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President Trump was quoted the other day saying “We have to look at the Internet because a lot of bad things are happening to young kids and young minds and their minds are being formed,” Trump said, according to a pool report, “and we have to do something about maybe what they’re seeing and how they’re seeing it. And also video games. I’m hearing more and more people say the level of violence on video games is really shaping young people’s thoughts.” But outside of broad assertions like this—that playing violent video games cause violent behavior—does it stack up to what the scientific literature says about it? In short, no, it does not. (A lot of publication bias exists in this debate, too.) Why do people think that violent video games cause violent behavior? Mostly due to the APA and their broad claims with little evidence.
Just doing a cursory Google search of ‘violence in video games pubmed‘ brings up 9 journal articles, so let’s take a look at a few of those.
The first article is titled The Effect of Online Violent Video Games on Levels of Aggression by Hollingdale and Greitemeyer (2014). They took 101 participants and randomized them to one of four experimental conditions: neutral, offline; neutral online; (Little Big Planet 2) violent offline; and violent online video games (Call of Duty: Modern Warfare). After they played said games, they answered a questionnaire and then measured aggression using the hot sauce paradigm (Lieberman et al, 1999) to measure aggressive behavior. Hollingdale and Greitemeyer (2014) conclude that “this study has identified that increases in aggression are not more pronounced when playing a violent video game online in comparison to playing a neutral video game online.”
Staude-Muller (2011) finds that “it was not the consumption of violent video games but rather an uncontrolled pattern of video game use that was associated with increasing aggressive tendencies.” Przybylski, Ryan, and Rigby (2009) found that enjoyment, value, and desire to play in the future were strongly related to competence in the game. Players who were high in trait aggression, though, were more likely to prefer violent games, even though it didn’t add to their enjoyment of the game, while violent content lent little overall variance to the satisfactions previously cited.
Tear and Nielsen (2013) failed to find evidence that violent video game playing leads to a decrease in pro-social behavior (Szycik et al, 2017 also show that video games do not affect empathy). Gentile et al (2014) show that “habitual violent VGP increases long-term AB [aggressive behavior] by producing general changes in ACs [aggressive cognitions], and this occurs regardless of sex, age, initial aggressiveness, and parental involvement. These robust effects support the long-term predictions of social-cognitive theories of aggression and confirm that these effects generalize across culture.” The APA (2015) even states that “scientific research has demonstrated an association between violent video game use and both increases in aggressive behavior, aggressive affect, aggressive cognitions and decreases in prosocial behavior, empathy, and moral engagement.” How true is all of this, though? Does playing violent video games truly increase aggression/aggressive behavior? Does it have an effect on violence in America and shootings overall?
Whitney (2015) states that the video-games-cause-violence paradigm has “weak support” (pg 11) and that, pretty much, we should be cautious before taking this “weak support” as conclusive. He concludes that there is not enough evidence to establish a truly causal connection between violent video game playing and violent and aggressive behavior. Cunningham, Engelstatter, and Ward (2016) tracked the sale of violent video games and criminal offenses after those games were sold. They found that violent crime actually decreased the weeks following the release of a violent game. Of course, this does not rule out any longer-term effects of violent game-playing, but in the short term, this is good evidence against the case of violent games causing violence. (Also see the PsychologyToday article on the matter.)
We seem to have a few problems here, though. How are we to untangle the effects of movies and other forms of violent media that children consume? You can’t. So the researcher(s) must assume that video games and only video games cause this type of aggression. I don’t even see how one can logically state that out of all other types of media that violent video games—and not violent movies, cartoons, TV shows etc—cause aggression/violent behavior.
Back in 2011, the Supreme Court case Brown vs. Entertainment Merchants Association concluding that since the effects on violent/aggressive behavior were so small and couldn’t be untangled from other so-called effects from other violent types of media. Ferguson (2015) found that violent video game playing had little effect on children’s mood, aggression levels, pro-social behavior or grades. He also found publication bias in this literature (Ferguson, 2017). Contrary to what those say about video games causing violence/aggressive behavior, video game playing was associated with a decrease in youth crime (Ferguson, 2014; Markey, Markey, and French, 2015 which is in line with Cunningham, Engelstatter, and Ward, 2016). You can read more about this in Ferguson’s article for The Conversation, along with his and others’ responses to the APA who state that violent video games cause violent behavior (with them stating that the APA is biased). (Also read a letter from 230 researchers on the bias in the APA’s Task Force on Violent Media.)
How would one actually untangle the effects of, say, violent video game playing and the effects of such other ‘problematic’ forms of media that also show aggression/aggressive acts towards others and actually pinpoint that violent video games are the culprit? That’s right, they can’t. How would you realistically control for the fact that the child grows up around—and consumes—so much ‘violent’ media, seeing others become violent around him etc; how can you logically state that the video games are the cause? Some may think it logical that someone who plays a game like, say, Call of Duty for hours on end a day would be more likely to be more violent/aggressive or more likely to commit such atrocities like school shootings. But none of these studies have ever come to the conclusion that violent video games may/will cause someone to kill or go on a shooting spree. It just doesn’t make sense. I can, of course, see the logic in believing that it would lead to aggressive behavior/lack of pro-social behavior (let’s say the kid played a lot of games and had little outside contact with people his age), but of course the literature on this subject should be enough to put claims like this to bed.
It’s just about impossible to untangle the so-called small effects of video games on violent/aggressive behavior from other types of media such as violent cartoons and violent movies. Who’s to say it’s not just the violent video games and not the violent movies and violent cartoons, too, that ’cause’ this type of behavior? It’s logically impossible to distinguish this, so therefore the small relationship between video games and violent behavior should be safely ignored. The media seems to be getting this right, which is a surprise (though I bet if Trump said the opposite—that violent video games didn’t cause violent behavior/shootings—that these same people would be saying that they do), but a broken clock is right twice a day.
So Trump’s claim (even if he didn’t outright state it) is wrong, along with anyone else who would want to jump in and attempt to say that video games cause violence. In fact, the literature shows a decrease in violence after games are released (Ferguson, 2014; Markey, Markey, and French, 2015; Cunningham, Engelstatter, and Ward, 2016). The amount of publication bias (also see Copenhaver and Ferguson, 2015 where they show how the APA ignores bias and methodological problems regarding these studies) in this field (Ferguson, 2017) should lead one to question the body of data we currently have, since studies that find an effect are more likely to get published than studies that find no effect.
Video games do not cause violent/aggressive behavior/school shootings. There is literally no evidence that they are linked to the deaths of individuals, and with the small effects noted on violent/aggressive behavior due to violent video game playing, we can disregard those claims. (One thing video games are good for, though, is improving reaction time (Benoit et al, 2017). The literature is strong here; playing these so-called “violent video games” such as Call of Duty improved children’s reaction time, so wouldn’t you say that these ‘violent video games’ have some utility?)
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.
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.
People don’t understand the relationship between testosterone, aggression, and crime. People hear the sensational media stating that testosterone causes crime, aggression, and anger. However, I have written numerous articles on this blog on the true nature of testosterone, what it’s really needed for and why we need it in high amounts. I’ve mused a lot on this hormone, which is one of my favorites to discuss due to the numerous misconceptions surrounding it.
Which way does causation run in regard to prisoners and their testosterone level?: heightened testosterone > aggression > violence or aggression > heightened testosterone > dominance > possibility (not necessarily, as I have written myself in the past) of violence.
People may use animal studies in support of their contention that testosterone causes aggressive behavior. However, for reasons I have discussed in the past, animal models only show avenues for future research and do not necessarily mean that this is the case for humans (as Mazur, 2006 point out). I don’t use animal studies. They’re good for future research, but to use them as evidence for causation in humans doesn’t make sense.
People may cite Dabbs et al showing that the more violent prisoners had higher levels of testosterone and therefore conclude that higher levels of testosterone drive the violent crime that they commit, however it is much more nuanced than that.
Does being a violent criminal raise testosterone or are violent people more likely to have high testosterone? Dabbs never untangles this; they just showed a correlation, which is small as evidenced by my other citations.
Testosterone is, as evidenced by numerous studies, related to dominance and dominance contests, however, during these dominance contests “a killing is rarely the outcome of a violent dominance contest” (Mazur, 2006: 25). Therefore, this throws a wrench in the testosterone-causes-crime hypothesis.
Some individuals may state that these dominance contests then lead to violence, however, as Mazur (2006) puts it: “Heightened testosterone is not a direct cause of male violence.”
Other animals assert dominance violently but we, necessarily, do not.
Mazur (2006) states that dominance contests rarely escalate to murder. Mazur also states that dominance contests also lead to increased T for the winners and decreased T for the losers, and these contests also don’t necessarily lead to murder/violent behavior. There is a feedback loop with high T causing behavior and behavior causing high T (Mazur, 2006) while this feedback loop may lead to “lethal effects” (Mazur and Booth, 2008).
It’s worth noting that Mazur seems to advocate for ‘testosterone-depressing drugs’. He concludes:
There are strong linkages between macro-level culture and the physiology of
individuals. We may find solutions to some of our social problems by altering these linkage.
Macro-level culture being white culture, black culture, Asian culture, etc.
The physiological differences are due to the preparation for dominance contests. So, his hypothesis goes, the culture of dominance among young black men with no education is why their T is so high. That low education was also associated with low education lends credence to the claim that this is changeable.
