sense! (Jensen, 1998: 92 further notes that “g tells us little if anything about its contents“.)
All in all, I thank Grey Enlightenment for his response to my article, though it leaves a lot to be desired and if he responds to this article then I hope that it’s much more nuanced. IQ has no construct validity, and as I’ve shown, the attempts at giving it validity are circular, and done by correlating it with other IQ tests and achievement tests. That’s not construct validity.
American Renaissance published an article the other day titled “Is ‘Racism’ Killing Black People?” and, for the most part, I largely agree with it. However, there are a few faults in it that I need to address.
First, off, as the article rightly noted, it’s not only perceived ‘racism’ that is the cause for these health disparities, but stress from other blacks as well. Gregory Hood (the author of the AmRen article) cites a new study showing that blacks who move out of the ‘hood’ see a subsequent decrease in BP (Kershaw et al, 2017). They followed 2,290 people 974 were men and 1,306 were women. This is data collected from the CARDIA study which has helped us to understand racial disparities in all types of different health outcomes. Blacks who lived in high segregation neighborhoods had higher levels of SBP (systolic blood pressure), and saw a decrease in their SBP when they moved to less segregated neighborhoods. The authors conclude that “policies that reduce segregation may have meaningful health benefits.” What kind of policies will ‘reduce segregation’? Most races/ethnic groups group together in an area, so I don’t see how this would happen.
In regards to the argument on black maternal mortality and ‘racism’, I think it’s much more nuanced. Black women are 2 to 6 times more likely to die giving birth than white women; while the leading causes of maternal death in black women is pregnancy-induced hypertension, and embolism (Chang et al, 2003), though reasons for the mortality rate are not explainable at present (Flanders-Stepans, 2002). Further, in regards to preeclampasia, women who get pregnant at younger ages are more likely to acquire the disease while pregnant, and blacks and other non-whites are more likely to get pregnant at younger ages than whites (Main et al, 2015).
However, there are ways to reduce maternal mortality in black women. In a RCT undertaken between the years of 1990-2011 in Memphis, Tennesee, black women were followed with their live-in children and placed into one of four groups: “treatment 1 (transportation for prenatal care [n = 166]), treatment 2 (transportation plus developmental screening for infants and toddlers [n = 514]), treatment 3 (transportation plus prenatal/postpartum home visiting [n = 230]), and treatment 4 (transportation, screening, and prenatal, postpartum, and infant/toddler home visiting [n = 228])” (Olds et al, 2014). They conclude that pre- and post-natal care greatly reduces maternal/infant mortality in black women, “living in highly disadvantaged settings.”
Further, the racial disparity in post-term neonates is largely driven by “CHD among term infants with US-born mothers is driven predominately by the postneonatal survival disadvantage of African-American infants” (Collins et al, 2017). Though, as can be seen in the study by Olds et al (2014), pre- and post-natal care can greatly reduce both infant and maternal mortality.
Stress can also be measured in pregnant women by measuring the level of blood cortisol (Gillespie et al, 2017). They show that, independent of adulthood stress, stress during childhood may shape birth timing, with cortisol being the biological mediator. This may be an explanation for what Gregory Hood notes. He states in his article that there has to be an explanation for why black women birth earlier, and while I am sympathetic to biological models ala Rushton (1997), Gillespie et al (2017) drive a hard argument that stress during childhood using cortisol as a biological mediator makes a lot of sense.
There are a few studies that attest to pre- and post-natal care having a large effect on the morality of black women, and that having the carers being black women seems to have a positive effect (Guerra-Reyes and Hamilton, 2017). They conclude that “Recognition, support, and increasing the number of African-American midwives and birth assistants is vital in tackling health inequalities.” In regards to infant mortality rate (IMR), 18 states will achieve racial equality by 2050 if current trends from 1999-2013 hold (Joedrecka et al, 2017).
Now for the main reason I decided to write this: the ‘Hispanic’ paradox. This paradox is that for the past twenty years, ‘Hispanics’ with low SES have similar or better health outcomes than whites (Franzini, Ribble, and Keddie, 2001). However, more recent analyses show that the ‘Hispanic’ paradox does not exist, mostly due to methodological problems and migrant selectivity (Crimmins et al, 2007; Teruya and Bazargan-Hezeji, 2013) and was not noticed in Chile either (Cabiesies, Tunstall, and Pickett, 2013). There is no migrant selectivity in regards to smoking, however (Fenelon, 2013, 2016).
Studies which advocate the validity of the Immigrant Paradox are countered by those which report specific, negative physical and mental health outcomes, and higher rates of substance use, especially among immigrant adolescents. Findings may also be compromised by fundamental methodological concerns such as migrant health selectivity, and approaches that consider only selectively healthy groups. Moreover, the Immigrant Paradox’s benefits do not appear to extend evenly and consistently to all races, ethnicities and subgroups. Similarly, the Hispanic Paradox does not protect consistently across all Latino ethnicities, age groups and genders, with Puerto Ricans and Cubans in particular found to enjoy fewer health advantages.
