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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.
Eat less and move more and you will lose weight. That’s the common mantra of everyone around the world because this is what has been repeated for decades. “The First Law of Thermodynamics states that energy can neither be created nor destroyed in an isolated system”. This Law is used in support of the CICO paradigm. But this kind of thinking does not make sense. The First Law only tells us that energy is conserved. That’s it. It says absolutely nothing about weight loss. Does anyone think that it’s weird that we’re given weight loss advice with physics (thermodynamics) and not advice for our physiology? This fallacy, what I term the CICO fallacy, then leads to the second fallacy: that a calorie is a calorie. The implication is this: the body does not discern between what type of macro you choose to ingest, it’s only worried about the amount of energy consumed. But, as I will show, this type of thinking does not work, either.
The First Law of Thermodynamics
The First Law states that energy can neither be created nor destroyed. A positive caloric balance must be associated with weight gain, but where the wrong conclusions come in is when people assume that the positive caloric balance is driving the weight gain. So if the First Law is interpreted correctly, then both conclusions—getting fat makes one consume more energy and consuming more energy makes one fat—are both valid hypotheses. The evidence and observations suggest that getting fat makes one consume more energy. (Jason Fung (2016: 33) writes: “Having studied a full year of thermodynamics in university, I can assure you that neither calories nor weight loss were mentioned even a single time.“)
Obesity researcher Jules Hirsch said to the New York Times:
There is an inflexible law of physics—energy taken in must exactly equal the number of calories leaving the system when fat storage is unchanged. Calories leave the system when food is used to fuel the body. To lower fat content—reduce obesity—one must reduce calories taken in, or increase activity, or both. This is true whether calories come from pumpkins or peanuts or pate de foie gras.
It’s this type of information that has caused the CICO paradigm to continue unabated. However, there are dissenting voices. People like Dr. Jason Fung, Gary Taubes, Zoe Harcombe, Nina Teicholz, Tim Noakes all go against the conventional wisdom regarding obesity and the cause for weight gain.
Another thing that is not taken into account is what occurs in the body when calories are reduced. One important thing to note is that the energy we consume and expend are not independent variables—they are dependent. Therefore, if we lower what we consume, what we expend will then lower as well. If you change one of them, the other will change too. For example, if you exercise more in an attempt to lose more weight you will eat more to compensate. If you eat less to lose more weight, your body’s metabolism will drop to match what the intake is. This is exactly what was seen in the Biggest Loser Study—shockingly lower RMRs in the contestants (see Fothergill et al, 2016). Biological systems are way more complex than to reduce it down to “eat less and move more=weight loss”, and that is easily shown.
Fliers and Maratos-Flier (2007: 74) write in Scientific American:
An animal whose food is suddenly restricted tends to reduce its energy expenditure both by being less active and by slowing energy use in cells, thereby limiting weight loss. It also experiences increased hunger so that once the restriction ends, it will eat more than its prior norm until the earlier weight is attained.
Take this example. Caloric excess in children is positively correlated with height increases. Though the caloric excess is not driving the height increases; they eat because they are growing.
The point that most people miss is the third storage system—fat storage. The three storage systems are kcal in/kcal out and fat storage. Insulin dictates fat storage, in the absence of insulin, the body cannot gain weight. Insulin shuttles fat into the adipocyte which is why insulin is fattening. That’s the point that CICO doesn’t work due to hormonal fluctuations. The most fattening hormone is insulin. The types of foods that elicit the highest insulin response are processed carbohydrates. Therefore, those are the most fattening foods. People who assume CICO state that a calorie is a calorie; that’s wrong.
Imagine a crowded room. The room is getting more crowded, and you ask me why the room is getting more crowded. I say ‘the room is more crowded because more people are entering it than leaving it.’ You say ‘duh, of course that’s true, but why is the room more crowded?’ Saying a room gets crowded because more people are entering than leaving it is redundant; saying that one gets fat because more calories are consumed than burned is redundant, it only says the same thing in two different ways so it is meaningless. Rooms that have more people enter them than leave them will become more crowded since there is no getting around the First Law, right?
Now take that same logic with obesity. Thermodynamics states that if we get fatter then more energy is entering our body than leaving it. Overeating means we’ve consumed more calories than we have expended. It’s tautological.
‘CICO could work’ but that is irrelevant, since what is assumed by the CICOers is that calories are calories; the assumption that once ingested, they go through the same metabolic pathways. This is false. The First Law says nothing about why we get fat. It is irrelevant to human physiology.
Taubes (2007: 293) writes:
Change in energy stores = Energy intake — Energy expenditure
The first law of thermodynamics dictates that weight gain—the increase in energy stored as fat and lean-tissue mass—will be accompanied by or associated with positive energy balance, but it does not say that it is caused by a positive energy balance—by “a plethora of calories,” as Russel Cecil and Robert Loeb’s 1951 Textbook of Medicine put it. There is no arrow of causality in the equation. It is equally possible, without violating this fundamental truth, for a change in energy stores, the left side of the above equation, to be the driving force in the cause and effect; some regulatory phenomenon could drive us to gai weight, which would in turn cause a positive energy balance—and thus overeating or sedentary behavior. Either way, the calories in will equal the calories out, as they must, but what is the cause in one cause is effect in the other.
And on pg 294:
The alternative hypothesis reverses the causality: we are driven to get fat by “primary metabolic or enzymatic effects,” as Hilde Bruch phrased it, and this fattening process induces the compensatory responses of overeating and/or physical inactivity. We eat more, move less, and have less energy to expend because we are metabolically or hormonally driven to get fat.
All the first law of thermodynamics tells us is that people can’t become more massive without taking in more energy than they expend since people who are heavier contain more energy than people who are lighter. That person has to consume more energy to accommodate said increasing mass. That person also cannot become lighter without expending more energy than they take in. That’s all the First Law tells us: energy is conserved. It says nothing about causation. The First Law literally only says that if something becomes more massive than more energy has to come in than leave. Nothing is said about cause and effect; it only tells us what has to happen if said thing does happen. That’s not causal information.
People only assume that the First Law has any relevance to obesity because of the ‘energy cannot be created nor destroyed’ part. But this shows no understanding of the Law. If you carefully read and understand it, you will see that it gives you absolutely no causal information. You can then reverse the commonly-held mantra—that eating more leads to obesity—to becoming obese leads one to eat more. It’s perfectly logical to reverse it and no Law is broken. People erroneously assume that the Laws of physics dictate weight gain and loss, but in complex metabolic systems, what is ingested is more important than how much is ingested (because we have hormones that let us know when to stop eating—which don’t get released while one eats carbohydrates).
The Second Law of Thermodynamics
The second weight loss fallacy is ‘a calorie is a calorie’, therefore, for weight loss, it doesn’t matter if a majority of my calories comes from fat, carbs or protein; the body will register the calories consumed and will regulate fat stores as dictated by the First Law (supposedly). The fallacy of invoking the First Law of thermodynamics ties directly into the fallacy of the Second Law of Thermodynamics—what the Second Law states is, that variation in metabolic pathways is to be expected, therefore, the mantra “a calorie is a calorie” violates the Second Law as a principle (Feinman and Fine, 2004, 2007).
A diet split of 55:30:15 CHO, fat, protein, yielded 1848 kcal. In fact, thermodynamics does not support the dictum that, all else being equal (i.e., two diets with the same amount of calories, but differing macro splits; one high-fat low carb the other high carb low-fat).
However, in 2004 Zoe Harcombe recalculated the figure from Feinman and Fein (2004) and found it to be wrong. The correct number ended up being 1825 kcal, not 1848 kcal, which strengthened Feinman and Fine’s (2004) point (Harcombe, 2004). She also writes:
I then repeated the calculations for a 10:30:60 high protein diet (keeping fat the same and swapping carbs out and protein in), and the calories available to the body dropped to 1,641. This is incredible. This means that two people can both eat 2000 calories a day and the high carbohydrate person is effectively getting nearly 200 calories more than the high protein person. Anyone still wonder why low-carbohydreate diets have a built in advantage?
So we can see that it’s ridiculous to ignore the thermic effect of food, seeing as it’s 20 percent for protein and 5 percent for CHO.
To put this into perspective, two people eating similar diets (but differing macro splits) only need to out-eat the other by 20 calories per day and that will be enough to gain more weight than the other person. Taubes (2011: 58) writes:
How many calories do we have to consume, but not expend, stashing them away in our fat tissue, to trsnsform ourselves, as many of us do, from lean twenty-five-year-olds to obese fifty-year-olds?
Twenty calories a day.
Twenty calories a day times the 365 days in a year comes to a little more than seven thousand calories stored as fat every year—two pounds of excess fat.
Multiply that by 10 and that’s twenty pounds gained in ten years—all from counting kcal wrong (Aamodt, 2016: 111-112). So with Harcomb’s (2004) example, the damage will be much worse in 10 years. This is all based on the assumption that ‘calories are calories’ which is false, as I have shown.