However, in his newer article on education, low testosterone and blacks he advocates for more sensible solutions (attempting an environmental change). I don’t know about you but I have big problems with using FDA/Big Pharma drugs to ‘reduce societal problems’, and it seems that Mazur has changed his view there. Mazur (2016) writes:
If high T does facilitate the high violence rate among young black men, there would be a troubling policy question of what, if anything, to do about it. Any notion of a medical or pharmaceutical fix, rather like prescribing Ritalin for hyperactivity, would reek of race-based chemical castration and should be regarded as outside the pale. However, social interventions might be workable and ethically acceptable.
I have railed against measures like this in the past, since proposing measures to attempt to ‘decrease crime through supposedly decreasing one of the main “causes”‘ is very Brave New World-ish, and I am highly against those measures. Social interventions are, in my view, the more sensible measures to undertake.
In regard to low education and testosterone, this same relationship was noticed by Assari, Caldwell, and Zimmerman (2014) where they note that testosterone was not associated with aggression in men, but low education was, which Mazur (2016) replicates, showing that blacks of the same age group with more education had lower levels of testosterone when compared to age-matched blacks. Mazur (2016) cites one study in support for his contention that education can decrease aggressive behavior (Carre et al, 2014)
The correlation is there, I agree. let’s take the middle value of .11 between Archer, Graham-Kevan, and Davies, 2005 at .08; and Book, Starzyk, and Quinsey, 2001 .14. So testosterone explains 3 percent of the the relationship with aggression. Not high at all.
Great evidence against the testosterone-causes-aggressive-behavior hypothesis are data on the Yanomami. About 50 percent of Yanomami men meet their deaths by other Yanomami men. So the Yanomami must have testosterone levels through the roof, right? Wrong. De Lima et al (2015) write:
We observed that Yanomamis present lower levels of testosterone (414 ng/dL) in relation to other ethnic groups (502/512 ng/dL), but still within normal limits (350-1000 ng/dL).
(Note that these values for “normal limits” changed, going into effect at the end of July.)
The Yanomami with an extremely high murder rate with nowhere near a modern society have T levels on the lower end of our range. So….. The Yanomami example is direct evidence against the assertion of testosterone directly causing crime, as some people assert (it is even evidence against an indirect cause). The evidence of the Yanomami having testosterone levels near our lower range is direct evidence against the testosterone/crime hypothesis. Clearly, other variables drive the high violence rate in this society that are not testosterone. More interestingly, these people have had little contact with Western societies, and their T levels are still low compared to ours despite constantly being vigilant for threats from other Yanomami.
Most dominance contests do not end violently in the first-world, there is numerous evidence to attest to this fact. So with the low correlation between testosterone and aggression (Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005), along with dominance contests rarely ending in murder/violent crime, then there are way more factors influencing these phenomena.
So the feedback loop goes: Testosterone rises in expectation of a challenge which then, after the dominance contest (which doesn’t always necessarily lead to violence), it affects both individuals differently depending on whether or not they won or lost that dominance contest and these values then persist over time if the dominance contests continuously end up the same.
Let’s say, for argument’s sake, that testosterone is a large cause for aggressive behavior in lower-educated blacks, what should be done about it? Mazur cites evidence that behavioral interventions seem to work to decrease violent behavior during certain circumstances (Carre et al, 2014), so that is a good way to lower violence in populations that have low education.
So heightened testosterone does lead to dominance which then facilitates a dominance contest between two individuals which does not necessarily lead to crime and aggressive, violent behavior (this outcome is rare in dominance contests among “higher primates” [Mazur’s words]) so, therefore, while testosterone does facilitate dominance contests, it rarely leads to violence in our species. Therefore, testosterone does not cause aggressive behavior and crime, but it does cause dominance which, for the most part, do not always result in violent, aggressive, murderous behavior.
I’ve shown that Mazur replicated other analyses that show that testosterone and aggressive behavior are related to lower education. Testosterone wasn’t associated with aggressive behavior in Assari, Caldwell, and Zimmerman’s (2014) study, and, as Mazur (2016) replicates, low education was. So one way to end this relationship is to educate people, as shown by Carre et al (2014), and with this education, crime will begin to fall. Heightened testosterone is not a direct cause of male violence.
(Note: I also believe that other factors such as sleep and depressed nutrition play a factor in crime, as well as racial differences in it. See Birch, 1972; Liu et al, 2003; Liu et al, 2004; Walker et al, 2007; Galler et al, 2011, 2012a, 2012b; Spratt et al, 2012; Gesch, 2013; Kuratko et al, 2013; Waber et al, 2014; Raine et al, 2015; Thompson et al, 2017 for more information, I will cover this in the future. I’m of course not daft enough to believe that no genetic differences between individuals/populations are the cause of a lot of crime between them, however, as I have laid out the case in regard to testosterone and MAOA numerous times, these two explanations for both individual differences in crime as well as racial differences in crime leave a lot to be desired. Other genetic factors, of course, influence these differences, however, I am only worried about refuting the popular notions of ‘testosterone and MAOA, the ‘warrior gene” cause crime. The relationship is a lot more nuanced as I have provided mountains of evidence for.)
Many long-time readers may know of the numerous tirades of been on in regards to the “testosterone causes crime and aggression” myth. It’s a fun subject to talk about because the intelligent human physiological system is an amazing system. However, people who are not privy to the literature on testosterone in regards to race, aggression, crime, sex differences etc are only aware of whatever they read in pop science articles. So since they never read the actual papers themselves, they get a clouded view of a subject.
In my last article, I wrote about how there are no “testosterone genes”. In previous articles on the hormone, I have proven that there is no causal link between testosterone and aggression. But when comparing the sexes, how do the results look? Do they look the same with men being more violent while women—who have substantially less testosterone than men—do not have any higher levels of aggression or crime? The most recent study I’m aware of is by Assari, Caldwell, and Zimmerman (2014) titled: Sex Differences in the Association Between Testosterone and Violent Behaviors.
To make a long story short, there was no relationship between testosterone and aggression in men, but a significant relationship between testosterone and aggression in women. This data comes from the Flint Adolescent Study, a longitudinal study conducted between the years of 1994 to 2012. In regards to testosterone collection, saliva was used which has a perfect correlation with circulating testosterone. The eligibility to be included in the testosterone assay was “provided consent for the procedure, not being pregnant, not having anything to eat, drinking nothing except water, and not using tobacco, 1 hour prior to collection” (Assari, Caldwell, and Zimmerman, 2014).
The adolescent who contributed saliva gave a whole slew of demographic factors including SES, demographics, psychological factors, family relations, religion, social relations, behavior, and health. They were aged 14 to 17 years of age. They collected data during face-to-face interviews,
Age and SES were used as control variables in their multivariate analysis. For violent behaviors, the authors write:
Youths were asked how often they had engaged in the following behaviors; ‘had a fight in school’, ‘taken part in a rumble where a group of your friends were against another group’, injured someone badly enough to need bandages or a doctor’, ‘hit a teacher or supervisor at work (work supervisor)’, used a knife or gun or other object (like a club) to get something romantic a person’, ‘carried a knife or razor’, or ‘carried a gun’. All items used a Likert response, ranging from 1 (0 times) to 5 (4 or more times). Responses to each item were averages to calculate the behavior during the last year. Total score was calculated as the average of all items. Higher scores indicated more violent behaviors (a = 0.79). This measure has shown high reliability and validity and it has been used previously in several published reports.
This is a great questionnaire. The only thing I can think of that’s missing is fighting/arguing with parents.
In regards to testosterone assaying, they were assayed after 11 am to “control for changes due to diurnal rhythm” (Assari, Caldwell, and Zimmerman, 2014). I’m iffy on that since testosterone levels are highest at 8 am but whatever. This analysis is robust. Saliva was not taken if the subject had smoked or ingested something other than water or if a subject was pregnant. Assays should be taken as close to 8 am, as that’s when levels are highest. However one study does argue to extend the range to 8 am to 2 pm (Crawford et al, 2015) while other studies show that this only should be the case for older males (Long, Nguyen, and Stevermer, 2015). Even then assays were done at the higher end of the range as stated by Crawford et al (2015), so differences shouldn’t be too much.
86.4 percent of the sample was black whereas 13.4 percent were white. 41.2 percent of the subjects had some college education whereas 58.2 percent of the subjects lived with a partner or relative. 21.4 percent of the subjects were unemployed.
The mean age was 20.5 for both men and women, however, which will be a surprise to some, testosterone did not predict aggressive behavior in men but did in women. Testosterone and aggressive behavior were positively correlated, whereas there was a negative correlation between education and testosterone and aggressive behavior. Though education was associated with aggressive behavior in men but not women. So sex and education was associated with aggressive behavior (the sex link being women more privy to aggressive behavior while men are more privy to aggressive behavior due to lack of education). Females who had high levels of education had lower levels of aggressive behavior. Again: testosterone wasn’t associated with violent behavior in men, but it was in women. This is a very important point to note.
This was a community sample, so, of course, there were different results when compared to a laboratory setting, which is not surprising. Laboratory settings are obviously unnatural settings whereas the environment you live in every day obviously is more realistic.
This study does contradict others, in that it shows that there is no association between testosterone and aggression in men. However, still other research shows that testosterone is not linked to aggression or impulsivity, but to sensation-seeking, sexual experience or sociality (Daitzman and Zuckerman, 1980; Zuckerman, 1984). Clearly, testosterone is a beneficial hormone and due to the low correlation of testosterone with aggression (between .08 and .14; Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005). This paper, yet again, buttresses my arguments in regards to testosterone and aggressive behavior.