This is good evidence that the people who migrate to America are healthier, and that the symptoms of low SES show in their children, but not in them because they are a self-selected population. There is no ‘Hispanic’ paradox (Smith and Bradshaw, 2006; Schoenthaler, 2016). Even a new meta-analysis on this ‘paradox’ states “Immigrant children and youth suffer from an immigrant mortality disadvantage” (Shor, Roelfs, and Vamg, 2017).
Lastly, Gregory Hood brings up stress and suicide, stating that if blacks were really more stressed than whites then blacks would have higher rates of suicide, but some studies show that whites have a higher rate of suicidal ideation, while others do not show this (Perez-Rodriguez et al, 2010). Though, as Balis and Postolache (2010) show, studies show that while there is conflicting evidence in regards to racial/ethnic differences in suicide, whites still attempt it the most. However, suicide for young black Americans is on the rise. Ahmedani et al (2016) show that “Nearly 27% of White individuals made a mental health visit versus less than 20% of Asian, Hawaiian/Pacific Islander, and Black individuals in this period. Within 4 weeks, all visits and mental health visits remained most common for White individuals (67.3% and 47.4%, respectively) and least common among Asian individuals (52.8% and 31.9%, respectively). Within 52-weeks, more than 90% made any visit. Alaskan Native/Native American (81.5%) and White individuals (79.5%) made mental health visits 10–25% more often than other groups.” However, at least in Fulton County, Georgia, black suicide decedents were less likely to report depression than white suicide decedents (Abe et al, 2008).
However, for whites, as noted in this 1982 New York Times article, suicidal feelings “reflects feelings of loneliness and hopelessness, which can be greater factors as one grows older; for instance, after loved ones have died” whereas for older white men, loss of status may be a cause, which would not be that prevalent in lower SES ethnicities. The article seems to implicate loss of status as a main cause for higher rates of suicide in white Americans, and states that as other, lower SES ethnies attain higher status, that suicide rates would rise for them as well.
Another cause could be prescription drugs, for instance in the Northeast which has been hit hard by the opiate/heroin crisis which leads to more white deaths. Robert Putnam puts this on “the links between poverty, hopelessness and health” and states that the suicide rate has declined for two groups, black males and males over the age of 75. Further, “divorce, economic strain, or political repression are often characterized as suicide risks.” Cheng et al (2010) show that “A high level of identification with one’s ethnic group was associated with lower rates of suicide attempts.” So, it seems that if one keeps their status, and has a high level of identification with their ethnic group, whites would then be protected against suicidal ideation. Nonmetropolitan counties also have higher rates of suicide than metropolitan counties (Ivey-Stephenson et al, 2017). People who livee in rural counties are less likely to seek help for mental problems (Carpenter-Song and Snell-Rood, 2016). Whites are also more likely to live in rural areas. This could explain higher rates of suicide in whites, along with loss of status, depression and drug use.
In conclusion, the ‘Hispanic’ paradox doesn’t exist; whites attempt/commit suicide more due to loss of status and since most whites live in rural areas, they do not seek help for their mental health problems which then leads to suicide. In regards to black maternal mortality/infant mortality rates, if they have midwives present during and after the birth, mortality rates have decreased. If these trends continue, there will be racial equality in terms of maternal/infant mortality in 18 states. The AmRen article was good and well written, but there were a few huge flaws. The author assumed that since the ‘Hispanic paradox’ exists, that this should have one disregard the effects of, say, stress on blood pressure in black Americans, as I have discussed in the past. But since the ‘Hispanic’ paradox does not exist, then you cannot say that (perceived) discrimination and ‘racism’ is not a cause for higher rates of mortality in blacks compared to whites.
The New York Times published an article on December the 8th titled What Doctors Should Ignore: Science has revealed how arbitrary racial categories are. Perhaps medicine will abandon them, too. It is an interesting article and while I do not agree with all of it, I do agree with some.
It starts off by talking about sickle cell anemia (SCA) and how was once thought of as a ‘black disease’ because blacks were, it seemed, the only ones who were getting the disease. I recall back in high-school having a Sicilian friend who said he ‘was black’ because Sicilians can get SCA which is ‘a black disease’, and this indicates ‘black genes’. However, when I grew up and actually learned a bit about race I learned that it was much more nuanced than that and that whether or not a population has SCA is not based on race, but is based on the climate/environment of the area which would breed mosquitoes which carry malaria. SCA still, to this day, remains a selective factor in the evolution of humans; malaria selects for the sickle cell trait (Elguero et al, 2015).
