Home » Crime » 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)

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)

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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 2002Rohrmann 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.

Rushton and Templer (2012: 6) write:

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 Itbut 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, shows that the proposed relationships are caused by the melanocortin system and Lift History Theory shows their ignorance of the human physiological system.



  1. HughCipher says:

    Ok I’ve learned a lot reading this. You have a lot of information that new to me here and I’ll be digesting it for a while. It’s rare for a person entrenched in a particular world view to accept new information and change or modify that belief system. I’m glad you have because you wouldn’t be educating people on this level. I mean this is deep stuff. Reading what you wrote about testosterone I think about boxing. I’m a big boxing fan and every time I see Vasly Lomanchenko, Billie Joe Saunders or say the new kid Pretty Boy Kelly fight I think about how these guys were trained from 6 and 8 yrs old using similar techniques Black boxers have used for ages and now dominate opponents. Race realist would have said Asians are hopefully doomed to be 5 ft 7 at their tallest before Jeremy Lin started slam dunking on Black guys. Jeremy Lin doesn’t have European or African genes. His ancestors simply moved to America changing their environment-specifically their dietary habits and a few generations later you have the epigenetic results of a 6ft plus Jeremy Lin and today many American born Asians are just as tall or taller than their Black and White countrymen. The race realist logic would dictate that these English, Irish and Eastern European fighters and Asian athletes could never dominate the way Blacks do no mater what they did. To me it proves environment and culture are key catalyst to human ability or lack thereof. This would be even more so when it concerns cognitive traits like IQ, temperament and sexuality. Cognitive expression is not just gene based and the way environment impacts the way one acts and thinks is mind bogglingly complicated. I think anyone looking for a biologically based causation for forms of human cognitive expression is just looking for an easy answer


  2. […] controlling (apparently) causally unrelated surface features. Fringe claims of melanin directly causing criminality notwithstanding, the HBD argument for racial disparities on behavioral traits holds up […]


  3. Michael says:

    You certainly gave an interesting analysis, and your self-reflective critical thinking is exactly what we need more of. In regards to the topic, while the study in question has numerous apparent flaws, including statements in regard to r-/K- theory, IQ, racial definitions, and various spurious causations that are very likely mere correlations, etc, I must comment that, standing apart from the rest of paper, the section on animal studies may hold merit and require further investigation.

    To explain, let me respond to this section where you wrote:
    “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).”

    I initially interpreted the statement you quoted (“The genes that control…”) in quite a different manner. Within the context of the genome, in regard to different downstream biological processes, it is the case that different genes hold different hierarchies of influence (depending on the environmental context). Some genes can indeed produce greater impacts upon phenotype that others. Within this interpretation, of correct, their statement seems reasonable.

    On another note, the major component I would like to address is the statement regarding genes as not being blueprints or recipes. This may be a semantic issue, however, as I often use the analogy of genes as recipes in my lectures. As you are aware, genes are recipes for protein production, and proteins are involved in phenotypic and behavioral mechanisms. The papers you cited by Noble explain the intertwined relationships between genes and environment, explaining that genes are not deterministic. Although, the genome should be thought of as an organism’s potential, what an organism CAN be, while the environment directs the genome into realizing what the organism becomes. Disregarding somatic mutations throughout life, once the genome is set initially, there enters a dynamic play between genetic signals and environmental signals (induced exogenously or endogenously; by environmental conditions, emotional and physical stresses, illness, nutrition, etc) that ultimately shapes the individual.

    What this ultimately means is that if the correlations between melanin and aggression/sexuality in fact have a true biological connection, it would most certainly NOT be a simple deterministic cause and effect case. Higher melanin levels would not CAUSE more aggression or sexual activity, but merely that the increased levels may positively influence the drive or inclination one has towards these tendencies, which, in the case of most humans, can be overcome by cognition. I say “most” because it must also be noted that many of these phenotypes (physical or behavioral) are not discrete on/off, but typically found in some form of distribution, or continuum, meaning that not all, or even few members of a species containing similar expression of one specific trait have the same degree of phenotypic expression of connected traits (displaying great intra-population diversity due to biological complexity of molecular interactions). Due to this, a dark skinned individual could be significantly less aggressive than a light-skinned one, but generalized trends may be only found when comparing the averages of different melanistically-homogenous groups or when comparing individuals at the extremes.

    If this melanin/behavior tendency connection was in fact true, this could actually present us with a possible parallel to correllations between genetic markers and addiction, for example. It is NOT AT ALL deterministic, but may present a possible increased tendency toward behavior for some members of a population which, if realized in the medical field, may allow us to better address potential social disparities and foster compassion in the understanding that these disparities are not just a manifestation of bad behavior or values as some claim, but that this is something that can be addressed or understood in more productive ways, through therapy and treatment as opposed to criminal courts and punishment.

    However, there looms the obvious potential for some select members of our society to interpret such information as a confirmation of racial supremacy, which is entirely what we want to avoid…

    On final note, I would have to wonder, too, how tanning and redheads would fit into this equation, given that tanning influences melanin levels and redheads have deiffering quantities of orange pheomelanin and standard brown eumelanin, relative to other human phenotypes.

    ——NOTE: If anything I listed is incorrect, requires clarification, or is disagreeable, please reply to this comment. For example, do all the animal studies listed agree on the results? Are there counter studies in non-nocturnal vertebrates? I found this topic very engaging and welcome discourse. Thank you for posting this 🙂


    • DaveM says:

      “select members of our society to interpret such information as a confirmation of racial supremacy”
      – Sooo in other words you want to conceal information for political correctness? Censorship, communism has murdered more people than any other ism. Makes me laugh at how the west think Hitler was the worst when he was no where near it. But I guess you are right in a sense because (((they))) are taught at very early age that they are superior to gentiles, how to infiltrate, to lie, attend special schools where they are trained in psychology, trained to subvert, destroy movements to keep everyone else under their heel. (((They))) do this with their children because they are paranoid, degenerate, schizos.
      But please tell me, what is the difference between “we are the master race” and “we are god’s chosen people”? Because it comes off as the same thing.


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