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What is the relationship between nutrition and antisocial behavior? Does not consuming adequate amounts of vitamins and minerals lead to an increased risk for antisocial behavior? If it does, then lower class people will have commit crimes at a higher rate, and part of the problem may indeed be dietary. Though, what kind of data is there that lends credence to the idea? It is well-known that malnutrition leads to antisocial behavior, but what kind of effect does it have on the populace as a whole?
About 85 percent of Americans lack essential vitamins and minerals. Though, when most people think of the word ‘malnutrition’ and the imagery it brings along with it, they assume that someone in a third-world country is being talked about, say a rail-thin kid somewhere in Africa who is extremely malnourished due to lack of kcal and vitamins and minerals. However, just because one lives in a first-world country and has access to kcal to where they’re “not hungry” doesn’t mean that vitamin and mineral deficiencies do not exist in these countries. This is known as “hidden hunger” when people can get enough kcal for their daily energy needs but what they are eating is lower-quality food, and thus, they become vitamin and nutrient deficient. What kind of effects does this have?
Infants are most at risk, more than half of American babies are at-risk for malnutrition; malnutrition in the postnatal years can lead to antisocial behavior and a lower ‘IQ’ (Galler and Ramsey, 1989; Liu et al, 2003; Galler et al, 2011, 2012a, 2012b; Gesch, 2013; Kuratko et al, 2013; Raine et al, 2015; Thompson et al, 2017). Clearly, not getting pertinent vitamins and minerals at critical times of development for infants leads to antisocial behavior in the future. These cases, though, can be prevented with a good diet. But the preventative measures that can prevent some of this behavior has been demonized for the past 50 or so years.
Poor nutrition leads to the development of childhood behavior problems. As seen in rat studies, for example, lack of dietary protein leads to aggressive behavior while rats who are protein-deficient in the womb show altered locomotor activity. The same is also seen with vitamins and minerals; monkeys and rats who were fed a diet low in tryptophan were reported to be more aggressive whereas those that were fed high amounts of tryptophan were calmer. Since tryptophan is one of the building blocks of serotonin and serotonin regulates mood, we can logically state that diets low in tryptophan may lead to higher levels of aggressive behavior. The role of omega 3 fatty acids are mixed, with omega 3 supplementation showing a difference for girls, but not boys (see Itomura et al, 2005). So, animal and human correlational studies and human intervention studies lend credence to the hypothesis that malnutrition in the womb and after birth leads to antisocial behavior (Liu and Raine, 2004).
We also have data from one randomized, placebo-controlled trial showing the effect of diet and nutrition on antisocial behavior (Gesch et al, 2002). They state that since there is evidence that offenders’ diets are lacking in pertinent vitamins and minerals, they should test whether or not the introduction of physiologically adequate vitamins, minerals and essential fatty acids (EFAs) would have an effect on the behavior of the inmates. They undertook an experimental, double-blind, placebo-controlled randomized trial on 231 adult prisoners and then compared their write-ups before and after nutritional intervention. The vitamin/mineral supplement contained 44 mg of DHA (omega 3 fatty acid docosahexaenoic acid; plays a key role in enhancing brain structure and function, stimulating neurite outgrowth), 80 mg of EPA (eicosapentaenoic acid; n3), and 1.26 g of ALA (alpha-linolenic acid), 1260mg of LA (linolic acid), and 160mg of GLA (gamma-Linolenic acid, n6) and a vegetable oil placebo. (Also see Hibbeln and Gow, 2015 for more information on n3 and nutrient deficits in childhood behavior disorders and neurodevelopment.)
Raine (2014: 218-219) writes:
We can also link micronutrients to specific brain structures involved in violence. The amygdala and hippocampus, which are impaired in offenders, are packed with zinc-containing neurons. Zinc deficiency in humans during pregnancy can in turn impair DNA, RNA, and protein synthesis during brain development—the building blocks of brain chemistry—and may result in very early brain abnormalities. Zinc also plays a role in building up fatty acids, which, as we have seen, are crucial for brain structure and function.
Gesch et al (2002) found pretty interesting results: those who were given the capsules with vitamins, minerals, and EFAs had 26.3 percent fewer offenses than those who got the placebo. Further, when compared with the baseline, when taking the supplement for two weeks, there was an average 35.1 percent reduction in offenses compared to the placebo group who showed little change. Gesch et al (2002) conclude:
Antisocial behaviour in prisons, including violence, are reduced by prisons, are reduced by vitamins, minerals and essential fatty acids with similar implications for those eating poor diets in the community.
Of course one could argue that these results would not transfer over to the general population, but to a critique like this, the observed effect of behavior is physiological; so by supplementing the prisoners’ diets giving them pertinent vitamins, minerals and EFAs, violence and antisocial behavior decreased, which shows some level of causation between nutrition/nutrient/fatty acid deprivation and antisocial behavior and violent activity.
Gesch et al (2002) found that some prisoners did not know how to construct a healthy diet nor did they know what vitamins were. So, naturally, since some prisoners didn’t know how to construct diets with an adequate amount of EFAs, vitamins and minerals, they were malnourished, though they consumed an adequate amount of calories. The intervention showed that EFA, vitamin and mineral deficiency has a causal effect on decreasing antisocial and violent behavior in those deficient. So giving them physiological doses lowered antisocial behavior, and since it was an RCT, social and ethnic factors on behavior were avoided.
Of course (and this shouldn’t need to be said), I am not making the claim that differences in nutrition explain all variance in antisocial and violent behavior. The fact of the matter is, this is causal evidence that lack of vitamin, mineral and EFA consumption has some causal effect on antisocial behavior and violent tendencies.