This is a good point brought up by the article: the assumption that SCA was a ‘black disease’ had us look over numerous non-blacks who had the sickle cell trait and could get the help they needed, when they were overlooked due to their race with the assumption that they did not have this so-called ‘black disease’. Though it is understandable why it got labeled ‘a black disease’; malaria is more prevalent near to the equator and people whose ancestors evolved there are more likely to carry the trait. In regards to SCA, it should be known that blacks are more likely to get SCA, but just because someone is black does not automatically mean that it is a foregone conclusion that one has the disease.
The article then goes on to state that the push to excise race from medicine may undermine a ‘social justice concept’: that is, the want to rid the medical establishment of so-called ‘unconscious bias’ that doctors have when dealing with minorities. Of course, I will not discount that this doesn’t have some effect—however small—on racial health disparities but I do not believe that the scope of the matter is as large as it is claimed to be. This is now causing medical professionals to integrate ‘unconscious bias training’, in the hopes of ridding doctors of bias—whether conscious or not—in the hopes to ameliorate racial health disparities. Maybe it will work, maybe it will not, but what I do know is that if you know someone’s race, you can use it as a roadmap to what diseases they may or may not have, what they may or may not be susceptible to and so on. Of course, only relying on one’s race as a single data point when you’re assessing someone’s possible health risks makes no sense at all.
The author then goes on to write that the terms ‘Negroid, Caucasoid, and Mongoloid’ were revealed as ‘arbitrary’ by modern genetic science. I wouldn’t say that; I would say, though, that modern genetic science has shown us the true extent of human variation, while also showing that humans cluster into 5 distinct geographic categories, which we can call ‘race’ (Rosenberg et al, 2002; but see Wills, 2017 for alternative view that the clusters identified by Rosenberg et al, 2002 are not races. I will cover this in the future). The author then, of course, goes on to use the continuum fallacy stating that since “there are few sharp divides where one set of traits ends and another begins“. A basic rebuttal would be, can you point out where red and orange are distinct? How about violet and blue? Blue and Cyan? Yellow and orange? When people commit the continuum fallacy then the only logical conclusion is that if races don’t exist because there are “few sharp divides where one set of traits ends and another begins“, then, logically speaking, colors don’t exist either because there are ‘few [if any] sharp divides‘ where one color ends and another begins.
The author also cites geneticist Sarah Tishkoff who states that the human species is too young to have races as we define them. This is not true, as I have covered numerous times. The author then cites this study (Ng et al, 2008) in which Craig Venter’s genome was matched with the (in)famous [I love Watson] James Watson and focused on six genes that had to do with how people respond to antipsychotics, antidepressants, and other drugs. It was discovered that Venter had two of the ‘Caucasian’ variants whereas Watson carried variants more common in East Asians. Watson would have gotten the wrong medicine based on the assumption of his race and not on the predictive power of his own personal genome.
The author then talks about kidney disease and the fact that blacks are more likely to have it (Martins, Agodoa, and Norris, 2012). It was assumed that environmental factors caused the disparity of kidney disease in blacks when compared to whites, however then the APOL1 gene variant was discovered, which is related to worse kidney outcomes and is in higher frequencies in black Americans, even in blacks with well-controlled blood pressure (BP) (Parsa et al, 2013). The author then discusses that black kidneys were seen as ‘more prone to failure’ than white kidneys, but this is, so it’s said, due to that one specific gene variant and so, race shouldn’t be looked at in regards to kidney disease but individual genetic variation.
In one aspect of the medical community can using medicine based on one’s race help: prostate cancer. Black men are more likely to be afflicted with prostate cancer in comparison to whites (Odedina et al, 2009; Bhardwaj et al, 2017) with it even being proposed that black men should get separate prostate screenings to save more lives (Shenoy et al, 2016). Then he writes that we still don’t know the genes responsible, however, I have argued in the past that diet explains a large amount—if not all of the variance. (It’s not testosterone that causes it like Ross et al, 1986 believe).
The author then discusses another medical professional who argues that racial health disparities come down to the social environment. Things like BP could—most definitely—be driven by the social environment. It is assumed that the darker one’s skin is, the higher chance they have to have high BP—though this is not the case for Africans in Africa so this is clearly an American-only problem. I could conjure up one explanation: the darker the individual, the more likely he is to believe he is being ‘pre-judged’ which then affects his state of mind and has his BP rise. I discussed this shortly in my previous article Black-White Differences in Physiology. Williams (1992) reviewed evidence that social, not genetic, factors are responsible for BP differences between blacks and whites. He reviews one study showing that BP is higher in lower SES, darker-skinned blacks in comparison to higher SES blacks whereas for blacks with higher SES no effect was noticed (Klag et al, 1991). Sweet et al (2007) showed that for lighter-skinned blacks, as SES rose BP decreased while for darker-skinned blacks BP increased as SES did while implicating factors like ‘racism’ as the ultimate causes.