The CICO paradigm is wrong. Consumption and expenditure are not independent variables, they are dependent. So if you decrease one of them, the other will decrease as well. This is the fatal flaw in the CICO paradigm. The First Law always holds, yes, but it tells us absolutely nothing about obesity or human physiology and is therefore irrelevant. The Second Law is violated when one states that ‘a calorie is a calorie’, but this is demonstrably false. The Second Law states that variation in metabolic pathway efficiency is to be expected. Therefore stating that “a calorie is a calorie” violates the Second Law. This has further implications. Using Taubes’ example of 20 calories per day, if people truly believe the CICO mantra then people eating the same exact number of calories will have different weight gains if the skew of carbs to fat is higher in one than the other. Couple that with what insulin does in the body and this exacerbates the problem.
Stating that thermodynamics has anything to do with weight loss is clearly fallacious.
Race Differences in Penis Size Revisited: Is Rushton’s r/K Theory of Race Differences in Penis Length Confirmed?
In 1985 JP Rushton, psychology professor at the University of Ontario, published a paper arguing that r/K selection theory (which he termed Differential K theory) explained and predicted outcomes of what he termed the three main races of humanity—Mongoloids, Negroids and Caucasoids (Rushton, 1985; 1997). Since Rushton’s three races differed on a whole suite of traits, he reasoned races that were more K-selected (Caucasoids and Mongoloids) had slower reproduction times, higher time preference, higher IQ etc in comparison to the more r-selected Negroids who had faster reproduction times, lower time preference, lower IQ etc (see Rushton, 1997 for a review; also see Van Lange, Rinderu, and Bushmen, 2017 for a replication of Rushton’s data not theory). Were Rushton’s assertions on race and penis size verified and do they lend credence to his Differential-K claims regarding human races?
Rushton’s so-called r/K continuum has a whole suite of traits on it. Ranging from brain size to speed of maturation to reaction time and IQ, these data points supposedly lend credence to Rushton’s Differential-K theory of human differences. Penis size is, of course, important for Rushton’s theory due to what he’s said about it in interviews.
Rushton’s main reasoning for penis size differences between race is “You can’t have both”, and that if you have a larger brain then you must have a smaller penis; if you have a smaller penis you must have a larger brain. He believed there was a “tradeoff” between brain size and penis size. In the book Darwin’s Athletes: How Sport Has Damaged Black America and Preserved the Myth of Race, Hoberman (1997: 312) quotes Rushton: “Even if you take something like athletic ability or sexuality—not to reinforce stereotypes or some such thing—but, you know, it’s a trade-off: more brain or more penis. You can’t have both.” This, though, is false. There is no type of evidence to imply that this so-called ‘trade-off’ exists. In my readings of Rushton’s work over the years, that’s always something I’ve wondered: was Rushton implying that large penises take more energy to have and therefore the trade-off exists due to this supposed relationship?
Andrew Joyce of the Occidental Observer published an article the other day in defense of Richard Lynn. Near the end of his article he writes:
Another tactic is to belittle an entire area of research by picking out a particularly counter-intuitive example that the public can be depended on to regard as ridiculous. A good example is J. Philippe Rushton’s claim, based on data he compiled for his classic Race, Evolution and Behavior, that average penis size varied between races in accord with the predictions of r/K theory. This claim was held up to ridicule by the likes of Richard Lewontin and other crusaders against race realism, and it is regularly presented in articles hostile to the race realist perspective. Richard Lynn’s response, as always, was to gather more data—from 113 populations. And unsurprisingly for those who keep up with this area of research, he found that indeed the data confirmedRushton’s original claim.
The claim was ridiculed because it was ridiculous. This paper by Lynn (2013) titled Rushton’s r-K life history theory of race differences in penis length and circumference examined in 113 populations is the paper that supposedly verifies Rushton’s theory regarding race differences in penis size, along with one of its correlates in Rushton’s theory (testosterone). Lynn (2013) proclaims that East Asians are the most K-evolved, then come Europeans, while Africans are the least K-evolved. This, then, is the cause of the supposed racial differences in penis size.
Lynn (2013) begins by briefly discussing Rushton’s ‘findings’ on racial differences in penis size while also giving an overview of Rushton’s debunked r/K selection theory. He then discusses some of Rushton’s studies (which I will describe briefly below) along with stories from antiquity of the supposed larger penis size of African males.
Our old friend testosterone also makes an appearance in this paper. Lynn (2013: 262) writes:
Testosterone is a determinant of aggression (Book, Starzyk, & Quinsey, 2001; Brooks & Reddon, 1996; Dabbs, 2000). Hence, a reduction of aggression and sexual competitiveness between men in the colder climates would have been achieved by a reduction of testosterone, entailing the race differences in testosterone (Negroids > Caucasoids > Mongoloids) that are given in Lynn (1990). The reduction of testosterone had the effect of reducing penis length, for which evidence is given by Widodsky and Greene (1940).
Phew, there’s a lot to unpack here. (I discuss Lynn 1990 in this article.) Testosterone does not determine aggression; see my most recent article on testosterone (aggression increases testosterone; testosterone does not increase aggression. Book, Starzyk and Quinsey, 2001 show a .14 correlation between testosterone and aggression, whereas Archer, Graham-Kevan, and Davies 2005 show the correlation is .08). This is just a correlation. Sapolsky (1997: 113) writes:
Okay, suppose you note a correlation between levels of aggression and levels of testosterone among these normal males. This could be because (a) testosterone elevates aggression; (b) aggression elevates testosterone secretion; (c) neither causes the other. There’s a huge bias to assume option a while b is the answer. Study after study has shown that when you examine testosterone when males are first placed together in the social group, testosterone levels predict nothing about who is going to be aggressive. The subsequent behavioral differences drive the hormonal changes, not the other way around.
Brooks and Reddon (1996) also only show relationships with testosterone and aggressive acts; they show no causation. This same relationship was noted by Dabbs (2000; another Lynn 2013 citation) in prisoners. More violent prisoners were seen to have higher testosterone, but there is a caveat here too: being aggressive stimulates testosterone production so of course they had higher levels of testosterone; this is not evidence for testosterone causing aggression.
Another problem with that paragraph quoted from Lynn (2013) is that it’s a just-so story. It’s an ad-hoc explanation. You notice something with data you have today and then you imagine a nice-sounding story to attempt to explain your data in an evolutionary context. Nice-sounding stories are cool and all and I’m sure everyone loves a nicely told story, but when it comes to evolutionary theory I’d like theories that can be independently verified of the data they’re trying to explain.
My last problem with that paragraph from Lynn (2013) is his final citation: he cites it as evidence that the reduction of testosterone affects penis length…..but his citation (Widodsky and Green, 1940) is a study on rats… While these studies can give us a wealth of information regarding our physiologic systems (at least showing us which types of avenues to pursue; see my previous article on myostatin), they don’t really mean anything for humans; especially this study on the application of testosterone to the penis of a rat. See, the fatal flaw in these assertions is this: would a, say, 5 percent difference in testosterone lead to a larger penis as if there is a dose-response relationship between testosterone and penis length? It doesn’t make any sense.
Lynn (2013), though, says that Rushton’s theory doesn’t propose that there is a direct causal relationship between “intelligence”‘ and penis length, but just that they co-evolved together, with testosterone reduction occurring when Homo sapiens migrated north out of Africa they needed to cooperate more so selection for lower levels of testosterone subsequently occurred which then shrunk the penises of Rushton’s Caucasian and Mongoloid races.
Lynn (2013) then discusses two “new datasets”, one of which is apparently in Donald Templer’s book Is Size Important (which is on my to-read list, so many books, so little time). Table 1 below is from Lynn reproducing Templer’s ‘work’ in his book.
The second “dataset” is extremely dubious. Lynn (2013) attempts to dress it up, writing that “The information in this website has been collated from data obtained by research centres and reports worldwide.” Ethnicmuse has a good article on the pitfalls of Lynn’s (2013) article. (Also read Scott McGreal’s rebuttal.)
Rushton attempted to link race and penis size for 30 years. In a paper with Bogaert (Rushton and Bogaert, 1987), they attempt to show that blacks had larger penises than whites who h ad longer penises than Asians which then supposedly verified one dimension of Rushton’s theory. Rushton (1988) also discusses race differences in penis size, citing a previous paper by Rushton and Bogaert, where they use data from Alfred Kinsey, but this data is nonrepresentative and nonrandom (see Zuckermann and Brody, 1988 and Weizmann et al, 1990: 8).
Still others may attempt to use supposed differences in IGF-1 (insulin-like growth factor 1) as evidence that there is, at least, physiological evidence for the claim that black men have larger penises than white men, though I discussed that back in December of 2016 and found it strongly lacking.
Rushton (1997: 182) shows a table of racial differences in penis size which was supposedly collected by the WHO (World Health Organization). Though a closer look shows this is not true. Ethnicmuse writes:
ANALYSIS: The WHO did not study penis sizes. It relied on three separate studies, two of which were not peer-reviewed and the data was included as “Appendix III” (which should have alerted Rushton that this was not an original study). The first study references Africans in the US (not Africa!) and Europeans in the US (not Europe!), the second Europeans in Australia (not Europe!) and the third, Thais.
So it seems to be bullshit all the way down.
Ajmani et al (1985) showed that 385 healthy Nigerians had an average penile length of 3.21 inches (flaccid). Orakwe and Ebuh (2007) show that while Nigerians had longer penises than other ethnies tested, the only statistical difference was between them and Koreans. Though Veale et al (2014: 983) write that “There are no indications of differences in racial variability in our present study, e.g. the study from Nigeria was not a positive outlier.”