In regards to the contrast in the literature the authors describe, they write:
One of the many factors that may explain the inconsistency in these findings is the community versus clinical setting, which has been shown to be a determinant of these associations. Literature has previously shown that many of the findings that can be found in clinical samples may not be easily replicated in a community setting (36).
This is like the (in)famous, unreplicable stereotype threat (see Stroessner and Good). It can only be replicated in a lab, not in an actual educational setting. And it also seems that this is the case for testosterone and aggressive behavior.
Just because women have lower testosterone and are less likely to engage in aggressive behavior, that doesn’t mean that a relationship does not exist between females. “It is also plausible to attribute sex differences in the above studies to differential variations in the amount of testosterone among men and women” (Assari, Caldwell, and Zimmerman, 2014). This view supports the case that testosterone is linked to aggression in females, even though their range of testosterone is significantly lower than men’s, while it may also be easier to assay women for testosterone due to less diurnal variation in comparison to men (Book, Starzyk, and Quinsey, 2001).
Assari, Caldwell, and Zimmerman, (2014) also write (which, again, buttresses my arguments):
Age may explain some of the conflicting results across the studies. A meta-analysis of community and selected samples suggested that there might be only low to modest association between testosterone and aggression, with mean weighted correlations ranging from 0.08 to 0.14, in males. Overall, these meta-analyses suggest that the testosterone-aggression association is equally strong in 12 to 21-year-olds, as it is in 22 to 35-year-olds, but that it may be less strong in age groups younger than 12, than in those who are older.
So, testosterone may be associated with aggressive behavior and violence in women but not in men. In men, the significant moderator was education. It’s interesting to note that Mazur (2016) noted that young black males with little education had higher levels of testosterone than age-matched samples of other blacks. This, along with the evidence provided here, may be a clue that if the social environment changes, then so will higher levels of testosterone (as I have argued here).
They, perhaps taking too large of a leap here, argue that “aggressive behaviors may be more social and less biologically based among men” (Assari, Caldwell, and Zimmerman, 2014). Obviously social factors are easier to change than biological ones (in theory), so, they argue, preventative measures may be easier for men than women. More studies need to be done on the complex interactions between sex, testosterone, aggression, biology and the social environment which then shapes the aggressive behaviors of those who live there.
Testosterone and aggression studies are interesting. However, you must know a good amount of the literature to be able to ascertain good studies from the bad, what researchers should and should not have controlled for, time of assay, etc because these variables (some not in the author’s hands, however) can and do lead to false readings if certain variables are not controlled for. All in all, the literature is clearly points to, though other studies contest this at times, the fact that testosterone does not cause aggressive behavior in men. The myth needs to die; the data is piling up for this point of view and those who believe that testosterone causes aggressive behavior and crime (which I have shown it does not, at least for men) will soon be left in the dust as we get a better understanding of this pivotal hormone.
(In case anyone was going to use this as evidence that black women have higher levels of testosterone than white women, don’t do it because it’s not true. You’ll only embarrass yourself like this guy did. Read the comments and see him say that you don’t need scientific measurements, you only need to ‘observe it’ and through ‘observation’ we can deduce that black women have higher levels of testosterone than white women. This is not true. Quoting Mazur, 2016:
The pattern [high testosterone] is not seen among teenage boys or among females.
There is no indication of inordinately high T among young black women with low education.
Whoever still pushes that myth is an idealogue; I have retracted my article ‘Black Women and Testosterone‘, but idealogues just gloss over it and read what they think will bolster their views when I have provided the evidence to the contrary. It pisses me off that people selectively read things then cite my article because they think it will confirm their pre-conceived notions. Well too bad, things don’t work like that.)
When I first got into HBD back in 2012, one of the first things I came across—along with the research on racial IQs from Rushton, Lynn, Jensen et al—was that the races differed in a gene called MAOA-L, which has a frequency in Caucasians at .1 percent (Beaver et al, 2013), 54 percent in Chinese people (Lu et al, 2013; 56 percent in Maoris (Lea and Chambers 2007) while about 60-65 percent of Japanese people have the low-frequency version of this gene (Way and Lieberman, 2007).
So if these ethnies have a higher rate of this polymorphism and it is true that this gene causes crime, then the Chinese and Japanese should have the highest rates of crime in the world, since even apparently the effect of MAOA and violence and antisocial behavior is seen even without child abuse (Ficks and Waldman, 2014). Except East Asian countries have lower rates of crime (Rushton, 1995; Rushton and Whytney, 2002). Though, Japan’s low crime rate is relatively recent, and when compared with other countries on certain measures “Japan fares the same or worse when compared to other nations” (Barberet 2009, 198). This goes against a lot of HBD theory, and I will save that for another day. (Japan has a 99 percent prosecution rate, which could be due to low prosecutorial budgets; Ramseyer and Rasmusen, 2001. I will cover this in the future.)
The media fervor—as usual—gave the MAOA gene the nickname “the warrior gene“, which is extremely simplistic (I will have much more to say on ‘genes for’ any trait towards the end of the article). I will show how this is a very simplistic view.
The MAOA gene was first discovered in 1993 in a Dutch family who had a history of extreme violence going as far back as the 1890s. Since the discovery of this gene, it has been invoked as an ultimate cause of crime. However, as some hereditarians do note, MAOA only ’causes’ violence if one has a specific MAOA genotype and if they have been abused as a child (Caspi et al, 2002; Cohen et al, 2006; Beaver et al, 2009; Ferguson et al, 2011; Cicchetti, Rogosch, Thibodeau, 2012;). People have invoked these gene variants as ultimate causes of crime—that is, people who have the low-expressing MAOA variants are more likely to commit more crime—but the relationship is not so simple.
Maoris are more four times more likely to have the low-expressing gene variant than Europeans, the same holding for African Americans and Europeans (Lea and Chambers, 2007).
There is, however, a protective effect that protects whites (and not non-whites in certain cases) against antisocial behavior/violent attitudes if one has a certain genotype (Widom and Brzustowicz, 2006), though the authors write on page 688: “For non-whites, the effect of child abuse and neglect on the juvenile VASB was not significant (beta .08, SE .11, t 1.19, ns), whereas the effect of child maltreatment on lifetime VASB composite approached significance (beta .13, SE .12, t 1.86, p .06). For non-whites (see Figure 2), neither gene (MAOA) environment (child abuse and neglect) interaction was significant: juvenile VASB (beta .06, SE .28, t .67, ns) and lifetime VASB (beta .01, SE .29, t .14, ns).” So as you can see, there are mixed results. Whites seem to be protected against the effect of antisocial behavior and violence but only if they have a certain genotype (which implies that if they have the other genotype, then if abused they will show violent and antisocial behavior). So, we can see that the relationship between MAOA and criminal behavior is not as simple as some would make it out to be.
MAOA, like other genetic variants, of course, has been linked to numerous other traits. Steven J. Heine, author of the book DNA is Not Destiny: The Remarkable and Completely Misunderstood Relationship Between You and Your Genes:
However, any labels like “the warrior gene” are highly problematic because they suggest that the this gene is specifically associated with violence. It’s not, just as alleles from other genes do not only have one outcome. Pleiotropy is the term for how a single genetic variant can influence multiple different phenotypes. MAOA is highly pleiotropic: the traits and conditions potientially connected to the MAOA gene invlude Alzheimer’s. anoerxia, autism, body mass index, bone mineral density, chronic fatigue syndrome, depression, extraversion, hypertension, individualism, insomnia, intelligence, memory, neuroticism, obesity, openness to experience, persistence, restless leg syndrome, schizophrenia, social phobia, sudden infant death syndrome, time perception and voting behavior. (59) Perhaps it would be more fitting to call MAOA “the everything but the kitchen sink gene. (Heine, 2017: 195)
Something that I have not seen brought up when discussions of race, crime, and MAOA come up is that Japanese people have the highest chance—even higher than blacks, Maoris, and whites—to have the low repeat MAOA variant (Way and Lieberman) yet have lower rates of crime. So MAOA cannot possibly be a ‘main cause’ of crime. It is way more complex than that. “However intuitively satisfying it may be to explain cultural differences in violence in terms of genes“, Heine writes, “as of yet there is no direct evidence for this” (Heine, 2017: 196).
Numerous people have used ‘their genes’ in an attempt to get out of criminal acts that they have committed. A judge even knocked off one year off of a murder’s sentence since he found the evidence for the MAOA gene’s link to violence “particularly compelling.” I find it “particularly ridiculous” that the man got less time in jail than someone who ‘had a choice’ in his actions to murder someone. Doesn’t it seem ridiculous to you that someone gets less time in jail than someone else, all because he may have the ‘crime/warrior gene’?
Aspinwall, Brown, and Tabery (2012) showed that when evidence of a ‘biomechanic’ cause of violence/psychopathy was shown to the judges (n=191), that they reduced their sentences by almost one year if they were reading a story in which the accused was found to have the low-repeat MAOA allele (13.93 to 12.83 years). So, as you can see, this can sway judges’ perception into giving one a lighter sentence since they believe that the evidence shows that one ‘can not control themselves’, which results in the judge giving assailants lighter sentences because ‘it’s in their genes’.
Further, people would be more lenient on sentences for criminals who are found to have these ‘criminal genes’ than those who were found to not have them (Cheung and Heine, 2015). Monterosso, Royzman, and Schwartz (2010) also write: “Physiologically explained behavior was more likely to be characterized as “automatic,” and willpower and character were less likely to be cited as relevant to the behavior. Physiological explanations of undesirable behavior may mitigate blame by inviting nonteleological causal attributions.” So, clearly, most college students would give a lighter sentence if the individual in question were found to have ‘criminal genes’. But, if these genes really did ’cause’ crime, shouldn’t they be given heavier sentences to keep them on the inside more so those with the ‘non-criminal genes’ don’t have to suffer from the ‘genetically induced’ crime?