There is evidence for the effect of psychosocial factors and BP (Marmot, 1985). In a 2014 review of the literature, Cuffee et al (2014) identify less sleep—along with other psychosocial factors—as another cause of higher BP. It just so happens that blacks average about one hour of sleep less than whites. This could cause a lot of the variation in BP differences between the races, so clearly in the case of this variable, it is useful to know one’s race, along with their SES. Keep in mind that any actual ‘racism’ doesn’t have to occur; the person only ‘needs to perceive it’, and their blood BP will rise in response to the perceived ‘racism’ (Krieger and Sidney, 1996). Harburg et al (1978) write in regards to Detroit blacks:
For 35 blacks whose fathers were from the West Indies, pressures were higher than those with American-born fathers. These findings suggest that varied gene mixtures may be related to blood pressure levels and that skin color, an indicator of possible metabolic significance, combines with socially induced stress to induce higher blood pressures in lower class American blacks.
Langford (1981) shows that when SES differences are taken into account that the black-white BP disparity vanishes. So there seems to be good evidence for the hypothesis that psychosocial factors, sleep deprivation, diet and ‘perceived discrimination’ (whether real or imagined) can explain a lot of this gap so race and SES need to be looked at when BP is taken into account. These things are easily changeable; educate people on good diets, teach people that, in most cases, no, people are not being ‘racist’ against you. That’s really what it is. This effect holds more for darker-skinned, lower-class blacks. And while I don’t deny a small part of this could be due to genetic factors, the physiology of the heart and how BP is regulated by even perceptions is pretty powerful and could have a lot of explanatory power for numerous physiological differences between races and ethnic groups.
Krieger (1990) states that in black women—not in white women—“internalized response to unfair treatment, plus non-reporting of race and gender discrimination, may constitute risk factors for high blood pressure among black women“. This could come into play in regards to black-white female differences in BP. Thomson and Lip (2005) show that “environmental influence and psychosocial factors may play a more important role than is widely accepted” in hypertension but “There remain many uncertainties to the relative importance and contribution of environmental versus genetic influences on the development of blood pressure – there is more than likely an influence from both. However, there is now evidence to necessitate increased attention in examining the non-genetic influences on blood pressure …” With how our physiology evolved to respond to environmental stimuli and respond in real time to perceived threats, it is no wonder that these types of ‘perceived discrimination’ causes higher BP in certain groups with lower SES.
Wilson (1988) implicates salt as the reason why blacks have higher BP than whites. High salt intake could affect the body’s metabolism by causing salt retention which influences blood plasma volume, cardiac output. However, whites have a higher salt intake than blacks, but blacks still ate twice the recommended amounts from the dietary guidelines (all ethnic subgroups they analyzed from America over-consumed salt as well) (Fulgoni et al, 2014). Blacks are also more ‘salt-sensitive’ than whites (Sowers et al 1988; Schmidlin et al, 2009; Sanada, Jones, and Jose, 2014) which is also heritable in blacks (Svetke, McKeown, and Wilson, 1996). A slavery hypothesis does exist to explain higher rates of hypertension in blacks, citing salt deficiency in the parts of Africa that supplied the slaves to the Americas, to the trauma of the slave trade and slavery in America. However, historical evidence does not show this to be the case because “There is no evidence that diet or the resulting patterns of disease and demography among slaves in the American South were significantly different from those of other poor southerners” (Curtin, 1992) whereas Campese (1996) hypothesizes that blacks are more likely to get hypertension because they evolved in an area with low salt.
The NYT article concludes:
Science seeks to categorize nature, to sort it into discrete groupings to better understand it. That is one way to comprehend the race concept: as an honest scientific attempt to understand human variation. The problem is, the concept is imprecise. It has repeatedly slid toward pseudoscience and has become a major divider of humanity. Now, at a time when we desperately need ways to come together, there are scientists — intellectual descendants of the very people who helped give us the race concept — who want to retire it.
Race is a useful concept. Whether in medicine, population genetics, psychology, evolution, physiology, etc it can elucidate a lot of causes for differences between races and ethnic groups—whether or not they are genetic or psychosocial in nature. That just attests to both the power of suggestion along with psychosocial factors in regards to racial differences in physiological factors.