Lynn and Dutton have attempted to use androgen differentials between the races as evidence for racial differences in penis size (this is another attempt at a physiological argument to attempt to show the existence of racial differences in penis size). Edward Dutton attempted to revive the debate on racial differences in penis size during a 2015 presentation where he, again, showed that Negroids have higher levels of testosterone than Caucasoids who have higher levels of androgens than Mongoloids. These claims, though, have been rebutted by Scott McGreal who showed that populations differences in androgen levels are meaningless while they subsequently fail to validate Rushton and Lynn’s claims on racial differences in penis size.
Finally, it was reported the other day that condoms from China were too small in Zimbabwe, per Zimbabwe’s health minister. This led Kevin MacDonald to proclaim that this was “More corroboration of race differences in penis size which was part of the data Philippe Rushton used in his theory of r/K selection (along with brain size, maturation rates, IQ, etc.)” This isn’t “more corroboration” for Rushton’s long-dead theory; nor is this evidence that blacks have longer penises. I don’t understand why people make broad and sweeping generalizations. It’s one country in Africa that complained about smaller condoms from a country in East Asia, therefore this is more corroboration for Rushton’s r/K selection theory? The logic doesn’t follow.
Asians have small condoms. Those condoms go to Africa. They complain condoms from China are too small. Therefore Rushton’s r/K selection theory is corroborated. Flawed logic.
In sum, Lynn (2013) didn’t verify Rushton’s theory regarding racial differences in penis size and I find it even funnier that Lynn ends his article talking about “falsification’ stating that this aspect of Rushton’s theory has survived two attempts at falsification, therefore, it can be regarded as a “progressive research program“, though obviously, with the highly flawed “data” that was used, one cannot rationally make that statement. Supposed hormonal differences between the races do not cause penis size differences; even if blacks had levels of testosterone significantly higher than whites (the 19 percent that is claimed by Lynn and Rushton off of one highly flawed study in Ross et al, 1986) they still would not have longer penises.
The study of physical differences between populations is important, but sometimes, stereotypes do not tell you anything, especially in this case. Though in this instance, the claim that blacks have the longest penis lies on shaky ground, and with what evidence we do have for the claim, we cannot logically make the inference (especially not from Lynn’s (2013) flimsy data). Richard Lynn did not “confirm” anything with this paper; the only thing he “confirmed” are his own preconceived notions; he did not ‘prove’ what he set out to.
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.
Lead has many known neurological effects on the brain (regarding the development of the brain and nervous system) that lead to many deleterious health outcomes and negative outcomes in general. Including (but not limited to) lower IQ, higher rates of crime, higher blood pressure and higher rates of kidney damage, which have permanent, persistent effects (Stewart et al, 2007). Chronic lead exposure, too, can “also lead to decreased fertility, cataracts, nerve disorders, muscle and joint pain, and memory or concentration problems” (Sanders et al, 2009). Lead exposure in vitro, in infancy, and in childhood can also lead to “neuronal death” (Lidsky and Schneider, 2003). While epigenetic inheritance also plays a part (Sen et al, 2015). How do blacks and whites differ in exposure to lead? How much is the difference between the two races in America, and how much would it contribute to crime? On the other hand, China has high rates of lead exposure, but lower rates of crime, so how does this relationship play out with the lead-crime relationship overall? Are the Chinese an outlier or is there something else going on?
The effects of lead on the brain are well known, and numerous amounts of effort have been put into lowering levels of lead in America (Gould, 2009). Higher exposure to lead is also found in poorer, lower class communities (Hood, 2005). So since higher levels of lead exposure are found more often in lower-class communities, then blacks should have higher blood-lead levels than whites. This is what we find.
Blacks had a 27 percent higher concentration of lead in their tibia, while having significantly higher levels of blood lead, “likely because of sustained higher ongoing lead exposure over the decades” (Theppeang et al, 2008). Other data—coming out of Detroit—shows the same relationships (Haar et al, 1979; Talbot, Murphy, and Kuller, 1982; Lead poisoning in children under 6 jumped 28% in Detroit in 2016; also see Maqsood, Stanbury, and Miller, 2017) while lead levels in the water contribute to high levels of blood-lead in Flint, Michigan (Hanna-Attisha et al, 2016; Laidlaw et al, 2016). Cassidy-Bushrow et al (2017) also show that “The disproportionate burden of lead exposure is vertically transmitted (i.e., mother-to-child) to African-American children before they are born and persists into early childhood.”
Children exposed to lead have lower brain volumes as children, specifically in the ventrolateral prefrontal cortex, which is the same region of the brain that is impaired in antisocial and psychotic persons (Cecil et al, 2008). The community that was tested was well within the ‘safe’ range set by the CDC (Raine, 2014: 224), though the CDC says that there is no safe level of lead exposure. There is a large body of studies which show that there is no safe level of lead exposure (Needleman and Landrigan, 2004; Canfield, Jusko, and Kordas, 2005; Barret, 2008; Rossi, 2008; Abelsohn and Sanborn, 2010; Betts, 2012; Flora, Gupta, and Tiwari, 2012; Gidlow, 2015; Lanphear, 2015; Wani, Ara, and Usmani, 2015; Council on Environmental Health, 2016; Hanna-Attisha et al, 2016; Vorvolakos, Aresniou, and Samakouri, 2016; Lanphear, 2017). So the data is clear that there is absolutely no safe level of lead exposure, and even small effects can lead to deleterious outcomes.
Further, one brain study of 532 men who worked in a lead plant showed that those who had higher levels of lead in their bones had smaller brains, even after controlling for confounds like age and education (Stewart et al, 2008). Raine (2014: 224) writes:
The fact that the frontal cortex was particularly reduced is very interesting, given that this brain region is involved in violence. This lead effect was equivalent to five years of premature aging of the brain.
So we have good data that the parts of the brain that relate to violent tendencies are reduced in people exposed to more lead had the same smaller parts of the brain, indicating a relationship. But what about antisocial disorders? Are people with higher levels of lead in their blood more likely to be antisocial?
Needleman et al (1996) show that boys who had higher levels of lead in their blood had higher teacher ratings of aggressive and delinquent behavior, along with higher self-reported ratings of aggressive behavior. Even high blood-lead levels later in life is related to crime. One study in Yugoslavia showed that blood lead levels at age three had a stronger relationship with destructive behavior than did prenatal blood lead levels (Wasserman et al, 2008); with this same relationship being seen in America with high blood lead levels correlating with antisocial and aggressive behavior at age 7 and not age 2 (Chen et al 2007).
Nevin (2007) showed a strong relationship between preschool lead exposure and subsequent increases in criminal cases in America, Canada, Britain, France, Australia, Finland, West Germany, and New Zealand. Reyes (2007) also shows that crime increased quicker in states that saw a subsequent large decrease in lead levels, while variations in lead levels within cities correlating with variations in crime rates (Mielke and Zahran, 2012). Nevin (2000) showed a strong relationship between environmental lead levels from 1941 to 1986 and corresponding changes to violent crime twenty-three years later in the United States. Raine (2014: 226) writes (emphasis mine):
So, young children who are most vulnerable to lead absorption go on twenty-three years later to perpetrate adult violence. As lead levels rose throughout the 1950s, 1960s, and 1970s, so too did violence correspondingly rise in the 1970s, 1980s and 1990s. When lead levels fell in the late 1970s and early 1980s, so too did violence fall in the 1990s and the first decade of the twenty-first century. Changes in lead levels explained a full 91 percent of the variance in violent offending—an extremely strong relationship.
From international to national to state to city levels, the lead levels and violence curves match up almost exactly.
But does lead have a causal effect on crime? Due to the deleterious effects it has on the developing brain and nervous system, we should expect to find a relationship, and this relationship should become stronger with higher doses of lead. Fortunately, I am aware of one analysis, a sample that’s 90 percent black, which shows that with every 5 microgram increase in prenatal blood-lead levels, that there was a 40 percent higher risk of arrest (Wright et al, 2008). This makes sense with the deleterious developmental effects of lead; we are aware of how and why people with high levels of lead in their blood show similar brain scans/brain volume in certain parts of the brain in comparison to antisocial/violent people. So this is yet more suggestive evidence for a causal relationship.
Jennifer Doleac discusses three studies that show that blood-lead levels in America need to be addressed, since they are related strongly to negative health outcomes.Aizer and Curry (2017) show that “A one-unit increase in lead increased the probability of suspension from school by 6.4-9.3 percent and the probability of detention by 27-74 percent, though the latter applies only to boys.” They also show that children who live nearer to roads have higher blood-lead levels, since the soil near highways was contaminated decades ago with leaded gasoline. Fiegenbaum and Muller (2016) show that cities’ use of lead pipes increased murder rates between the years o921 and 1936. Finally, Billings and Schnepnel (2017: 4) show that their “results suggest that the effects of high levels of [lead] exposure on antisocial behavior can largely be reversed by intervention—children who test twice over the alert threshold exhibit similar outcomes as children with lower levels of [lead] exposure (BLL<5μg/dL).”
A relationship with lead exposure in vitro and arrests at adulthood. The sample was 90 percent black, with numerous controls. They found that prenatal and post-natal blood-lead exposure was associated with higher arrest rates, along with higher arrest rates for violent acts (Wright et al, 2008). To be specific, for every 5 microgram increase in prenatal blood-lead levels, there was a 40 percent greater risk for arrest. This is direct causal evidence for the lead-causes-crime hypothesis.