Heine (2017: 198-199) also writes:
But is someone really less any responsible for their actions if his or her genes are implicated? A problem with this argument is that we would be hard-pressed to find any actions that we engage in where our genes are not involved—our behaviors do not occur in any gene-free zones. Or, consider this: there actually is a particular genetic variant that, if you possess it, makes you about 40 times more likely to engage in same-sex homicides than those who possess a different variant. (66) It’s known as the Y chromosome—that is, people who possess it are biologically male. Given this, should we infer that Y chromosomes cause murders, and thus give a reduced sentence to anyone who is the carrier of such a chromosome because he is really not responsible for his actions? The philosopher Stephen Morse calls the tendency to excuse a crime because of a biological basis the “fundamental psycholegal error.” (67) The problem with this tendency is that it involves separating yout genes from yourself. Saying “my genes made me do it” doesn’t make sense because there is no “I” that is independent of your genetic makeup. But curiously, once genes are implicaed, people see, to feel that the accused is no longer fully in control of his or her actions.
Further, in the case of a child pornographer, one named Gary Cossey, the court said:
The court predicted that some fifty years from now Cossey’s offense conduct would likely be discovered to be caused by “a gene you were born with. And it’s not a gene you can get rid of.” The court expressed its belief that although Cossey was in therapy, it “can only lead, in my view, to a sincere effort on your part to control, but you can’t get rid of it. You are what you’re born with. And that’s the only explanation for what I see here.”
However, this judge punished Cossey more severely due to the ‘possibility’ that scientists may find ‘genes for’ child pornography use in 50 years. Cossey was then given another, unbiased judge, and was given a ‘more lenient’ sentence than the genetic determinist judge did.
Sean Last over at The Alternative Hypothesis is also a big believer in this so-called MAOA-race difference that explains racial differences in crime. However, as reviewed above (and as he writes), MAOA can be called the “everything but the kitchen sink gene” (Heine, 2017: 195), as I will touch on briefly below, to attribute ’causes’ to genes is not the right way to look at them. It’s not so easy to say that since one ‘has the warrior gene’ that they’d automatically be violent. Last cites a study saying that even those who have the MAOA allele who were not abused showed higher rates of violent behavior (Ficks and Waldman, 2014). They write (pg. 429):
The frequency of the ‘‘risk’’ allele in nonclinical samples of European ancestry ranges from 0.3 to 0.4, although the frequency of this allele in individuals of Asian and African ancestry appears to be substantially higher (*0.6 in both groups; Sabol et al. 1998).
So, why don’t Asians have higher rates of crime—along with blacks—if MAOA on its own causes violent and antisocial behavior? Next I know that someone would claim that “AHA! TESTOSTERONE ALSO MEDIATES THIS RELATIONSHIP!!” However, as I’ve talked about countless times (until I’m blue in the face), blacks do not have/have lower levels of testosterone than whites (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Hu et al, 2014; Richard et al, 2014). Though young black males have higher levels of testosterone due to the environment (honor culture) (Mazur, 2016). So that canard cannot be trotted out.
All in all, these simplistic and reductionist approaches to ‘figuring out’ the ’causes’ of crime do not make any sense. To point at one gene and say that this is ‘the cause’ of that do not make sense.
One last point on ‘genes as causes’ for behavior. This is something that deserves a piece of its own, but I will just provide a quote from Eva Jablonska and Marion Lamb’s book Evolution in Four Dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life (Jablonska and Lamb, 2014: 17; read chapter one of the book here; I have the nook version so the page number may be different):
Although many psychiatrists, biochemists, and other scientists who are not geneticists (yet express themselves with remarkable facility on genetic issues) still use the language of genes as simple causal agents, and promise their audience rapid solutions to all sorts of problems, they are no more than propagandists whose knowledge or motives must be suspect. The geneticists themselves now think and talk (most of the time) in terms of genetic networks composed of tens or hundreds of genes and gene products, which interact with each other and together affect the development of a particular trait. They recognize that whether or not a trait (a sexual preference, for example) develops does not depend, in the majority of cases, on a difference in a single gene. It involves interactions among many genes, many proteins and other types of molecule, and the environment in which an individual develops.
So to say that those who have low-functioning MAOA variants have an ‘excuse’ as to why they commit crime is incorrect. I know that most people know this, but when you read some people’s writings on things like this it’s like they think that these singular genes/polymorphisms/etc cause these things on their own. In actuality, you need to look at how the whole system interacts with these things, and not reduce whole complex physiological systems to a sum of its parts. This is why implicating singular genes/polymorphisms as explanations for racial differences in crime does not make sense (as can be seen with the Japanese example).
To reduce behaviors simply to gene X and not look at the whole system does not make any sense. There are no ‘genes for’ anything, except a few Mendelian diseases (Ropers, 2010). Stating that certain genes ’cause’ X, as I have shown does not make sense and, wrongly, in my opinion, gives criminals less of a sentencing since judges find stuff like this ‘very compelling’. If that’s the case, why implicate any murderer? ‘Their genes made them do it’, right? Though, things are not that simple to implicate one gene as a cause for crime or any other complex behavior; in this sense—like for most things to do with the human body—holism makes way more sense and not reductionism. We need to look at how these genes that are ‘implicated’ in criminal behavior interact with the whole system. Only then can we understand the causes of criminal behavior. Looking at singular genes impedes us from figuring out the true underlying reasons why people commit crime.
Remember: we can’t blame “warrior genes” for violent crime. If someone does have a ‘genetic predisposition to crime’ from the MAOA gene, then wouldn’t it make more sense to give them more time? Though, the relationship is not so simple as I have covered. So to close, there is no ‘simple relationship’ between race, crime and MAOA. Not in the way that other hereditarians would like you to believe. Because if this relationship were so simple, then East Asians (Chinese, Japanese) would have the highest rates of crime, and they do not.
I came across this video on YouTube last night by a geneticist/science writer Steve Jones. He is also the Emeritus Professor of genetics at University College London. This makes what he says in the video I will speak about below very troubling—especially to a man of his caliber with the knowledge he has—views he has on the hormone.
In the very beginning of the video titled Testosterone and Crime: What Can Genes Tell Us About Behavior?, Jones says “But in fact, there are genes—there is a gene—for crime, which causes nearly all the crime, and is widely used and we understand a great deal about it. It’s a chemical gene it produces a particular chemical, which we understand in detail is the chemical testosterone. Testosterone—we all have it but some of us have rather more than others—testosterone is of course a gene that is made—switched on by the Y chromosome and makes males male. Women have a small amount but only a small amount and as they get older … Now testosterone is a dangerous, dangerous thing to have. I don’t recommend it, those of you who have it, don’t get it. And if you’ve got some, don’t get any more.” What bullshit! This guy is a literal genetics Ph.D. saying this; this is proof that knowledge/educational attainment does not stop you from saying dumb, untrue things.
“I don’t know that this character does it, but certainly plenty of bodybuilders inject steroids—testosterone—into themselves. They damage themselves severely. Their life expectancy goes down strikingly. They die for all those male reasons. They die from violence, they die from suicide, they die from car accidents, they die from heart disease, all those things are true of males. … But even if you look at males and females in general, there is kind of a depressing picture for half of the room, I’m not sure which half.” Jones then talks about how men die at a much higher rate than women for a slew of reasons. This is his logic: Men have higher testosterone than women. Testosterone is shown to cause violence, aggression, heart disease, risk-taking, etc. Men have way more testosterone than women. Therefore testosterone is the reason why men die more than women and commit more violence than women. This is horrible logic—coming from a geneticist no less!
“Men actually—less expectedly perhaps—are much less good at dealing with parasites and infectious disease than women are. And that’s because testosterone—the male hormone—suppresses the immune system. Now the immune system fights off the parasites and we don’t do nearly as well.” There is actually some empirical data for his argument here. Back in 2013, it was shown that testosterone, gene expression, and the immune system were linked. They discovered that higher levels of testosterone prevented Module 52 genes from turning on. So higher levels of testosterone result in more Module 52 expression. Testosterone also does exert immune-suppressing effects, “increasing the severity of malaria, leishmaniasis, amebiasis, and tuberculosis, while at the same time supporting the clearance of toxoplasmosis (Bernin & Lotter, 2014; Nhamoyebonde & Leslie, 2014)” (Giefing-Kroll et al, 2015). The suppressive effects of testosterone on the immune system and how down-regulates “the systemic immune response by cell type specific effects in the context of immunological disorders.” (Trigunaite, Dimo, and Jorgensen, 2015).
The effects of testosterone replacement therapy (TRT) on the immune system have not been looked into, but it has a positive effect on elderly men (Osterberg, Bernie, and Ramasamy, 2014). However, Braude, Tang-Martinez, and Taylor (1999) challenge the wisdom that testosterone is an immuno-depressor. This is Jones’ only claim that is not outright wrong; there is data out there for both positions (of course I think that Braude, Tang-Martinez and Taylor, 1999 drive a solid argument against the testosterone-causes-immuno-suppression hypothesis).