Finally let’s see what the literature says about race in medicine. Bonham et al (2009) showed that both black and white doctors concluded that race is medically relevant but couldn’t decide why however they did state that genetics did not explain most of the disparity in relation to race and disease aside from the obvious disorders like Tay Sachs and sickle cell anemia. Philosophers accept the usefulness of race in the biomedical sciences (Andreason, 2009; Efstathiou, 2012; Hardimon, 2013; Winther, Millstein, and Nielsen, 2015; Hardimon, 2017) whereas Risch et al (2002) and Tang et al (2002) concur that race is useful in the biomedical sciences. (See also Dorothy Roberts’ Ted Talk The problem with race-based medicine which I will cover in the future). Richard Lewontin, naturally, has hang-ups here but his contentions are taken care of above. Even if race were a ‘social construct‘, as Lewontin says, it would still be useful in a biomedical sense; but since there are differences between races/ethnic groups then they most definitely are useful in a biomedical sense, even if at the end of the day individual variation matters more than racial variation. Just knowing someone’s race and SES, for instance, can tell you a lot about possible maladies they may have, even if, utltimately, individual differences in physiology and anatomy matter more in regards to the biomedical context.
In conclusion, race is most definitely a useful concept in medicine, whether race is a ‘social construct’ or not. Just using Michael Hardimon’s race concepts, for instance, shows that race is extremely useful in the biomedical context, despite what naysayers may say. Yes, individual differences in anatomy and physiology trump racial differences, but just knowing a few things like race and SES can tell a lot about a particular person, for instance with blood pressure, resting metabolic rate, and so on. Denying that race is a useful concept in the biomedical sciences will lead to more—not less—racial health disparities, which is ironic because that’s exactly what race-deniers do not want. They will have to accept a race concept, and they would accept Hardimon’s socialrace concept because that still allows it to be a ‘social construct’ while acknowledging that race and psychosocial factors interact to cause higher physiological variables. Race is a useful concept in medicine, and if the medical establishment wants to save more lives and actually end the racial disparities in health then they should acknowledge the reality of race.
Black-white differences in physiology can tell a lot about how the two groups have evolved over time. On traits like resting metabolic rate (RMR), basal metabolic rate (BMR), adiposity, heart rate, Vo2 max, etc. These differences in physiological variables between groups, then, explain part of the reason why there are different outcomes in terms of life quality/mortality between the two groups.
Right away, by looking at the average black and average white, you can see that there are differences in somatype. So if there are differences in somatype, then there must be differences in physiological variables, and so, this may be a part of the cause of, say, differing obesity rates between black and white women (Albu et al, 1997) and even PCOS (Wang and Alvero, 2013).
Resting metabolic rate
Resting metabolic rate is your body’s metabolism at rest, and is the largest component of the daily energy budget in modern human societies (Speakman and Selman, 2003). So if two groups, on average, differ in RMR, then one with the lower RMR may have a higher risk of obesity than the group with the higher RMR. And this is what we see.
Black women do, without a shadow of a doubt, have a lower BMR, lower PAEE (physical activity energy expenditure) and TDEE (total daily expenditure) (Gannon, DiPietro, and Poehlman, 2000). Knowing this, then it is not surprising to learn that black women are also the most obese demographic in the United States. This could partly explain why black women have such a hard time losing weight. Metabolic differences between ethnic groups in America—despite living in similar environments—show that a genetic component is responsible for this.
There are even predictors of obesity in post-menopausal black and white women (Nicklas et al, 1999). They controlled for age, body weight and body composition (variables that would influence the results—no one tell me that “They shouldn’t have controlled for those because it’s a racial confound!”) and found that despite having a similar waist-to-hip ratio (WHR) and subcutaneous fat area, black women had lower visceral fat than white women, while fasting glucose, insulin levels, and resting blood pressure did not differ between the groups. White women also had a higher Vo2 max, which remained when lean mass was controlled for. White women could also oxidize fat at a higher rate than black women (15.4 g/day, which is 17% higher than black women). When this is expressed as percent of total kcal burned in a resting state, white women burned more fat than black women (50% vs 43%). I will cover the cause for this later in the article (one physiologic variable is a large cause of these differences).
We even see this in black American men with more African ancestry—they’re less likely to be obese (Klimentidis et al 2016). This, too, goes back to metabolic rate. Black American men have lower levels of body fat than white men (Vickery et al, 1988; Wagner and Heyward, 2000). All in all, there are specific genetic variants and physiologic effects, which cause West African men to have lower central (abdominal) adiposity than European men and black women who live in the same environment as black men—implying that genetic and physiologic differences between the sexes are the cause for this disparity. Whatever the case may be, it’s interesting and more studies need to be taken out so we can see how whatever gene variants are *identified* as protecting against central adiposity work in concert with the system to produce the protective effect. Black American men have lower body fat, therefore they would have, in theory, a higher metabolic rate and be less likely to be obese—while black women have the reverse compared to white women—a lower metabolic rate.