One study showed that in post-Katrina New Orleans, decreasing lead levels in the soil caused a subsequent decrease in blood lead levels in children (Mielke, Gonzales, and Powell, 2017). Sean Last argues that, while he believes that lead does contribute to crime, that the racial gaps have closed in the recent decades, therefore blood-lead levels cannot be a source of some of the variance in crime between blacks and whites, and even cites the CDC ‘lowering its “safe” values’ for lead, even though there is no such thing as a safe level of lead exposure (references cited above). White, Bonilha, and Ellis Jr., (2015) also show that minorities—blacks in particular—have higher rates of lead in their blood. Either way, Last seems to downplay large differences in lead exposure between whites and blacks at young ages, even though that’s when critical development of the mind/brain and other important functioning occurs. There is no safe level of lead exposure—pre- or post-natal—nor are there safe levels at adulthood. Even a small difference in blood lead levels would have some pretty large effects on criminal behavior.
Sean Last also writes that “Black children had a mean BLL which was 1 ug/dl higher than White children and that this BLL gap shrank to 0.9 ug/dl in samples taken between 2003 and 2006, and to 0.5 ug/dl in samples taken between 2007 and 2010.” Though, still, there are problems here too: “After adjustment, a 1 microgram per deciliter increase in average childhood blood lead level significantly predicts 0.06 (95% confidence interval [CI] = 0.01, 0.12) and 0.09 (95% CI = 0.03, 0.16) SD increases and a 0.37 (95% CI = 0.11, 0.64) point increase in adolescent impulsivity, anxiety or depression, and body mass index, respectively, following ordinary least squares regression. Results following matching and instrumental variable strategies are very similar” (Winter and Sampson, 2017).
Naysayers may point to China and how they have higher levels of blood-lead levels than America (two times higher), but lower rates of crime, some of the lowest in the world. The Hunan province in China has considerably lowered blood-lead levels in recent years, but they are still higher than developed countries (Qiu et al, 2015). One study even shows ridiculously high levels of lead in Chinese children “Results showed that mean blood lead level was 88.3 micro g/L for 3 – 5 year old children living in the cities in China and mean blood lead level of boys (91.1 micro g/L) was higher than that of girls (87.3 micro g/L). Twenty-nine point nine one per cent of the children’s blood lead level exceeded 100 micro g/L” (Qi et al, 2002), while Li et al (2014) found similar levels. Shanghai also has higher levels of blood lead than the rest of the developed world (Cao et al, 2014). Blood lead levels are also higher in Taizhou, China compared to other parts of the country—and the world (Gao et al, 2017). But blood lead levels are decreasing with time, but still higher than other developed countries (He, Wang, and Zhang, 2009).
Furthermore, Chinese women, compared to American women, had two times higher BLL (Wang et al, 2015). With transgenerational epigenetic inheritance playing a part in the inheritance of methylation DNA passed from mother to daughter then to grandchildren (Sen et al, 2015), this is a public health threat to Chinese women and their children. So just by going off of this data, the claim that China is a safe country should be called into question.
Reality seems to tell a different story. It seems that the true crime rate in China is covered up, especially the murder rate:
In Guangzhou, Dr Bakken’s research team found that 97.5 per cent of crime was not reported in the official statistics.
Of 2.5 million cases of crime, in 2015 the police commissioner reported 59,985 — exactly 15 less than his ‘target’ of 60,000, down from 90,000 at the start of his tenure in 2012.
The murder rate in China is around 10,000 per year according to official statistics, 25 per cent less than the rate in Australia per capita.
“I have the internal numbers from the beginning of the millennium, and in 2002 there were 52,500 murders in China,” he said.
Instead of 25 per cent less murder than Australia, Dr Bakken said the real figure was closer to 400 per cent more.”
Guangzhou, for instance, doesn’t keep data for crime committed by migrants, who commit 80 percent of the crime in this province. Out of 2.5 million crimes committed in Guangzhou, only 5,985 crimes were reported in their official statistics, which was 15 crimes away from their target of 6000. Weird… Either way, China doesn’t have a similar murder rate to Switzerland:
The murder rate in China does not equal that of Switzerland, as the Global Times claimed in 2015. It’s higher than anywhere in Europe and similar to that of the US.
China also ranks highly on the corruption index, higher than the US, which is more evidence indicative of a covered up crime rate. So this is good evidence that, contrary to the claims of people who would attempt to downplay the lead-crime relationship, that these effects are real and that they do matter in regard to crime and murder.
So it’s clear that we can’t trust the official Chinese crime stats since there much of their crime is not reported. Why should we trust crime stats from a corrupt government? The evidence is clear that China has a higher crime—and murder rate—than is seen on the Chinese books.
Lastly, effects of epigenetics can and do have a lasting effect on even the grandchildren of mothers exposed to lead while pregnant (Senut et al, 2012; Sen et al, 2015). Sen et al (2015) showed lead exposure during pregnancy affected the DNA methylation status of the fetal germ cells, which then lead to altered DNA methylation on dried blood spots in the grandchildren of the mother exposed to lead while pregnant.—though it’s indirect evidence. If this is true and holds in larger samples, then this could be big for criminological theory and could be a cause for higher rates of black crime (note: I am not claiming that lead exposure could account for all, or even most of the racial crime disparity. It does account for some, as can be seen by the data compiled here).
In conclusion, the relationship between lead exposure and crime is robust and replicated across many countries and cultures. No safe level of blood lead exists, even so-called trace amounts can have horrible developmental and life outcomes, which include higher rates of criminal activity. There is a clear relationship between lead increases/decreases in populations—even within cities—that then predict crime rates. Some may point to the Chinese as evidence against a strong relationship, though there is strong evidence that the Chinese do not report anywhere near all of their crime data. Epigenetic inheritance, too, can play a role here mostly regarding blacks since they’re more likely to be exposed to high levels of lead in the womb, their infancy, and childhood. This could also exacerbate crime rates, too. The evidence is clear that lead exposure leads to increased criminal activity, and that there is a strong relationship between blood lead levels and crime.
People look different depending on where their ancestors derived from; this is not a controversial statement, and any reasonable person would agree with that assertion. Though what most don’t realize, is that even if you assert that biological races do not exist, but allow for patterns of distinct visible physical features between human populations that then correspond with geographic ancestry, then race—as a biological reality—exists because what denotes the physical characters are biological in nature, and the geographic ancestry corresponds to physical differences between continental groups. These populations, then, can be shown to be real in genetic analyses, and that they correspond to traditional racial groups. So we can then say that Eurasian, East Asian, Oceanian, black African, and East Asians are continental-level minimalist races since they hold all of the criteria needed to be called minimalist races: (1) distinct facial characters; (2) distinct morphologic differences; and (3) they come from a unique geographic location. Therefore minimalist races exist and are a biological reality. (Note: There is more variation within races than between them (Lewontin, 1972; Rosenberg et al, 2002; Witherspoon et al, 2007; Hunley, Cabana, and Long, 2016), but this does not mean that the minimalist biological concept of race has no grounding in biology.)
Minimalist race exists
The concept of minimalist race is simple: people share a peculiar geographic ancestry unique to them, they have peculiar physiognomy (facial features like lips, facial structure, eyes, nose etc), other physical traits (hair/hair color), and a peculiar morphology. Minimalist races exist, and are biologically real since minimalist races can survive findings from population genetics. Hardimon (2017) asks, “Is the minimalist concept of race a social concept?” on page 62. He writes that social concepts are socially constructed in a pernicious sense if and only if it “(i) fails to represent any fact of the matter and (ii) supports and legitimizes domination.” Of course, populations who derive from Africa, Europe, and East Asia have peculiar facial morphology/morphology unique to that isolated population. Therefore we can say that minimalist race does not conform to criteria (i). Hardimon (2017: 63) then writes:
Because it lacks the nasty features that make the racialist concept of race well suited to support and legalize domination, the minimalist race concept fails to satisfy condition (ii). The racialist concept, on the other hand, is socially constructed in the pernicious sense. Since there are no racialist races, there are no facts of the matter it represents. So it satisfies (i). To elaborate, the racialist race concept legtizamizes racial domination by representing the social hierarchy of race as “natural” (in a value-conferring sense): as the “natural” (socially unmediated and inevitable) expression of the talent and efforts of the inidividuals who stand on its rungs. It supports racial domination by conveying the idea that no alternative arrangment of social institutions could possibly result in racial equality and hence that attempts to engage in collective action in the hopes of ending the social hierarchy of race are futile. For these reasons the racialist race concept is also idealogical in the prejorative sense.
Knowing what we know about minimalist races (they have distinct physiognomy, distinct morphology and geographic ancestry unique to that population), we can say that this is a biological phenomenon, since what makes minimalist races distinct from one another (skin color, hair color etc) are based on biological factors. We can say that brown skin, kinky hair and full lips, with sub-Saharan African ancestry, is African, while pale/light skin, straight/wavy/curly hair with thin lips, a narrow nose, and European ancestry makes the individual European.
These physical features between the races correspond to differences in geographic ancestry, and since they differ between the races on average, they are biological in nature and therefore it can be said that race is a biological phenomenon. Skin color, nose shape, hair type, morphology etc are all biological. So knowing that there is a biological basis to these physical differences between populations, we can say that minimalist races are biological, therefore we can use the term minimalist biological phenomenon of race, and it exists because there are differences in the patterns of visible physical features between human populations that correspond to geographic ancestry.