The Jones says one of the dumbest things I’ve ever heard “And men, of course, are murdered much more than women. And who murders them—of course—other men. … Men murder at a much higher rate than women. … And that effect is striking—that effect is true worldwide—all over the world men, testosterone, murder at 10 times the rate of women. … So it’s a universal, it’s a biological universal, it’s clearly due to testosterone. There’s no question. The evidence is absolutely clear. So it’s a genetic phenomenon, it’s a gene for crime.” Should I be nice here and assume that whatever ‘gene’ he’s proposing that ’causes’ testosterone production actually causes the crime? Or should I take what he said at face value—that testosterone is a literal gene that causes crime? I think I’ll go with the second one.
“It’s certainly genetic, it’s also environmental. And you can’t disentangle it. You can change part of it—the environment—you can’t change the other part—the genes. And I always find it kind of odd that the public is so interested in the bit you can’t change—the genes—and is so uninterested in the bit you can—the environment.” This is wrong. Not all of it, but most of it. I don’t think that people are more interested in genes and toss aside environment—especially for testosterone. Because, as I documented yesterday, hereditarians assume that since testosterone has a heritability of around .6 then it must be mostly genetic in nature. This is wrong. As Jones said, the environment effects testosterone production too (though he didn’t go into the mechanisms).
The Left goes to the environment side—change the environment, change hormone production (this is true)—whereas the Right goes to the genes side—can’t change genes and environment is a product of genes so nothing can be done. (Oversimplified, don’t crucify me.) Both are wrong. Strong genetic determinism (gene G almost always leads to the development of trait T. (G increases the probability of T and the probability of T, given G, is 95% or greater) doesn’t make sense because a large majority of traits are moderately or weakly determined by genetics (Resnick and Vorhaus, 2006).
In sum, Jones is clueless about testosterone. He only really said one thing that is not outright wrong (but it is questionable). It doesn’t cause crime, it doesn’t cause men to murder more. The press has gotten all of these views into people’s heads because they want to demonize men—and the hormone that is largely responsible for male-ness. It’s incredible that this guy is both a geneticist, science writer and professor of genetics and still calls testosterone a ‘gene’ saying that it is responsible for ‘most of the crime’ committed. Anyone who has been reading this blog for the past year or so since I have began revising many of my main views knows how wrong this is. People really need to get a clue on testosterone and stop spreading bullshit. I know that I’ll have to keep correcting misconceptions on testosterone for a good long time (like with r/K theory) but I enjoy writing about both things so it’s not too big a deal. I just wish people would actually educated themselves on basic physiology so that the trainwreck of a video that Jones made does not get made.
No, Black Women Do Not Have Higher Testosterone than White Women (And More On Hereditarian Claims on Racial Testosterone Differences)
It has been over a year since I wrote the article Black Women and Testosterone, and I really regret it. Yes, I did believe that black women had higher levels of testosterone than white women due to one flimsy study and another article on pregnant black women. I then wised up to the truth about testosterone and aggression/crime/race/sex and revised the articles (like I have done with r/K selection theory). However, after I revised my views on the supposed differences in testosterone between black men/white men and black women/white women, people still cite the article, disregarding the disclaimer at the top of the article. I quoted Mazur (2016), who writes (emphasis mine):
The pattern [high testosterone] is not seen among teenage boys or among females.
There is no indication of inordinately high T among young black women with low education.
Honor cultures are cast as male affairs, but with T data in hand for both sexes, it is worth exploring whether or not a similar pattern exists among women. Mean T was calculated as a function of age for the four combinations of race and education used in Table 1 but now for women. All plots show T declining with age, from about 35 ng/dL in the 20–29 age group to about 20 ng/dL among women 60 years and older. The four plots essentially overlap without discernible differences among them. Given the high skew of T among adult females, both raw and ln-transformed values were analyzed with similar results. There is no indication of inordinately high T among young black women with low education.
In the present study, at least, the sexes differ because the very high T seen among young black men with low education does not occur among young black women with low education.
This is very clear… Mazur (2016) analyzed the NHANES 2011-2012 data and this is what he found. I understand that most HBD bloggers do believe this, well, like a lot of their strong assertions (which I have rebutted myself), they’re wrong. They don’t get it. They do not understand the hormone.
The reason why I’m finally writing this (which is long overdue) is that I saw a referral from this website today: https://www.minds.com/RedPillTV who writes about the aforementioned black women and testosterone article:
It is known that blacks have the highest levels of testosterone out of the major races of humanity. However, what’s not known is that black women have higher rates than white women. The same evolutionary factors that make it possible for black men to have high testosterone make it possible for women as well.
…..No. It seems that people just scroll on by the disclaimer at the top that is bolded and italicized and just go to the (now defunct) article and attempt to prove their assertion that black women have higher testosterone than white women with an article that I have stated myself I no longer believe and have provided the rationale/data for the position. This shows that people have their own biases and no matter what the author writes about their views that have changed due to good arguments/data, they will still attempt to use the article to prove their assertion.
I’ve written at length that testosterone does not cause 1) aggression, 2) crime and 3) prostate cancer. People are scared of testosterone mostly due to the media fervor of any story that may have a hint of ‘toxic masculinity’. They (most alt-righters) are scared of it because of Lynn/Rushton/Templer/Kanazawa bullshit on the hormone. Richard Lynn doesn’t know what he’s talking about on testosterone. No, Europeans did not need lower levels of aggression in the cold; Africans didn’t need higher levels of aggression (relative to Europeans) to survive in the tropics. The theory that supposed differential testosterone differences between the races are “the physiological basis in males of the racial differences in sexual drive which form the core of the different r/K reproduction strategies documented by J.P. Rushton” (Lynn, 1990: 1203). The races, on average, do not differ in testosterone as I have extensively documented. So hereditarians like Lynn and others need to look for other reasons to explain blacks’ higher rate of sexual activity.
Rushton’s views on the testosterone and supposed r/K continuum have been summarily rebutted by me. These psychologists’ views on the hormone (that they don’t understand the production of nor do they understand the true reality of the differences between the races) are why people are afraid of testosterone. No, testosterone is not some ‘master switch’ as Rushton (1999) asserts. Rushton asserts that racial differences in temperament are mediated by the hormone testosterone. He further dives into this assertion stating “Testosterone level correlates with temperament, self-concept, aggression, altruism, crime, and sexuality, in women as well as in men (Harris, Rushton, Hampson, & Jackson, 1996). It may ‘correlate’ with aggression and crime, but as I have documented, they do not cause either.
The aggression/testosterone correlation is only .08 (Archer, Graham-Kevan, and Davies, 2005). Furthermore, the diurnal variation in testosterone does not directly correlate to when testosterone levels are highest in the day (at 8 am and drop thereafter), with adults peaking in crime at 10 pm and kids at 3 pm, with rises at 8 pm and 12 pm (not surprisingly, kids go in to school around 8 am, go to recess at 12 and leave at 3).
If you’ve read as much Rushton as I have, you’ll notice that he begins to sound like a broken record when talking about certain things. One of the most telling is Rushton’s repeated assertions that blacks average 3-19 percent higher testosterone than whites. The 3 percent number comes from Ellis and Nyborg (1992) and the 19 percent number comes from Ross et al (1986) (which Rushton should know that after adjustments for confounding, it decreased to 13 percent). These are the only studies that hereditarians ever cite for these claims that blacks average higher testosterone than whites. That seems a bit fishy to me. Cite a 30-year-old study along with a 25-year-old study (with such huge variation from Rushton and those who cite him for this matter—3-19 percent!!) as ‘proof’ that blacks average such higher levels of testosterone in comparison to whites.
Ross et al (1986) is one of the most important studies to rebut for this hereditarian claim that testosterone causes all of these maladies in black American populations. Ross et al (1986) propose that higher levels of the hormone lead to the higher rates of prostate cancer in black American populations. However, meta-analyses do not show this (Zagars et al, 1998; Sridhar et al, 2010).
Rushton et al’s assertions—largely—lie on this supposed testosterone difference between the races and how it supposedly leads to higher rates of crime, prostate cancer, aggression, and violence. However, the truth of the matter is, this is all just hereditarian bullshit. Larger analyses—as I have extensively documented—do not show this trend. And even accepting the claim that blacks have, say, 19 percent higher levels of testosterone than whites, it still would not explain the supposed prostate cancer rates between the races (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even if blacks had 19 percent higher testosterone than whites, it would not explain higher levels of crime nor aggression due to such a hilariously low correlation of .08 (Archer, Graham-Kevan, and Davies, 2005).
Finally, I have a few words for Michael Hart and his (albeit sparse) claims on testosterone in his 2007 book Understanding Human History.
Hart (2007) writes:
(Many of these differences in sexual behavior may be a consequence of the fact that
blacks, on average, have higher levels of testosterone than whites.7) (pg. 127)
And….. footnote number 7 is…. surprisingly (not): 7) Ross, R., et al. (1986). Not going to waste my time on this one, again. I’ve pointed out numerous flaws in the study. (I will eventually review the whole thing.)
It seems unlikely, though, that the higher testosterone level in blacks — which is largely genetic in origin — has no effect on their sexual behavior (pg. 128; emphasis mine)
This is bullshit. People see the moderately high heritability of testosterone (.60; Harris, Vernon, and Boomsma, 1998) and jump right to the “It’s genetics!!!” canard without even understanding its production in the body (it is a cholesterol-based hormone which is indirectly controlled by DNA, there are no ‘genes for’ testosterone). Here are the steps: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone
I have documented numerous lines of evidence showing that testosterone is extremely sensitive to environmental factors (Mazur and Booth, 1998; Mazur, 2016), and due to the homeodynamic physiology we have acquired due to ever-changing environments (Richardson, 2017), this allows our hormones to up- or down-regulate depending on what occurs in the environment. The quote from Hart is bullshit; he doesn’t know what he’s talking about.