Skeletal muscle fiber
Skeletal muscle fibers are the how and why of black domination in explosive sports. This is something I’ve covered in depth. Type II fibers contract faster than type I. This has important implications for certain diseases that black men are more susceptible to. Though the continuous contraction of the fibers during physical activity leads to a higher disease susceptibility in black men—but not white men (Tanner et al, 2001). If you’re aware of fiber type differences between the races (Ama et al, 1986; Entine, 2000; Caeser and Henry, 2015); though see Kerr (2010’s) article The Myth of Racial Superiority in Sports for another view. That will be covered here in the future.
Nevertheless, fiber typing explains racial differences in sports, with somatype being another important variable in explaining racial disparities in sports. Two main variables that work in concert are the somatype (pretty much body measurements, length) and the fiber type. This explains why blacks dominate baseball and football; this explains why ‘white men can’t jump and black men can’t swim’. Physiological variables—not only ‘motivation’ or whatever else people who deny these innate differences say—largely explain why there are huge disparities in these sports. Physiology is important to our understanding of how and why certain groups dominate certain sports.
This is further compounded by differing African ethnies excelling in different running sports depending on where their ancestors evolved. Kenyans have an abundance of type I fibers whereas West Africans have an abundance of type II fibers. (Genetically speaking, ‘Jamaicans’ don’t exist; genetic testing shows them to come from a few different West African countries.) Lower body symmetry—knees and ankles—show that they’re more symmetrical than age-matched controls (Trivers et al, 2014). This also goes to show that you can’t teach speed (Lombardo and Deander, 2014). Though, of course, training and the will to want to do your best matter as well—you just cannot excel in these competitions without first and foremost having the right physiologic and genetic make-up.
Further, although it’s only one gene variant, ACTN3 and ACE explain a substantial percentage of sprint time variance, which could be the difference between breaking a world record and making a final (Papadimitriou et al, 2016). So, clearly, certain genetic variants matter more than others—and the two best studied are ACTN3 and ACE. Some authors, though, may deny the contribution of ACTN3 to elite athletic performance—like one researcher who has written numerous papers on ACTN3, Daniel MacArthur. However, elite sprinters are more likely to carry the RR ACTN3 genotype compared to the XX ACTN3 genotype, and the RR ACTN3 genotype—when combined with type II fibers and morphology—lead to increased athletic performance (Broos et al, 2016). It’s also worth noting that 2 percent of Jamaicans carry the XX ACTN3 genotype (Scott et al, 2010), so this is another well-studied variable that lends to superior running performance in Jamaicans.
In regards to Kenyans, of course when you are talking about genetic reasons for performance, some people don’t like it. Some may say that certain countries dominate in X, and that for instance, North Africa is starting to churn out elite athletes, should we begin looking for genetic advantages that they possess (Hamilton, 2000)? Though people like Hamilton are a minority view in this field, I have read a few papers that there is no evidence that Kenyans possess a pulmonary system that infers a physiologic advantage over whites (Larsen and Sheel, 2015).
People like these three authors, however, are in the minority here and there is a robust amount of research that attests to East African running dominance being genetic/physiologic in nature—though you can’t discredit SES and other motivating variables (Tucker, Onywera, and Santos-Concejero, 2015). Of course, a complex interaction between SES, genes, and environment are the cause of the success of the Kalenjin people of Kenya, because they live and train in such high altitudes (Larsen, 2003), though the venerable Bengt Saltin states that the higher Vo2 max in Kenyan boys is due to higher physical activity during childhood (Saltin et al, 1995).
The last variable I will focus on (I will cover more in the future) is blood pressure. It’s well known that blacks have higher blood pressure than whites—with black women having a higher BP than all groups—which then leads to other health implications. Some reasons for the cause are high sodium intake in blacks (Jones and Hall, 2006); salt (Lackland, 2014; blacks had a similar sensitivity than whites, but had a higher blood pressure increase); while race and ethnicity was a single independent predictor of hypertension (Holmes et al, 2013). Put simply, when it comes to BP, ethnicity matters (Lane and Lip, 2001).
While genetic factors are important in showing how and why certain ethnies have higher BP than others, social factors are arguably more important (Williams, 1992). He cites stress, socioecologic stress, social support, coping patterns, health behavior, sodium, calcium, and potassium consumption, alcohol consumption, and obesity. SES factors, of course, lead to higher rates of obesity (Sobal and Stunkard, 1989; Franklin et al, 2015). So, of course, environmental/social factors have an effect on BP—no matter if the discrimination or whatnot is imagined by the one who is supposedly discriminated against, this still causes physiologic changes in the body which then lead to higher rates of BP in certain populations.
Poverty does affect a whole slew of variables, but what I’m worried about here is its effect on blood pressure. People who are in poverty can only afford certain foods, which would then cause certain physiologic variables to increase, exacerbating the problem (Gupta, de Wit, and McKeown, 2007). Whereas diets high in protein predicted lower BP in adults (Beundia et al, 2015). So this is good evidence that the diets of blacks in America do increase BP, since they eat high amounts of salt, low protein and high carb diets.