Hardimon then talks about how eliminativist philosophers and others don’t deny that above premises above the minimalist biological phenomenon of race, but they allow these to exist. Hardimon (2017: 68-69) then quotes a few prominent people who profess that there are, of course, differences in physical features between human populations:
… Lewontin … who denies that biological races exist, freely grants that “peoples who have occupied major geographic areas for much of the recent past look different from one another. Sub-Saharan Africans have dark skin and people who have lived in East Asia tend to have a light tan skin and an eye color and eye shape that is difference from Europeans.” Similarly, population geneticist Marcus W. Feldman (final author of Rosenberg et al., “Genetic Stucture of Human Populations” ), who also denies the existence of biological races, acknowledges that “it has been known for centuries that certain physical features of humans are concentrated within families: hair, eye, and skin color, height, inability to digest milk, curliness of hair, and so on. These phenotypes also show obvious variation among people from different continents. Indeed, skin color, facial shape, and hair are examples of phenotypes whose variation among populations from different regions is noticeable.” In the same vein, eliminative anthropologist C. Loring Brace concedes, “It is perfectly true that long term residents of various parts of the world have patterns of features that we can identify as characteristic of they area from which they come.”
So even these people who claim to not believe in “biological races”, do indeed believe in biological races because what they are describing is biological in nature and they, of course, do not deny that people look different while their ancestors came from different places so therefore they believe in biological races. We can then use the minimalist biological phenomenon of race to get to the existence of minimalist races.
Hardimon (2017: 69) writes:
Step 1. Recognize that there are differences in patterns of visible physical features of human beings that correspond to their differences in geographic ancestry.
Step 2. Observe that these patterns are exhibited by groups (that is, real existing groups).
Step 3. Note that the groups that exhibit these patterns of visible physical features correspond to differences in geographical ancestry satisfy the conditions of the minimalist concept of race.
Step 4. Infer that minimalist race exists.
Those individuals mentioned previously who deny biological races but allow that people with ancestors from differing geographic locales look differently do not disagree with step 1, nor does anyone really disagree with step 2. Step 4’s inference immediately flows from the premise in step 3. “Groups that exhibit patterns or visible physical features that correspond to differences in geographical ancestry satisfy the conditions of the minimalist concept of race. Call (1)-(4) the argument from the minimalist biological phenomenon of race” (Hardimon, 2017: 70). Of course, the argument does not identify which populations may be called races (see further below), it just shows that race is a biological reality. Because if minimalist races exist, then races exist because minimalist races are races. Minimalist races exist, therefore biological races exist. Of course, no one doubts that people come from Europe, sub-Saharan Africa, East Asia, the Americas, and the Pacific Islands, even though the boundaries between them are ‘blurry’. They exhibit patterns of visible physical characters that correspond to their differing geographic ancestry, they are minimalist races therefore minimalist races exist.
Pretty much, the minimalist concept of race is just laying out what everyone knows and arguing for its existence. Minimalist races exist, but are they biologically real?
Minimalist races are biologically real
Of course, some who would assert that minimalist races do not exist would say that there are no ‘genes’ that are exclusive to one certain population—call them ‘race genes’. Of course, these types of genes do not exist. Whether or not one individual is a part of one race or not does not rest on the basis of his physical characters, but is determined by who his parents are, because one of the three premises for the minimalist race argument is ‘must have a peculiar geographic ancestry’. So it’s not that members of races share sets of genes that other races do not, it’s based on the fact that they share a distinctive set of visible physical features that then correspond with geographic ancestry. So of course if the minimalist concept of race is a biological concept then it entails more than ‘genes for’ races.
Of course, there is a biological significance to the existence of minimalist biological races. Consider that one of the physical characters that differ between populations is skin color. Skin color is controlled by genes (about half a dozen within and a dozen between populations). Lack of UV rays for individuals with dark skin will lead to diseases like prostate cancer, while darker skin is a protectant against UV damage to human skin (Brenner and Hearing, 2008; Jablonksi and Chaplin, 2010). Since minimalist race is biologically significant and minimalist races are partly defined by differences in skin color between populations then skin color has both medical and ecological significance.
(1) Consider light skin. People with light skin are more susceptible to skin cancer since they evolved in locations with poor UVR radiation (D’Orazio et al, 2013). The body needs vitamin D to absorb and use calcium for maintaining proper cell functioning. People who evolved near the equator don’t have to worry about this because the doses of UVB they absorb are sufficient for the production of enough previtamin D. While East Asians and Europeans on the other hand, became adapted to low-sunlight locations and therefore over time evolved lighter skin. This loss of pigmentation allowed for better UVB absorption in these new environments. (Also read my article on the evolution of human skin variation and also how skin color is not a ‘tell’ of aggression in humans.)
(2) While darker-skinned people have a lower rate of skin cancer “primarily a result of photo-protection provided by increased epidermal melanin, which filters twice as much ultraviolet (UV) radiation as does that in the epidermis of Caucasians” (Bradford, 2009). Dark skin is thought to have evolved to protect against skin cancer (Greaves, 2014a) but this has been contested (Jablonski and Chaplin, 2014) and defended (Greaves, 2014b). So therefore, using (1) and (2), skin color has evolutionary signifigance.
So as humans began becoming physically adapted to their new niches they found themselves in, they developed new features distinct from the location they previously came from to better cope with the new lifestyle due to their new environments. For instance “Northern Europeans tend to have light skin because they belong to a morphologically marked ancestral group—a minimalist race—that was subject to one set of environmental conditions (low UVR) in Europe” (Hardimon, 2017: 81). Of course explaining how human beings survived in new locations falls into the realm of biology, while minimalist races can explain why this happened.
Minimalist races clearly exist since minimalist races constitute complex biological patterns between populations. Hardimon (2017: 83) writes:
It [minimalist race] also enjoys intrinsic scientific interest because it represents distinctive salient systematic dimension of human biological diversity. To clarify: Minimalist race counts as (i) salient because human differences of color and shape are striking. Racial differences in color and shape are (ii) systematic in that they correspond to differences in geographic ancestry. They are not random. Racial differences are (iii) distinctive in that they are different from the sort of biological differences associated with the other two salient systematic dimensions of human diversity: sex and age.
An additional consideration: Like sex and age, minimalist race constitutes one member of what might be called “the triumverate of human biodiversity.” An account of human biodiversity that failed to include any one of these three elements would be obviously incomplete. Minimalist race’s claim to be biologically real is as good as the claim of the other members of the triumverate. Sex is biologically real. Age is biologically real. Minimalist race is biologically real.
Real does not mean deep. Compared to the biological associated with sex (sex as contrasted with gender), the biological differences associated with minimalist race are superficial.
Of course, the five ‘clusters’ and ‘populations’ identified by Rosenberg et al’s (2002) K=5 graph, which told structure to produce 5 genetic clusters, corresponds to Eurasia, Africa, East Asia, Oceania, and the Americas, are great candidates for minimalist biological races since they correspond to geographic locations, and even corroborates what Fredrich Blumenbach said about human races back in the 17th century. Hardimon further writes (pg 85-86):
If the five populations corresponding to the major areas are continental-level minimalist races, the clusters represent continental-level minimalist races: The cluster in the mostly orange segment represents the sub-Saharan African continental-level minimalist race. The cluster in the mostly blue segment represents the Eurasian continental-level minimal race. The cluster in the mostly pink segment represents the East Asian continental-level minimalist race. The cluster in the mostly green segment represents the Pacific Islander continental-level minimalist race. And the cluster in the mostly purple segment represents the American continental-level minimalist race.
The assumption that the five populations are continental-level minimalist races entitles us to interpret structure as having the capacity to assign individuals to continental-level minimalist races on the basis of markers that track ancestry. In constructing clusters corresponding to the five continental-level minimalist races on the basis of objective, race-neutral genetic markers, structure essentially “reconstructs” those races on the basis of a race-blind procedure. Modulo our assumption, the article shows that it is possible to assign individuals to continental-level races without knowing anything about the race or ancestry of the individuals from whose genotypes the microsattelites are drawn. The populations studied were “defined by geography, language, and culture,” not skin color or “race.”
Of course, as critics note, the researchers predetermine how many populations that structure demarcates, for instance, K=5 indicates that the researchers told the program to delineate 5 clusters. Though, these objections do not matter. For the 5 populations that come out in K=5 “are genetically structured … which is to say, meaningfully demarcated solely on the basis of genetic markers” (Hardimon, 2017: 88). K=6 brings one more population, the Kalash, a group from northern Pakistan who speak an Indo-European language. Though “The fact that structure represents a population as genetically distinct does not entail that the population is a race. Nor is the idea that populations corresponding to the five major geographic areas are minimalist races undercut by the fact that structure picks out the Kalash as a genetically distinct group. Like the K=5 graph, the K=6 graph shows that modulo our assumption, continental-level races are genetically structured” (Hardimon, 2017: 88).