For females in Siberia, the disadvantages of failing to find a man who would
provide for her and her children during their childhood were much greater than they were in tropical climates, and females who were not careful to do so were much less likely to pass on their genes. Furthermore, because females in harsh climates were so demanding on this point, males who seemed unlikely to provide the needed assistance found it hard to find mates. In other words, there was a marked sexual selection against such males. Such selection could result, for example, in the peoples living in northerly climates gradually evolving lower levels of testosterone than the peoples living in subSaharan Africa. (pg. 131)
This is a bullshit just-so story. Africans in Africa have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006).
Note also that a difference in testosterone level frequently affects not
only the sexual behavior of a young male, but also his aggressiveness.
No it does not (Archer, Graham-Kevan, and Davies, 2005).
Thankfully, that’s all he wrote about testosterone. There is so much bullshit out there. Though, people who like and seek out the truth will learn that there are no racial differences and that testosterone does not cause crime/aggression/prostate cancer and that it’s just hereditarian bullshit.
The evidence I have amassed and the arguments I have given point to a few things: 1) the races do not differ in testosterone/there is a small negligible difference; 2) testosterone does not cause crime; 3) testosterone does not cause aggression; 4) black women do not have higher levels of testosterone than white women; 5) high levels of testosterone do not cause prostate cancer; and 6) even allowing a 19 percent black/white difference will not have hereditarian claims hold true.
So for anyone who comes across my old articles on testosterone and sex/race, do a bit more reading of my newer material here to see my new viewpoints/arguments. DO NOT cite these articles as proof for your claims of higher levels of black men/women. DO cite the old articles ALONG WITH the new ones to show how and why my views changed along with the studies I have cited that changed my view. (Actually understanding the production of testosterone in the body was a huge factor too, which I talk about in Why Testosterone Does Not Cause Crime.)
I enjoy reading what other bloggers write about testosterone and its supposed link to crime, aggression, and prostate cancer; I used to believe some of the things they did, since I didn’t have a good understanding of the hormone nor its production in the body. However, once you understand how its produced in the body, then what others say about it will seem like bullshit—because it is. I’ve recently read a few articles on testosterone from the HBD-blog-o-sphere and, of course, they have a lot of misconceptions in them—some even using studies I have used myself on this blog to prove my point that testosterone does not cause crime!! Now, I know that most people don’t read studies that are linked, so they would take what it says on face value because, why not, there’s a cite so what he’s saying must be true, right? Wrong. I will begin with reviewing an article by someone at The Alternative Hypothesis and then review one article from Robert Lindsay on testosterone.
The Alternative Hypothesis
Faulk has great stuff here, but the one who wrote this article, Testosterone, Race, and Crime, 1) doesn’t know what he’s talking about and 2) clearly didn’t read the papers he cited. Read this article, you’ll see him make bold claims using studies I have used for my own arguments that testosterone doesn’t cause crime! Let’s take a look.
One factor which explains part of why Blacks have higher than average crime rates is testosterone. Testosterone is known to cause aggression, and Blacks are known to at once have more of it and, for genetic reasons, to be more sensitive to its effects.
- No it doesn’t.
- “Testosterone is known to cause aggression“, but that’s the thing: it’s only known that it ’causes’ aggression, it really doesn’t.
- Evidence is mixed on blacks being “… for genetic reasons … more sensitive to its effects” (Update on Androgen Receptor gene—Race/History/Evolution Notes).
Testosterone activity has been linked many times to aggression and crime. Meta-analyses show that testosterone is correlated with aggression among humans and non human animals (Book, Starzyk, and Quinsey, 2001).
Why doesn’t he say what the correlation is? It’s .14 and this study, while Archer, Graham-Kevan and Davies, (2005) reanalyzed the studies used in the previous analysis and found the correlation to be .08. This is a dishonest statement.
Women who suffer from a disease known as congenital adrenal hyperplasia are exposed to abnormally high amounts of testosterone and are abnormally aggressive.
Abnormal levels of androgens in the womb for girls with CAH are associated with aggression, while boys with and without CAH are similar in aggression/activity level (Pasterski et al, 2008), yet black women, for instance, don’t have higher levels of testosterone than white women (Mazur, 2016). CAH is just girls showing masculinized behavior; testosterone doesn’t cause the aggression (See Archer, Graham-Kevan and Davies, 2005)
Actually, no. Supraphysiological levels of testosterone administered to men (200 and 600 mg weekly) did not increase aggression or anger (Batrinos, 2012).
Finally, people in prison have higher than average rates of testosterone (Dabbs et al., 2005).
Dabbs et al don’t untangle correlation from causation. Environmental factors can explain higher testosterone levels (Mazur, 2016) in inmates, and even then, some studies show socially dominant and aggressive men have the same levels of testosterone (Ehrenkraz, Bliss, and Sheard, 1974).
Thus, testosterone seems to cause both aggression and crime.
No, it doesn’t.
Furthermore, of the studies I could find on testosterone in Africans, they have lower levels than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006) so, along with the studies and articles cited on testosterone, aggression, and crime, that’s another huge blow to the testosterone/crime/aggression hypothesis.
Richard et al. (2014) meta-analyzed data from 14 separate studies and found that Blacks have higher levels of free floating testosterone in their blood than Whites do.
They showed that blacks had 2.5 to 4.9 percent higher testosterone than whites, which could not explain the higher prostate cancer incidence (which meta-analyses call in to question; Sridhar et al 2010; Zagars et al 1998). That moderate amount would not be enough to cause differences in aggression either.
Exacerbating this problem even further is the fact that Blacks are more likely than Whites to have low repeat versions of the androgen receptor gene. The androgen reception (AR) gene codes for a receptor by the same name which reacts to androgenic hormones such as testosterone. This receptor is a key part of the mechanism by which testosterone has its effects throughout the body and brain.
The rest of the article talks about CAG repeats and aggressive/criminal behavior, but it seems that whites have fewer CAG repeats than blacks.
This one is much more basic, and tiring to rebut but I’ll do it anyway. Lindsay has a whole slew of articles on testosterone on his blog that show he doesn’t understand the hormone, but I’ll just talk about this one for now: Black Males and Testosterone: Evolution and Perspectives.
It was also confirmed by a recent British study (prostate cancer rates are somewhat lower in Black British men because a higher proportion of them have one White parent)
Jones and Chinegwundoh (2014) write: “Caution should be taken prior to the interpretation of these results due to a paucity of research in this area, limited accurate ethnicity data, and lack of age-specific standardisation for comparison. Cultural attitudes towards prostate cancer and health care in general may have a significant impact on these figures, combined with other clinico-pathological associations.”
This finding suggests that the factor(s) responsible for the difference in rates occurs, or first occurs, early in life. Black males are exposed to higher testosterone levels from the very start.
In a study of women in early pregnancy, Ross found that testosterone levels were 50% higher in Black women than in White women (MacIntosh 1997).
I used to believe this, but it’s much more nuanced than that. Black women don’t have higher levels of testosterone than white women (Mazur, 2016; and even then Lindsay fails to point out that this was pregnant women).
According to Ross, his findings are “very consistent with the role of androgens in prostate carcinogenesis and in explaining the racial/ethnic variations in risk” (MacIntosh 1997).
Testosterone has been hypothesized to play a role in the etiology of prostate cancer, because testosterone and its metabolite, dihydrotestosterone, are the principal trophic hormones that regulate growth and function of epithelial prostate tissue.
Testosterone doesn’t cause prostate cancer (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Diet explains any risk that may be there (Hayes et al, 1999; Gupta et al, 2009; Kheirandish and Chinegwundoh, 2011; Williams et al, 2012; Gathirua-Mingwai and Zhang, 2014). However in a small population-based study on blacks and whites from South Carolina, Sanderson et al (2017) “did not find marked differences in lifestyle factors associated with prostate cancer by race.”
Regular exercise, however, can decrease PCa incidence in black men (Moore et al, 2010). A lot of differences can be—albeit, not too largely— ameliorated by environmental interventions such as dieting and exercising.
Many studies have shown that young Black men have higher testosterone than young White men (Ellis & Nyborg 1992; Ross et al. 1992; Tsai et al. 2006).
Ellis and Nyborg (1992) found 3 percent difference. Ross et al (1992) have the same problem as Ross et al (1986), which used University students (~50) for their sample. They’re not representative of the population. Ross et al (1992) also write:
Samples were also collected between 1000 h and 1500 h to avoid confounding
by any diurnal variation in testosterone concentrations.
Testosterone levels should be measured near to 8 am. This has the same time variation too, so I don’t take this study seriously due to that confound. Assays were collected “between” the hours of 10 am and 3 pm, which means it was whenever convenient for the student. No controls on activities, nor attempting to assay at 8 am. People of any racial group could have gone at whatever time in that 5 hour time period and skew the results. Assaying “between” those times completely defeats the purpose of the study.
This advantage [the so-called testosterone advantage] then shrinks and eventually disappears at some point during the 30s (Gapstur et al., 2002).
This makes it very difficult if not impossible to explain differing behavioral variables, including higher rates of crime and aggression, in Black males over the age of 33 on the basis of elevated testosterone levels.
See above where I talk about crime/testosterone/aggression.
Critics say that more recent studies done since the early 2000’s have shown no differences between Black and White testosterone levels. Perhaps they are referring to recent studies that show lower testosterone levels in adult Blacks than in adult Whites. This was the conclusion of one recent study (Alvergne et al. 2009) which found lower T levels in Senegalese men than in Western men. But these Senegalese men were 38.3 years old on average.