Still, others argue that differences in BP between blacks and whites may not be explained by ancestry, but by differences in education, rather than genetic factors (Non, Gravlee, and Mulligan, 2012). Their study suggests that educating black Americans on the dangers and preventative measures of high BP will reduce BP disparities between the races. This is in-line with Williams (1992) in that the social environment is the cause for the higher rates of BP. One hypothesis explored to explain why this effect with education was greater in blacks than whites was that BP-related factors, such as stress, poverty and racial discrimination (remember, even if no racial discrimination occurs, any so-called discrimination is in the eye of the beholder so that will contribute to a rise in physiologic variables) and maybe social isolation may be causes for this phenomenon. Future studies also must show how higher education causes lower BP, or if it only serves as other markers for the social environment. Nevertheless, this is an important study in our understanding of how and why the races differ in BP and it will go far to increase our understanding of this malady.
This is not an exhaustive list—I could continue writing about other variables—but these three are some of the most important as they are a cause for higher mortality rates in America. Understanding the hows and whys of these variables will have us better equipped to help those who suffer from diseases brought on by these differences in physiological factors.
The cause for some of these physiologic differences come down to evolution, but still others may come down to the immediate obesogenic environment (Lake and Townshend, 2006) which is compounded by lower SES. Since high carbs diets increase BP, this explains part of the reason why blacks have higher BP, along with social and genetic factors. Muscle fiber typing is set by the second trimester, and no change is seen after age 6 (Bell, 1980). Resting metabolic rate gap differences between black and white women can be closed, but not completely, if black women were to engage in exercise that use their higher amounts of type II muscle fibers (Tanner et al, 2001). This research is important to understand differences in racial mortality; because when we understand them then we can begin to theorize on how and why we see these disparities.
Physiologic differences between the races are interesting, they’re easily measurable and they explain both disparities in sports and mortality by different diseases. Once we study these variables more, we will be better able to help people with these variables—race be dammed. Race is a predictor here, only because race is correlated with other variables that lead to negative health outcomes. So once we understand how and why these differences occur, then we can help others with similar problems—no matter their race.
Last month I argued that there was more to weight loss than CI/CO. One of the culprits is a virus called Ad-36. Obese people are more likely to have Ad-36 antibodies in comparison to lean people, which implies that they have/had the virus and could be a part of the underlying cause of obesity. However, a paper was recently published that your stool can predict whether or not you can lose weight. This is due to how certain bacteria in the gut respond to different macronutrients ingested into the body.
ScienceDaily published an article a few days ago titled Your stools reveal whether you can lose weight. In the article, they describe the diets of the cohort, which followed 31 people, some followed the New Nordic Diet (NND), while others followed the Average Danish Diet (ADD) (Hjorth et al, 2017; I can’t find this study!! I’ll definitely edit this article after I read the full paper when it is available). So 31 people ate the NDD for 26 weeks, and lost 3.5 kg (7.72 pounds for those of us who use freedom numbers) while those who ate the ADD lost an average of 1.7 kg (3.75 pounds for those of us who use freedom numbers). So there was a 1.8 kg difference in pounds lost between the two diets. Why?
Here’s the thing: when people were divided by their microbiota, those who had a higher proportion of Prevotella to Bacteriodoites lost 3.5 more kg (7.72 pounds) in 26 weeks when they ate the NND in comparison to the ADD. Those who had a lower proportion of Prevotella to Bacteriodoites lost no additional weight on the NND. Overall, they say, about 50 percent of the population would benefit from the NND, while the rest of the population should diet and exercise until new measures are found.
The New Danish Diet is composed of grains, fruits, and vegetables. The diet worked for one-half of the population, but not for the other. The researchers state that people should try other diets and to exercise for weight loss while they study other measures. This is important to note: the same diet did not induce weight loss in a population; the culprit here is the individual microbiome.
Now that those Bacteroidotes have come up again, this quote from Allana Collen’s 2014 book 10% Human: How Your Body’s Microbes Hold the Key to Health and Happiness:
But before we get too excited about the potential for a cure for obesity, we need to know how it all works. What are these microbes doing that make us fat? Just as before, the microbiotas in Turnbaugh’s obese mice contained more Firmicutes and fewer Bacteroidetes, and they somehow seemed to enable the mice to extract more energy from their food. This detail undermines one of the core tenets of the obesity equation. Counting ‘calories-in’ is not as simple as keeping track of what a person eats. More accurately, it is the energy content of what a person absorbs. Turnbaugh calculated that the mice with the obese microbiota were collecting 2 per cent more calories from their food. For every 100 calories the lean mice extracted, the obese mice squeezed out 102.