Though of course there are naysayers. Svante Paabo and David Serre, Hardimon writes, state that when individuals are sampled from homogeneous populations from around the world, the gradients of the allele frequencies that are found are distributed randomly across the world rather than clustering discretely. Though Rosenberg et al responded by verifying that the clusters they found are not artifacts of sampling as Paabo and Serre imply, but reflect features of underlying human variation. Though Rosenberg et al agree with Paabo and Serre in that that human genetic diversity consists of clines in variation in allele frequencies (Hardimon, 2017: 89). Other naysayers also state that all Rosenberg et al show is what we can “see with our eyes”. Though a computer does not partition individuals into different populations based on something that can be done with eyes, it’s based on an algorithm.
Hardimon also accepts that black Africans, Caucasians, East Asians, American Indians and Oceanians can be said to be races in the basic sense because “they constitute a partition of the human species“, and that they are distinguishable “at the level of the gene” (Hardimon, 2017: 93). And of course, K=5 shows that the 5 races are genetically distinguishable.
Hardimon finally discusses some medical significance for minimalist races. He states that if you are Caucasian that it is more likely that you have a polymorphism that protects against HIV compared to a member of another race. Meanwhile, East Asians are more likely to carry alleles that make them more susceptible to Steven-Johnson syndrome or another syndrome where their skin falls off. Though of course, the instances where this would matter in a biomedical context are rare, but still should be at the back of everyone’s mind (as I have argued), even though instances where medical differences between minimalist races are rare, there are times where one’s race can be medically significant.
Hardimon finally states that this type of “metaphysics of biological race” can be called “deflationary realism.” Deflationary because it “consists in the repudiation of the ideas that racialist races exist and that race enjoys the kind of biological reality that racialist race was supposed to have” and realism which “consists in its acknowledgement of the existence of minimalist races and the genetically grounded, relatively superficial, but still significant biological reality of minimalist race” (Hardimon, 2017: 95-96).
Minimalist races exist. Minimalist races are a biological reality because distinct visible patterns show differences between geographically isolated populations. This is enough for the classification of the five classic races we know of to be called race, be biologically real, and have a medical significance—however small—because certain biological/physical traits are tied to different geographic populations—minimalist races.
Hardimon (2017: 97) shows an alternative to racialism:
Deflationary realism provides a worked-out alternative to racialism—it it a theory that represents race as a genetically grounded, relatively superficial biological reality that is not normatively important in itself. Deflationary realism makes it possible to rethink race. It offers the promise of freeing ourselves, if only imperfectly, from the racialist background conception of race.
It is clear that minimalist races exist and are biologically real. You do not need to speak about supposed mental traits between these minimalist races, they are irrelevant to the existence of these minimalist biological races. As Hardimon (2017: 67) writes: “No reference is made to normatively important features such as intelligence, sexuality, or morality. No reference is made to essences. The idea of sharp boundaries between patterns of visible physical features or corresponding geographical regions is not invoked. Nor again is reference made to the idea of significant genetic differences. No reference is made to groups that exhibit patterns of visible physical features that correspond to geographic ancestry.”
The minimalist biological concept of race stands up to numerous lines of argumentation, therefore we can say without a shadow of a doubt that minimalist biological race exists and is real.
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.
In 1972 Richard Lewontin, studying the blood groups of different races, came to the conclusion that “Human racial classification is of no social value and is positively destructive of social and human relations. Since such racial classification is now seen to be of virtually no genetic or taxonomic significance either, no justification can be offered for its continuance” (pg 397). He also found that “the difference between populations within a race account for an additional 8.3 percent, so that only 6.3 percent is accounted for by racial classification.” This has lead numerous people to, along with Lewontin, conclude that race is ‘of virtually no genetic or taxonomic significance’ and conclude that, due to this, race does not exist.
Lewontin’s main reasoning was that since there is more variation within races than between them (85 percent of differences were within populations while 15 percent was within them) then since a lion’s share of human diversity is distributed within races, not between them, then race is of no genetic nor taxonomic use. Lewontin is correct that there is more variation within races than between them, but he is incorrect that this means that racial classification ‘is of no social value’, since knowing and understanding the reality of race (even our perceptions of them, whether they are true or not) influence things such as medical outcomes.
Though, like Lewontin, people have cited this paper as evidence against the existence of human races, for if there is way more genetic variation between races, and that most human genetic variation is within races, then race cannot be of any significance for things such as medical outcomes since most genetic variation is within races not between them.
Rosenberg et al (2002) also confirmed and replicated Lewontin’s analysis, showing that within-population genetic variation accounts for 93-95 percent of human genetic variation, while 3 to 5 percent of human genetic variation lies between groups. Philosopher Michael Hardimon (2017) uses these arguments to buttress his point that ‘racialist races’ (as he calls them) do not exist. His criteria being:
(a) The fraction of human genetic diversity between populations must exceed the fraction of diversity between them.
(b) The fraction of human genetic diversity within populations must be small.
(c) The fraction of diversity between populations must be large.
(d) Most genes must be highly differentiated by race.
(e) The variation in genes that underlie obvious physical differences must be typical of the genome in general.
(f) There must be several important genetic differences between races apart from the genetic differences that underlie obvious physical differences.
Note: (b) says that racialist races are genetically racially homogeneous groups; (c)-(f) say that racialist races are distinguised by major biological differences.
Call (a)-(f) the racialist concept of race’s genetic profile. (Hardimon, 2017: 21)
He clearly strawmans the racialist position, but I’ll get into that another day. Hardimon writes about how both of these studies lend credence to his above argument on racialist races (pg 24):
Rosenberg and colleagues also confirm Lewontin’s findings that most genes are not highly differentiated by race and that the variation in genes that underlie obvious physical differences is not typical of the variation of the genome in general. They also suggest that it is not the case that there are many important genetic differences between races apart from the genetic differences that underlie the obvious physical differences. These considerations further buttress the case against the existence of racialist races.
The results of Lewontin’s 1972 study and Rosenberg and colleagues’ 2002 study strongly suggest that it is extremely unlikely that there are many important genetic differences between races apart from the genetic differences that underlie the obvious physical differences.
(Hardimon also writes on page 124 that Rosenberg et al’s 2002 study could also be used as evidence for his populationist concept of race, which I will return to in the future.)
Though, my reasoning for writing this article is to show that the findings by Lewontin and Rosenberg et al regarding more variation within races than between them are indeed true, despite claims to the contrary. There is one article, though, that people cite as evidence against the conclusions by Lewontin and Rosenberg et al, though it’s clear that they only read the abstract and not the full paper.
Witherspoon et al (2007) write that “sufficient genetic data can permit accurate classification of individuals into populations“, which is what the individuals who cite this study as evidence for their contention mean, though they conclude (emphasis mine):
The fact that, given enough genetic data, individuals can be correctly assigned to their populations of origin is compatible with the observation that most human genetic variation is found within populations, not between them. It is also compatible with our finding that, even when the most distinct populations are considered and hundreds of loci are used, individuals are frequently more similar to members of other populations than to members of their own population. Thus, caution should be used when using geographic or genetic ancestry to make inferences about individual phenotypes.
Witherspoon et al (2007) analyzed the three classical races (Europeans, Africans and East Asians) over thousands of loci and came to the conclusion when genetic similarity is measured over thousands of loci, the answer to the question “How often is a pair of individuals from one population genetically more dissimilar than two individuals chosen from two different populations?” is “never“.
Hunley, Cabana, and Long (2016: 7) also confirm Lewontin’s analysis, writing “In sum, we concur with Lewontin’s conclusion that Western-based racial classifications have no taxonomic significance, and we hope that this research, which takes into account our current understanding of the structure of human diversity, places his seminal finding on firmer evolutionary footing.” But the claim that “racial classifications have no taxonomic significance” is FALSE.
This is a point that Edwards (2003) rebutted in depth. While he did agree with Lewontin’s (1972) analysis that there was more variation within races than between them (which was confirmed through subsequent analysis), he strongly disagreed with Lewontin’s conclusion that race is of no taxonomic significance. Richard Dawkins, too disagreed with Lewontin, though as Dawkins writes in his book The Ancestors Tale: “Most of the variation among humans can be found within races as well as between them. Only a small admixture of extra variation distinguishes races from each other. That is all correct. What is not correct is the inferene that race is therefore a meaningless concept.” The fact that there is more variation within races than between them is irrelevant to taxonomic classification, and classifying races by phenotypic differences (morphology, and facial features) along with geographic ancestry shows that just by looking at the average phenotype that race exists, though these concepts make no value-based judgements on anything you can’t ‘see’, such as mental and personality differences between populations.
Though while some agree with Edwards’ analysis of Lewontin’s argument about race’s taxonomic significance, they don’t believe that he successfully refuted Lewontin. For instance, Hardimon (2017: 22-23) writes that Lewontin’s argument against—what Hardimon (2017) calls ‘racialist race’ (his strawman quoted above)—the existence of race because the within-race component of genetic variation is greater than the genetic variation between races “is untouched by Edwards’ objections.”
Though Sesardic (2010: 152) argues that “Therefore, contra Lewontin, the racial classification that is based on a number of genetic differences between populations may well be extremely reliable and robust, despite the fact that any single of those genetic between-population differences\ remains, in itself, a very poor predictor of racial membership.” He also states that the 7 to 10 percent difference between populations “actually refers to the inter-racial portion of variation that is averaged over the separate contributions of a number of individual genetic indicators that were sampled in different studies” (pg 150).