Alvergne, Fauri, and Raymond (2009) show that the differences are due to environmental factors:
This study investigated the relationship between mens’ salivary T and the trade-off between mating and parenting efforts in a polygynous population of agriculturists from rural Senegal. The men’s reproductive trade-offs were evaluated by recording (1) their pair-bonding/fatherhood status and (2) their behavioral profile in the allocation of parental care and their marital status (i.e. monogamously married; polygynously married).
They also controlled for age, so his statement “But these Senegalese men were 38.3 years old on average” is useless.
These critics may also be referring to various studies by Sabine Rohrmann which show no significance difference in T levels between Black and White Americans. Age is poorly controlled for in her studies.
That is one study out of many that I reference. Rohrmann et al (2007) controlled for age. I like how he literally only says “age is poorly controlled for in her studies“, because she did control for age.
That study found that more than 25% of the samples for adults between 30 and 39 years were positive for HSV-2. It is likely that those positive samples had been set aside, thus depleting the serum bank of male donors who were not only more polygamous but also more likely to have high T levels. This sample bias was probably worse for African American participants than for Euro-American participants.
Why would they use diseased samples? Do you even think?
Young Black males have higher levels of active testosterone than European and Asian males. Asian levels are about the same as Whites, but a study in Japan with young Japanese men suggested that the Japanese had lower activity of 5-alpha reductase than did U.S. Whites and Blacks (Ross et al 1992). This enzyme metabolizes testosterone into dihydrotestosterone, or DHT, which is at least eight to 10 times more potent than testosterone. So effectively, Asians have the lower testosterone levels than Blacks and Whites. In addition, androgen receptor sensitivity is highest in Black men, intermediate in Whites and lowest in Asians.
Ethnicmuse also showed that, contrary to popular belief, Asians have higher levels of testosterone than Africans who have higher levels of testosterone than Caucasians in his meta-analysis. (Here is his data.)
Let us look at one study (Ross et al 1986) to see what the findings of a typical study looking for testosterone differences between races shows us. This study gives the results of assays of circulating steroid hormone levels in white and black college students in Los Angeles, CA. Mean testosterone levels in Blacks were 19% higher than in Whites, and free testosterone levels were 21% higher. Both these differences were statistically significant.
Assay times between 10 am and 3 pm, unrepresentative sample of college men, didn’t have control for waist circumference. Horribly study.
A 15% difference in circulating testosterone levels could readily explain a twofold difference in prostate cancer risk.
No, it wouldn’t (if it were true).
Higher testosterone levels are linked to violent behavior.
Causation not untangled.
Studies suggest that high testosterone lowers IQ (Ostatnikova et al 2007). Other findings suggest that increased androgen receptor sensitivity and higher sperm counts (markers for increased testosterone) are negatively correlated with intelligence when measured by speed of neuronal transmission and hence general intelligence (g) in a trade-off fashion (Manning 2007).
Who cares about correlations? Causes matter more. High testosterone doesn’t lower IQ. Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut.
Racial differences in testosterone don’t exist/are extremely small in magnitude (as I’ve covered countless times). The one article from TAH literally misrepresents studies/leaves out important figures in the testosterone differences between the two races to push a certain agenda. Though if you read the studies you see something completely different. It’s the same with Lindsay. He misunderstood a few studies to push his agenda about testosterone and crime and prostate cancer. They’re both wrong, though.
Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut. People read and write about things they don’t understand, which is the cause of these misconceptions with the hormone, as well as, of course, misinterpreting studies. Learn about the hormone and you won’t fear it. It doesn’t cause crime, prostate cancer nor aggression; these people who write these articles have one idea in their head and they just go for it. They don’t understand the intricacies of the endocrine system and how sensitive it is to environmental influence. I will cover more articles that others have written on testosterone and aggression to point out what they got wrong.
A commenter by the name of bbloggz alerted me to a new paper by Lee Ellis published this year titled Race/ethnicity and criminal behavior: Neurohormonal influences in which Ellis (2017) proposed his theory of ENA (evolutionary neuroandrogenic theory) and applied it to racial/ethnic differences in crime. On the face, his theory is solid and it has great explanatory power for the differences in crime rates between men and women, however, there are numerous holes in the application of the theory in regards to racial/ethnic differences in crime.
In part I, he talks about racial differences in crime. No one denies that, so on to part II.
In part II he talks about environmental causes for the racial discrepancies, that include economic racial disparities, racism and societal discrimination and subordination, a subculture of violence (I’ve been entertaining the honor culture hypothesis for a few months; Mazur (2016) drives a hard argument showing that similarly aged blacks with some college had lower levels of testosterone than blacks with less than high school education which fits the hypothesis of honor culture. Though Ellis’ ENA theory may account for this, I will address this below). However, if the environment that increases testosterone is ameliorated (i.e., honor culture environments), then there should be a subsequent decrease in testosterone and crime, although I do believe that testosterone has an extremely weak association with crime, nowhere near high enough to account for racial differences in crime, the culture of honor could explain a good amount of the crime gap between blacks and whites.
Ellis also speaks about the general stress/strain explanation, stating that blacks have higher rates of self-esteem and Asians the lowest, with that mirroring their crime rates. This could be seen as yet another case for the culture of honor in that blacks with a high self-esteem would feel the need to protect their ‘name’ or whatever the case may be and feel the need for physical altercation based on their culture.
In part III, Ellis then describes his ENA theory, which I don’t disagree with on its face as it’s a great theory with good explanatory power but there are some pretty large holes that he rightly addresses. He states that, as I have argued in the past, females selected men for higher rates of testosterone and that high rates of testosterone masculinize the brain, changing it from its ‘default feminine state’ and that the more androgens the brain is exposed to, the more likely it is for that individual to commit crime.
Ellis cites a study by Goodpaster et al (2006) in which he measured the races on the isokinetic dynamometry, pretty much a leg extension. However, one huge confound is that participants who did not return for follow-up were more likely to be black, obese and had more chronic disease (something that I have noted before in an article on racial grip strength). I really hate these study designs, but alas, it’s the best we have to go off of and there are a lot of holes in them that must be addressed. Though I applaud the researchers’ use of the DXA scan (regular readers may recall my criticisms on using calipers to assess body fat in the bench press study, which was highly flawed itself; Boyce et al, 2014) to assess body fat as it is the gold standard in the field.
Ellis (2017: 40) writes: “as brain exposure to testosterone surges at puberty, the prenatally-programmed motivation to strive for resources, status, and mating opportunities will begin to fully activate.” This is true on the face, however as I have noted the correlation between physical aggression and testosterone although positive is low at .14 (Archer, 1991; Book et al, 2001). Testosterone, as I have extensively documented, does cause social dominance and confidence which do not lead to aggression. However, when other factors are coupled with high testosterone (as noted by Mazur, 2016), high rates of crime may occur and this may explain why blacks commit crime; a mix of low IQ, high testosterone and low educational achievement making a life of crime ‘the smart way’ to live seeing as, as Ellis points out, and that intelligent individuals find legal ways to get resources while less intelligent individuals use illegal ways.
ENA theory may explain racial differences in crime
In part IV he attempts to show how his ENA theory may explain racial differences in crime—with testosterone sitting at the top of his pyramid. However, there are numerous erroneous assumptions and he does rightly point out that more research needs to be done on most of these variables and does not draw any conclusions that are not warranted based on the data he does cite. He cites one study in which testosterone levels were measured in the amniotic fluid of the fetus. The sample was 59 percent white and due to this, the researchers lumped blacks, ‘Hispanics’ and Native Americans together which showed no significant difference in prenatal testosterone levels (Martel and Roberts, 2014).
Umbilical cord and testosterone exposure
Ellis then talks about testosterone in the umbilical cord, and if the babe is exposed to higher levels of testosterone in vitro, then this should account for racial/ethnic differences in crime. However, the study he cited (Argus-Collins et al, 2012) showed no difference in testosterone in the umbilical cord while Rohrmann et al (2009) found no difference in testosterone between blacks and whites but found higher rates of SHBG (sex hormone-binding globulin) which binds to testosterone and makes it unable to leave the blood which largely makes testosterone unable to affect organ development. Thusly, if the finding of higher levels of SHBG in black babes is true, then they would be exposed to less androgenic hormones such as testosterone which, again, goes against the ENA theory.
He also cites two more studies showing that Asian babes have higher levels of umbilical cord testosterone than whites (Chinese babes were tested) (Lagiou et al, 2011; Troisi et al, 2008). This, again, goes against his theory as he rightly noted.
Next he talks about circulating differences in testosterone between blacks and whites. He rightly notes that testosterone must be assayed in the morning within an hour after waking as that’s when levels will be highest, yet cites Ross et al (1986) where assay times were all over the place and thusly testosterone cannot be said to be higher in blacks and whites based on that study and should be discarded when talking about racial differences in testosterone due to assay time being between 10 am and 3 pm. He also cites his study on testosterone differences (Eliss and Nyborg, 1993), but, however, just as Ross et al (1986) did not have a control for WC (waist circumference) Ellis and Nyborg (1993) did not either, so just like the other study that gets cited to show that there is a racial difference in testosterone, they are pretty hugely flawed and should not be used in discussion when discussing racial differences in testosterone. Why do I not see these types of critiques for Ross et al (1986) in major papers? It troubles me…
He also seems to complain that Lopez et al (2013) controlled for physical activity (which increases testosterone) and percent body fat (which, at high levels, decreases testosterone). These variables, as I have noted, need to be controlled for. Testosterone varies and fluctuated by age; WC and BMI vary and fluctuate by age. So how does it make sense to control for one variable that has hormone levels fluctuate by age and not another? Ellis also cites studies showing that older East Asian men had higher levels of testosterone (Wu et al, 1995). Nevertheless, there is no consensus; some studies show Chinese babes have higher levels of testosterone than whites and some studies show that whites babes have higher levels of testosterone than Chinese babes. Indeed, this meta-analysis by Ethnicmuse shows that Asians have the highest levels, followed by Africans then Europeans, so this needs to be explained to save the theory that testosterone is the cause of black overrepresentation of violence (as well as what I showed that testosterone is important for vital functioning and is not the boogeyman the media makes it out to be).