Not much, perhaps, but over the course of a year or more, it adds up. Let’s take a woman of average height. 5 foot 4 inches, who weights 62 kg (9st 11 lb) and a healthy Body Mass Index (BMI: weight (kg) /(height (m)^2) of 23.5. She consumes 2000 calories per day, but with an ‘obese’ microbiota, her extra 2 per cent calorie extraction adds 40 more calories each day. Without expending extra energy, those further 40 calories per day should translate, in theory at least, to a 1.9 kg weight gain over a year. In ten years, that’s 19 kg, taking her weight to 81 kg (12 st 11 lb) and her BMI to an obese 30.7. All because of just 2 percent extra calories extracted from her food by her gut bacteria.
This corresponds with the NND/ADD study on weight loss… This proves that there is more than the simplistic CI/CO to weight loss, and that an individual’s microbiome/physiology definitely does matter in regards to weight loss. Clearly, to understand the population-wide problem of obesity we must understand the intricate relationship between the microbiome/brain/gut/body relationship and how it interacts with what we eat. Because evidence is mounting that the individual’s microbiome houses the key to weight loss/gain.
Exercise does not induce weight loss. A brand new RCT (randomized controlled trial) showed that in a cohort of children who were made to do HIIT (high-intensity interval training) did show better cardiorespiratory fitness, but there were no concomitant reductions in adiposity and bio blood markers (Dias et al, 2017). What this tells me is that people should exercise for health and that ‘high’ that comes along with it; if people exercise for weight loss they will be highly disappointed. Note, I am NOT saying to not exericse, I’m only saying to not have any unrealistic expectations that cardio will induce it, it won’t!
Bjornara et al (2016) showed that, when the NND was compared to the ADD, there was better adherence to the NND when compared to the ADD. Poulskin et al (2015) showed that the NND provided higher satisfaction, and body weight reduction with higher compliance with the NND and with physical activity (I disagree there, see above).
This study is important for our understanding of weight loss for the population as a whole. More recent evidence has shown that our microbiome and body clock work together to ‘pack on the pounds‘. This recent study found that the microbiome “regulate[s] lipid (fat) uptake and storage by hacking into and changing the function of the circadian clocks in the cells that line the gut.” The individual microbiome could induce weight gain, especially when they consume a Western diet, which of course is full of fat and sugar. One of the most important things they noticed is that mice without a microbiome fared much better on a high-fat diet.
The microbiome ‘talks’ to the gut lining. Germ-free mice were genetically unable to make NFIL3 in the cell lining of the gut. So germ-free mice lack a microbiome and lower than average production of NFIL3, meaning they take up and store fewer lipids than those with a microbiome.
So the main point about this study is the circadian rhythm. The body’s circadian clock recognizes the day/night system, which of course are linked to feeding times, which turn the body’s metabolism on and off. Cells are not directly exposed to light, but they capture light cues from visual and nervous systems, which then regulates gene expression. The gut’s circadian clock then regulates the expression of NFIL3 and the lipid metabolic machinery which is controlled NFIL3. So this study shows how the microbiome interacts with and impacts metabolism. This could also, as the authors state, explain how and why people who work nights and have shift-work disorder and the concurrent metabolic syndromes that come along with it.
In regards to the microbiome and weight loss, it is poorly understood at the moment (Conlon and Bird, 2015), though a recent systematic review showed that restrictive diets and bariatric surgery “reduce microbial abundance and promote changes in microbial composition that could have long-term detrimental effects on the colon.” They further state that “prebiotics might restore a healthy microbiome and reduce body fat“(Segenfrado et al, 2017). Wolf and Lorenz (2012) show that using “good” probiotic bacteria may induce changes in the obese phenotype. Bik (2015) states that learning more about the microbiome, dysbiosis (Carding et al, 2015), and how the microbiome interacts with our metabolism, brain, and physiology, then we can better treat those with obesity due to the dysbiosis of the microbiome. Clark et al (2012) show how the mechanisms behind the microbiota and obesity.
Weight loss is, clearly, more than CI/CO, and once we understand other mechanisms of weight loss/gain/regulation then we can better treat people with these metabolic syndromes that weirdly are all linked to each other. Diets affect the diversity of the microbiome, the diversity of the microbiome already there though, may need other macro/micro splits in order to show differing weight loss, in the case of the NND and ADD study reviewed above. Changes in weight do change the diversity of the microbiome of an individual, however, the heritable component of the microbiome may mean that some people need to eat different foods compared to others who have a different microbiome. Over time, new studies will show how and why the macro/micronutrient content matters for weight loss/gain.
Clearly, reducing the complex physiological process of weight gain/loss to numbers and ignoring the physiological process and how the microbiome induces weight gain/loss and works together with our other body’s cells. As the science grows here we will have a much greater understanding of our body’s weight loss mechanisms. Once we do that, then we can better help people with this disease.