I personally avoid all of this talk about genes/allele frequencies between populations and jump straight to using Hardimon’s minimalist race concept—a concept that, according to Hardimon is “stripped down to its barest bones” since it captures enough of the racialist concept of race to be considered a race concept.
In sum, variation within races is greater than variation between races, but this does not mean anything for the reality of race since race can still be delineated based on peculiar physical features and peculiar geographic ancestry to that group. Using a few indicators (morphology, facial features such as nose, lips, cheekbones, facial structure, and hair along with geographic ancestry), we can group races based on these criteria and we can show that race does indeed exist in a physical—not social—sense and that these categories are meaningful in a medical context (Hardimon, 2013, 2017). So even though genetic variation is greater within races than between them, this does not mean that there is no taxonomic significance to race, as other authors have argued. Hardimon (2017: 23) agrees, writing (emphasis his) “… Lewontin’s data do not preclude the possibility that racial classification might have taxonomic significance, but they do preclude the possibility that racialist races exist.”
Hardimon’s strawman of the racialist concept notwithstanding (which I will cover in the future), his other three race concepts (minimalist, populationist and socialrace concepts) are logically sound and stand up to a lot of criticism. Either way, race does exist, and it does not matter if the apportionment of human genetic diversity is greatest within races than between them.
Steroids get a bad reputation. It largely comes from movies and people’s anecdotal experiences and repeating stories they hear from the media and other forms of entertainment, usually stating that there is a phenomenon called ‘roid rage’ that makes steroid users violent. Is this true? Are any myths about steroids true, such as a shrunken penis? Are there ways to off-set it? Steroids and their derivatives are off-topic for this blog, but it needs to be stressed that there are a few myths that get pushes about steroids and what it does to behavior, its supposed effects on aggression and so forth.
With about 3 million AAS (ab)users (anabolic-androgenic steroids) in America (El Osta et al, 2016), knowing the effects of steroids and similar drugs such as Winny (a cutting agent) would have positive effects, since, of course, athletes mostly use them.
This is, perhaps, one of the most popular. Though the actual myth is that AAS use causes the penis to shrink (which is not true), in reality, AAS use causes the testicles to shrink by causing the Leydig cells to decrease natural testosterone production which then decreases the firmness and shape of the testicles which then results in a loss of size.
In one study of 772 gay men using 6 gyms between the months of January and February (and you need to think of the type of bias there that those people who are ‘Resolutioners’ would be more likely to go to the gym those months), a questionnaire was given to the men. 15 .2 percent of the men had used, with 11.7 percent of them injecting within the past 12 months. HIV positive men were more likely to have used in the past compared to negative men (probably due to scripts). Fifty-one percent of them reported testicular atrophy, and they were more likely to report suicidal thoughts (Bolding, Sherr, and Elford, 2002). They conclude:
One in seven gay men surveyed in central London gyms in 2000 said they had used steroids in the previous 12 months. HIV positive men were more likely to have used steroids than other men, some therapeutically. Side effects were reported widely and steroid use was associated with having had suicidal thoughts and feeling depressed, although cause and effect could not be established. Our findings suggest that steroid use among gay men may have serious consequences for both physical and mental health.
Of course, those who (ab)use substances have more psychological problems than those who do not. Another study of 203 bodybuilders found that 8 percent (n = 17) found testicular atrophy (for what it’s worth, it was an internet survey of drug utilization) (Perry et al, 2005). Another study found that out of 88 percent of individuals who abused the drug complained of side-effects of AAS use, about 40 percent described testicular atrophy (Evans, 1997), while testicular atrophy was noted in about 50 percent of cases (sample size n = 24) (Darke et al, 2016).
One study of steroid users found that only 17 percent of them had normal sperm levels (Torres-Calleja et al, 2001), this is because exogenous testosterone will result in the atrophy of germinal cells which cause a decrease in spermatogenesis. Though, too, increased AAS (ab)use later into life may lead to infertility later in life. Knuth et al (1989) also studied 41 bodybuilders with an average age of 26.7. They went through a huge laundry list of different types of steroids they have taken over their lives. Nineteen of the men were still using steroids at the time of the investigation (group I), whereas 12 of them (group II) stopped taking steroids 3 months prior, while 10 of them (group III) stopped steroid use 4 to 24 months prior.
They found that only 5 of them had sperm counts below the average of 20 million sperm per square ml, while 24 of the bodybuilders showed these symptoms. No difference between group I and II was noticed and group III (the group that abstained from use for 4 to 24 months) largely had sperm levels in the normal range. So, the data suggests that even in cases of severe decrease of sensitivity to androgens due to AAS (ab)use, spermatogenesis may still continue normally in some men, even when high levels of androgens are administered exogenously, while even after prolonged use it seems it is possible for sperm levels to go back to the normal range (Knuth et al 1989).
Aggression and crime
Now it’s time for the fun part and my reason for writing this article. Does (ab)using steroids cause someone to go into an uncontrollable rage, a la the Incredible Hulk when they inject themselves with testosterone? The media has latched into the mind of many, with films and TV shows showing the insanely aggressive man who has been (ab)using AAS. But how true is this? A few papers have shown that this phenomenon is indeed true (Konacher and Workman, 1989; Pope and Katz, 1994), but how true is it on its own, since AAS (ab)users are known to use multiple substances???
Konacher and Workman (1989) is a case study done on one man who had no criminal history, who began taking AASs three months before he murdered his wife, and they conclude that AAS can be said to be a ‘personality changer’. Piacetino et al (2015) conclude in their review of steroid use and psychopathology in athletes that “AAS use in athletes is associated with mood and anxiety disturbances, as well as reckless behavior, in some predisposed individuals, who are likely to develop various types of psychopathology after long-term exposure to these substances. There is a lack of studies investigating whether the preexistence of psychopathology is likely to induce AAS consumption, but the bulk of available data, combined with animal data, point to the development of specific psycho-pathology, increased aggressiveness, mood destabilization, eating behavior abnormalities, and psychosis after AAS abuse/dependence.” I, too, would add that since most steroid abuse are polysubstance abusers (they use multiple illicit drugs on top of AAS), that the steroids per se are not causing crime or aggressive behavior, it’s the other drugs that the steroid (ab)user is also taking. And there is evidence for this assertion.
Lundholm et al (2015) showed just that: that AAS (ab)use was confounded with other substances used while the individual in question was also taking AAS. They write:
“We found a strong association between self-reported lifetime AAS use and violent offending in a population-based sample of more than 10,000 men aged 20-47 years. However, the association decreased substantially and lost statistical significance after adjusting for other substance abuse. This supports the notion that AAS use in the general population occurs as a component of polysubstance abuse, but argues against its purported role as a primary risk factor for interpersonal violence. Further, adjusting for potential individual-level confounders initially attenuated the association, but did not contribute to any substantial change after controlling for polysubstance abuse.“
Even The National Institute of Health (NIH) writes: “In summary, the extent to which steroid abuse contributes to violence and behavioral disorders is unknown. As with the health complications of steroid abuse, the prevalence of extreme cases of violence and behavioral disorders seems to be low, but it may be underreported or underrecognized.” We don’t know whether steroids cause aggression or more aggressive athletes are more likely to use the substance (Freberg, 2009: 424). Clearly, the claims of steroids causing aggressive behavior and crime are overblown and there has yet to be a scientific consensus on the matter. A great documentary on the matter is Bigger, Stronger, Faster, which goes through the myths of testosterone while chronicling the use of illicit drugs in bodybuilding and powerlifting.
This, too, was even seen in one study where men were administered supraphysiologic doses of testosterone to see its effects on muscle size and strength since it had never been tested; no changes in mood or behavior occurred (Bhasin et al, 1996). Furthermore, injecting individuals with supraphysiological doses of testosterone as high as 200 and 600 mg per week does not cause heightened anger or aggression (Tricker et al, 1996; O’Connor et, 2002). Testosterone is one of the most abused AASs around, and if a heightened level of T doesn’t cause crime, nor can testosterone levels being higher this week compared to last seem to be a trigger for crime, we can safely disregard any claims of ‘roid rage’ since they coincide with other drug use (polysubstance abuse). So since we know that supraphysiologic doses of testosterone don’t cause crime nor aggression, we can say that AAS use, on its own (and even with other drugs) does not cause crime or heightened aggression since aggression elevates testosterone secretion, testosterone doesn’t elevate aggression.
One review also suggests that medical issues associated with AAS (ab)use are exaggerated to deter their use by athletes (Hoffman and Ratamess, 2006). They conclude that “Existing data suggest that in certain circumstances the medical risk associated with anabolic steroid use may have been somewhat exaggerated, possibly to dissuade use in athletes.”
Racial differences in steroid use
Irving et al (2002) found that 2.1 percent of whites used steroids, whereas 7.6 percent of blacks did; 6.1 percent of ‘Hispanics’ use them within the past 12 months, and a whopping 14.1 percent of Hmong Chinese used them; 7.9 percent of ‘other Asians’ used them, and 3,1 percent of ‘Native Americans’ did with 11.3 percent of mixed race people using them within the past 12 months to gain muscle. Middle schoolers were more likely to use than high schoolers, while people from lower SES brackets were more likely to use than people in higher SES brackets.