Bone density and crime
Nevertheless, the next variable Ellis talks about is bone density and its relationship to crime. Some studies find that blacks are taller than whites while other show no difference. Whites are also substantially taller than Asian males. Blacks have greater bone density than the other three races, but according to Ellis, this measure has not been shown to have a relationship to crime as of yet.
Penis size, race and crime
Now on to penis size. In two articles, I have shown that there is no evidence for the assertion that blacks have larger penises than whites. However, states that penis length was associated with higher levels of testosterone in Egyptian babes. He states that self-reported penis size correlates with self-reports of violent delinquency (Ellis and Das, 2012). Ellis’ main citations for the claim that blacks have larger penises than other races comes from Nobile (1982), the Kinsey report, and Rushton and Boagert (1987) (see here for a critique of Rushton and Boagert, 1987), though he does cite a study stating that blacks had a longer penis than whites (blacks averaging 5.77 inches while whites averaged 5.53 inches). An HBDer may go “Ahah! Evidence for Rushton’s theory!”, yet they should note that the difference is not statistically significant; just because there is a small difference in one study also doesn’t mean anything for the totality of evidence on penis size and race—that there is no statistical difference!
He then cites Lynn’s (2013) paper which was based on an Internet survey and thus, self-reports are over-measured. He also cites Templer’s (2002) book Is Size Important?, which, of course, is on my list of books to read. Nevertheless, the ‘evidence’ that blacks average larger penises than whites is extremely dubious, it’s pretty conclusive that the races don’t differ in penis size. For further reading, read The Pseudoscience of Race Differences in Penis Size, and read all of Ethnicmuses’ posts on penis size here. It’s conclusive that there is no statistical difference—if that—and any studies showing a difference are horribly flawed.
2d/4d ratio and race
Then he talks about 2d/4d ratio, which supposedly signifies higher levels of androgen exposure in vitro (Manning et al, 2008) however these results have been challenged and have not been replicated (Koehler, Simmons, and Rhodes, 2004; Yan et al, 2008, Medland et al, 2010). Even then, Ellis states that in a large analysis of 250,000 respondents, Asians had the lowest 2d/4d ratio, which if the hypothesis of in vitro hormones affecting digit length is to be believed, they have higher levels of testosterone than whites (the other samples had small ns, around 100).
Prostate-specific antigens, race, and prostate cancer
He then talks about PSA (prostate-specific antigen) rates between the races. Blacks are two times more likely to get prostate cancer, which has been blamed on testosterone. However, I’ve compiled good evidence that the difference comes down to the environment, i.e., diet. Even then, there is no evidence that testosterone causes prostate cancer as seen in two large meta-analyses (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even then, rates of PCa (prostate cancer) are on the rise in East Asia (Kimura, 2012; Chen et al, 2015; Zhu et al, 2015) which is due to the introduction of our Western diet. I will cover the increases in PCa rates in East Asia in a future article.
He then reviews the evidence of CAG repeats. There is, however, no evidence that the number of CAG repeats influences sensitivity to testosterone. However, intra-racially, lower amounts of CAG repeats are associated with higher spermatozoa counts—but blacks don’t have higher levels of spermatozoa (Mendiola et al, 2011; Redmon et al, 2013). Blacks do have shorter CAG repeats, and this is consistent with the racial crime gap of blacks > whites > Asians. However, looking at the whole of the evidence, there is no good reason to assume that this has an effect on racial crime rates.
Intelligence and education
Next he talks about racial differences in intelligence and education, which have been well-established. Blacks did have higher rates of learning disabilities than whites who had higher levels of learning disabilities then Asians in a few studies, but other studies show whites and South Asians having different rates, for instance. He then talks about brain size and criminality, stating that the head size of males convicted for violent crimes did not differ from males who committed non-violent crimes (Ikaheimo et al, 2007). I won’t bore anyone with talking about what we know already: that the races differ in average brain size. However, a link between brain size and criminality—to the best of my knowledge—has yet to been discovered. IQ is implicated in crime, so I do assume that brain size is as well (no matter if the correlation is .24 or not; Pietschnig et al, 2015).
Prenatal androgen exposure
Now to wrap things up, the races don’t differ in prenatal androgen exposure, which is critical to the ENA theory; there is a small difference in the umbilical cord favoring blacks, and apparently, that predicts a high rate of crime. However, as noted, blacks have higher levels of SHBG at birth which inhibits the production of testosterone on the organs. Differences in post-pubertal testosterone are small/nonexistent and one should not talk about them when talking about differences in crime or disease acquisition such as PCa. DHT only shows a weak positive correlation with aggression—the same as testosterone (Christiansen and Winkler, 1992; however other studies show that DHT is negatively correlated with measures of physical aggression; Christiansen and Krussmann, 1987; further, DHT is not so evil after all).
Summing it all up
Blacks are not stronger than whites, indeed evidence from the races’ differing somatype, grip strength and leverages all have to do with muscular strength. Furthermore, the study that Ellis cites as ‘proof’ that blacks are stronger than whites is on one measure; an isokinetic dynamometry machine which is pretty much a leg extension. In true tests of strength, whites blow blacks away, which is seen in all major professional competitions all around the world. Blacks do have denser bones which is due to androgen production in vitro, but as of yet, there has been no research done into bone density and criminality.
The races don’t differ on penis size—and if they do it’s by tenths of an inch which is not statisitcally significant and I won’t waste my time addressing it. It seems that most HBDers will see a racial difference of .01 and say “SEE! Rushton’s Rule!” even when it’s just that, a small non-significant difference in said variable. That’s something I’ve encountered a lot in the past and it’s, frankly, a waste of time to converse about things that are not statistically significant. I’ve also rebutted the theory on 2d/4d ration as well. Finally, Asians had a similar level of androgen levels compared to blacks, with whites having the least amount. Along with a hole in the theory for racial differences in androgen causing crime, it’s yet another hole in the theory for racial differences in androgens causing racial differences in penis size and prostate cancer.
On intelligence scores, no one denies that blacks have scored about 1 SD lower than whites for 100 years, no one denies that blacks have a lower educational attainment. In regards to learning disabilities, blacks seem to have the highest rates, followed by Native Americans, than non-Hispanic whites, East Asians and the lowest rates found in South Asians. He states only one study links brain size to criminal behavior and it showed a significant inverse relationship with crime but not other types of offenses.
This is a really good article and I like the theory, but it’s full of huge holes. Most of the variables described by Ellis have been shown to not vary at all or much between the races (re: penis size, testosterone, strength [whites are stronger] prostate cancer caused mainly by diet, 2d/4d ratio [no evidence of it showing a digit ratio difference], and bone density not being studied). Nevertheless, a few of his statements do await testing so I await future studies on the matter. He says that androgen exposure ‘differs by race and ethnicity’, yet the totality of evidence shows ‘not really’ so that cannot be the cause of higher amounts of crime. Ellis talks about a lot of correlates with testosterone, but they do not pass the smell test. Most of it has been rebutted. In fact, one of the central tenets of the ENA theory is that the races should differ in 2d/4d ratio due to exposure of differing levels of the hormone in vitro. Alas, the evidence to date has not shown this—it has in fact shown the opposite.
ENA theory is good in thought, but it really leaves a lot to be desired in regards to explaining racial differences in crime. More research needs to be looked into in regards to intelligence and education and its effect on crime. We can say that low IQ people are more likely to drop out of school and that is why education is related to crime. However, in Mazur (2016) shows that blacks matched for age had lower levels of testosterone if they had some college under their belt. This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have the lowest rate of crime in the worle!
This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have some of the lowest rate of crime in the world (Rushton, 1995)! So this is something that needs to be explained if it is to be shown that testosterone facilitates aggression and therefore, crime.
I’ve shown—extensively—that there is a low positive correlation between testosterone and physical aggression, why testosterone does not cause crime, and have definitively shown that, by showing how flawed the other studies are that purport to show blacks have higher testosterone levels than whites, along with citing large-scale meta-analyses, that whites and blacks either do not differ or the differences is small to explain any so-called differences in disease acquisition or crime. One final statement on the CAG repeats, they are effect by obesity, men who had shorter CAG repeats were more likely to be overweight, which would skew readings (Gustafsen, Wen, and Koppanati, 2003). So depending on the study—and in most of the studies I cite whites have a higher BMI than blacks—BMI and WC should be controlled for due to the depression of testosterone.
It’s pretty conclusive that testosterone itself does not cause crime. Most of the examples cited by Ellis have been definitively refuted, and his other claims lack evidence at the moment. Even then, his theory rests on the 2d/4d ratio and how blacks may have a lower 2d/4d ratio than whites. However, I’ve shown that there is no significant relationship between 2d/4d ratio and traits mediated by testosterone (Kohler, Simmons, and Rhodes, 2004) so that should be enough to put the theory to bed for good.