Stilger and Yesalis (1999: 134) write (emphasis mine):
Of the 873 high school football players participating in the study, 54 (6.3%) reported having used or currently using AAS. Caucasians represented 85% of all subjects in the survey. Nine percent were African-American while the remainder (6%) consisted of Hispanics, Asian, and other. Of the AAS users, 74% were Caucasian, 13% African American, 7% Hispanic, and 3% Asian, x2 (4,854 4) 4.203, p 4 .38. The study also indicated that minorities are twice as likely to use AAS as opposed to Caucasians. Cross tabulated results indicate that 11.2% of all minorities use/used AAS as opposed to 6.5% of all Caucasians (data not displayed).
One study even had whites and blacks reporting the same abuse of steroids in their sample (n = 10,850 ‘Caucasians’ and n = 1,883 black Americans), with blacks reporting, too, lower levels of other drug abuse (Green et al, 2001). Studies indeed find higher rates of drug use for white Americans than other ethnies, in college (McCabe et al, 2007). Black Americans also frequently underreport and lie about their drug use (Ledgerwood et al, 2008; Lu et al, 2001). Blacks are also more likely to go to the ER after abusing drugs than whites (Drug Abuse Warning Network, 2011). Bauman and Ennett (1994) also found that blacks underreport drug use whereas whites overreport.
So can we really believe the black athletes who state that they do not (ab)use AAS? No, we cannot. Blacks like about any and all drug use, so believing that they are being truthful about AAS (ab)use in this specific instance is not called for.
Like with all things you use and abuse, there are always side-effects. Though, the media furor one hears regarding AAS and testosterone (ab)use are largely blown out of proportion. The risks associated with AAS (ab)use are ‘transient’, and will subside after one discontinues using the drugs. Blacks seem to take more AAS than whites, even if they do lie about any and all drug use. (And other races, too, seem to use it at higher rates than whites.) Steroid use does not seem to be ‘bad’ if one knows what they’re doing and are under Doctor’s supervision, but even then, if you want to know the truth about AAS, then you need to watch the documentary Bigger, Stronger, Faster. I chalk this up to the media themselves demonizing testosterone itself, along with the ‘toxic masculinity’ and the ‘toxic jock effect‘ (Miller, 2009; Miller, 2011). Though, if you dig into the literature yourself you’ll see there is scant evidence for AAS and testosterone (ab)use causing crime, that doesn’t stop papers like those two by Miller talking about the effects of ‘toxic jocks’ and in effect, deriding masculine men and with it the hormone that makes Men men: testosterone. If taken safely, there is nothing wrong with AAS/testosterone use.
(Note: Doctor’s supervision only, etc)
People seem to be confused on the definition of the term ‘phrenology’. Many people think that just the measuring of skulls can be called ‘phrenology’. This is a very confused view to hold.
Phrenology is the study of the shape and size of the skull and then drawing conclusions from one’s character from bumps on the skull (Simpson, 2005) to overall different-sized areas of the brain compared to others then drawing on one’s character and psychology from these measures. Franz Gall—the father of phrenology—believed that by measuring one’s skull and the bumps etc on it, then he could make accurate predictions about their character and mental psychology. Gall had also proposed a theory of mind and brain (Eling, Finger, and Whitaker, 2017). The usefulness of phrenology aside, the creator Gall contributed a significant understanding to our study of the brain, being that he was a neuroanatomist and physiologist.
1.The brain is the organ of the mind.
2. The mind is composed of multiple, distinct, innate faculties.
3. Because they are distinct, each faculty must have a separate seat or “organ” in the brain.
4. The size of an organ, other things being equal, is a measure of its power.
5. The shape of the brain is determined by the development of the various organs.
6. As the skull takes its shape from the brain, the surface of the skull can be read as an accurate index of psychological aptitudes and tendencies.
Gall’s work, though, was imperative to our understanding of the brain and he was a pioneer in the inner workings of the brain. They ‘phrenologized’ by running the tips of their fingers or their hands along the top of one’s head (Gall liked using his palms). Here is an account of one individual reminiscing on this (around 1870):
The fellow proceeded to measure my head from the forehead to the back, and from one ear to the other, and then he pressed his hands upon the protuberances carefully and called them by name. He felt my pulse, looked carefully at my complexion and defined it, and then retired to make his calculations in order to reveal my destiny. I awaited his return with some anxiety, for I really attached some importance to what his statement would be; for I had been told that he had great success in that sort of work and that his conclusion would be valuable to me. Directly he returned with a piece of paper in his hand, and his statement was short. It was to the effect that my head was of the tenth magnitude with phyloprogenitiveness morbidly developed; that the essential faculties of mentality were singularly deficient; that my contour antagonized all the established rules of phrenology, and that upon the whole I was better adapted to the quietude of rural life rather than to the habit of letters. Then the boys clapped their hands and laughed lustily, but there was nothing of laughter in it for me. In fact, I took seriously what Rutherford had said and thought the fellow meant it all. He showed me a phrenological bust, with the faculties all located and labeled, representing a perfect human head, and mine did not look like that one. I had never dreamed that the size or shape of the head had anything to do with a boy’s endowments or his ability to accomplish results, to say nothing of his quality and texture of brain matter. I went to my shack rather dejected. I took a small hand- mirror and looked carefully at my head, ran my hands over it and realized that it did not resemble, in any sense, the bust that I had observed. The more I thought of the affair the worse I felt. If my head was defective there was no remedy, and what could I do? The next day I quietly went to the library and carefully looked at the heads of pictures of Webster, Clay, Calhoun, Napoleon, Alexander Stephens and various other great men. Their pictures were all there in histories.
This—what I would call skull/brain-size fetishizing—is still evident today, with people thinking that raw size matters (Rushton and Ankney, 2007; Rushton and Ankney, 2009) for cognitive ability, though I have compiled numerous data that shows that we can have smaller brains and have IQs in the normal range, implying that large brains are not needed for high IQs (Skoyles, 1999). It is also one of Deacon’s (1990) fallacies, the “bigger-is-smarter” fallacy. Just because you observe skull sizes, brain size differences, structural brain differences, etc, does not mean you’re a phrenologist. you’re making easy and verifiable claims, not like some of the outrageous claims made by phrenologists.
What did they get right? Well, phrenologists stated that the most-used part of the brain would become bigger, which, of course, was vindicated by modern research—specifically in London cab drivers (McGuire, Frackowiak, and Frith, 1997; Woolett and McGuire, 2011).
It seems that phrenologists got a few things right but their theories were largely wrong. Though those who bash the ‘science’ of phrenology should realize that phrenology was one of the first brain ‘sciences’ and so I believe phrenology should at least get some respect since it furthered our understanding of the brain and some phrenologists were kind of right.
People see the avatar I use which is three skulls, one Mongoloid, the other Negroid and the other Caucasoid and then automatically make that leap that I’m a phrenologist based just on that picture. Even, to these people, stating that races/individuals/ethnies have different skull and brain sizes caused them to state that what I was saying is phrenology. No, it isn’t. Words have definitions. Just because you observe size differences between brains of, say either individuals or ethnies, doesn’t mean that you’re making any value judgments on the character/mental aptitude of that individual based on the size of theur skull/brain. On the other hand, noting structural differences between brains like saying “the PFC is larger here but the OFC is larger in this brain than in that brain” yet no one is saying that and if that’s what you grasp from just the statement that individuals and groups have different sized skulls, brains, and parts of the brain then I don’t know what to tell you. Stating that one brain weighs more than another, say one is 1200 g and another is 1400 g is not phrenology. Stating that one brain is 1450 cc while another is 1000 cc is not phrenology. For it to be phrenology I have to outright state that differences in the size of certain areas of the brain or brains as a whole cause differences in character/mental faculties. I am not saying that.
A team of neuroscientists just recently (recently as in last month, January, 2018) showed, in the “most exhaustive way possible“, tested the claims from phrenological ‘research’ “that measuring the contour of the head provides a reliable method for inferring mental capacities” and concluded that there was “no evidence for this claim” (Jones, Alfaro-Almagro, and Jbabdi, 2018). That settles it. The ‘science’ is dead.
It’s so simple: you notice physical differences in brain size between two corpses. That one’s PFC was bigger than OFC and with the other, his OFC was bigger than his PFC. That’s it. I guess, using this logic, neuroanatomists would be considered phrenologists today since they note size differences between individual parts of brains. Just noting these differences doesn’t make any type of judgments on potential between brains of individuals with different size/overall size/bumps etc.
It is ridiculous to accuse someone of being a ‘phrenologist’ in 2018. And while the study of skull/brain sizes back in the 17th century did pave the way for modern neuroscience and while they did get a few things right, they were largely wrong. No, you cannot see one’s character from feeling the bumps on their skull. I understand the logic and, back then, it would have made a lot of sense. But to claim that one is a phrenologist or is pushing phrenology just because they notice physical differences that are empirically verifiable does not make them a phrenologist.
In sum, studying physical differences is interesting and tells us a lot about our past and maybe even our future. Stating that one is a phrenologist because they observe and accept physical differences in the size of the brain, skull, and neuroanatomic regions is like saying that physical anthropologists and forensic scientists are phrenologists because they measure people’s skulls to ascertain certain things that may be known in their medical history. Chastizing someone because they tell you that one has a different brain size than the other by calling them outdated names in an attempt to discredit them doesn’t make sense. It seems that even some people cannot accept physical differences that are measurable again and again because it may go against some long-held belief.