Schoenthaler et al (1996) also showed how correcting low values of vitamins and minerals in those deficient led to a reduction in violence among juvenile delinquents. Though it has a small n, the results are promising. (Also see Zaalberg et al, 2010.) These simple studies show how easy it is to lower antisocial and violent behavior: those deficient in nutrients just need to take some vitamins and eat higher-quality food and there should be a reduction in antisocial and violent behavior.
Liu, Zhao, and Reyes (2015) propose “a conceptual framework whereby epigenetic modifications (e.g., DNA methylation) mediate the link between micro- and macro-nutrient deficiency early in life and brain dysfunction (e.g., structural aberration, neurotransmitter perturbation), which has been linked to development of behavior problems later on in life.” Their model is as follows: macro- and micro-nutrient deficiencies are risk-factors for psychopathologies since they can lead to changes in the epigenetic regulation of the genome (along with other environmental variables such as lead consumption, which causes abnormal behavior and also epigenetic changes which can be passed through the generations; Senut et al, 2012; Sen et al, 2015) which then leads to impaired brain development, which then leads to externalizing behavior, internalizing behavior and autism and schizophrenia (two disorders which are also affected by the microbiome; Strati et al, 2017; Dickerson, 2017).
Clearly, since the food we eat gives us access to certain fatty acids that cannot be produced de novo in the brain or body, good nutrition is needed for a developing brain and if certain pertinent vitamins, minerals or fatty acids are missing, negative outcomes could occur for said individual in the future due to lack of brain development from being nutrient, vitamin, and mineral deficient in childhood. Further, interactions between nutrient deficiencies and exposure to toxic chemicals may be a cause of a large amount of antisocial behavior (Walsh et al, 1997; Hubbs-Tait et al, 2005; Firth et al, 2017).
Looking for a cause for this interaction between metal consumption and nutrient deficiencies, Liu, Zhao, and Reyes (2015) state that since protein and fatty acids are essential to brain growth, lack of consumption of pertinent micro- and macro-nutrients along with consumption of high amounts of protein both in and out of the womb contribute to lack of brain growth and, at adulthood, explains part of the difference in antisocial behavior. What you can further see from the above studies is that metals consumed by an individual can interact with the nutrient deficiencies in said individual and cause more deleterious outcomes, since, for example, lead is a nutrient antagonist—that is, it inhibits the physiologic actions of whatever bioavailable nutrients are available to the body for us.
Good nutrition is, of course, imperative since it gives our bodies what it needs to grow and develop as we grow in the womb, as adolescents and even into old age. So, therefore, developing people who are nutrient deficient will have worse behavioral outcomes. Further, lower class people are more likely to be nutrient deficient and consume lower quality diets than higher, more affluent classes, though it’s hard to discover which way the causation goes (Darmon and Drewnowski, 2008). Of course, the logical conclusion is that being deficient in vitamins, minerals and EFAs causes changes to the epigenome and retards brain development, therefore this has a partly causal effect on future antisocial, violent and criminal behavior. So, some of the crime difference between classes can be attributed to differences in nutrition/toxic metal exposure that induces epigenetic changes that change the structure of the brain and doesn’t allow full brain development due to lack of vitamins, minerals, and EFAs.
There seems to be a causal effect on criminal, violent and antisocial behavior regarding nutrient deficiencies in both juveniles and adults (which starts in the womb and continues into adolescence and adulthood). However, it has been shown in a few randomized controlled trials that nutritional interventions decrease some antisocial behavior, with the effect being strongest for those individuals who showed worse nutrient deficiencies.
If the relationship between nutrition/interaction between nutrient deficiencies and toxins can be replicated successfully then this leads us to one major question: Are we, as a society, in part, causing some of the differences in crime due to how our society is regarding nutrition and the types of food that are advertised to our youth? Are people’s diets which lead to nutrient deficiencies a driving factor in causing crime? The evidence so far on nutrition and its effects on the epigenome and its effects on the growth of the brain in the womb and adolescence requires us to take a serious look at this relationship. That lower class people are exposed to more neurotoxins such as lead (Bellinger, 2008) and are more likely to be nutrient deficient (Darmon and Drewnowski, 2008; Hackman, Farrah, and Meaney, 2011) then if they were educated on which foods to eat to avoid nutrient deficiencies along with avoiding neurotoxins such as lead (which exacerbate nutrient deficiencies and cause crime), then a reduction in crime should occur.
Nutrition is important for all living beings; and as can be seen, those who are deficient in certain nutrients and have less access to good, whole, nutritious food (who also have an increased risk for exposure to neurotoxins) can lead to negative outcomes. These things can be prevented, it seems, with a few vitamins/minerals/EFA consumption. The effects of sleep, poor diet (which also lead to metabolic syndromes) can also exacerbate this relationship, between individuals and ethnicities. The relationship between violence and antisocial behavior and nutrient deficiencies/the interaction with nutrient deficiencies and neurotoxins is a great avenue for future research to reduce violent crime in our society. Lower class people, of course, should be the targets of such interventions since there seems to be a causal effect—-however small or large—on behavior, both violent and nonviolent—and so nutrition interventions should close some of the crime gaps between classes.
The logic is very simple: nutrition affects mood (Rao et al, 2008; Jacka, 2017) which is, in part, driven by the microbiome’s intimate relationship with the brain (Clapp et al, 2017; Singh et al, 2017); nutrition also affects the epigenome and the growth and structure of the brain if vitamin and mineral needs are not met by the growing body. This then leads to differences in gene expression due to the foods consumed, the microbiome (which also influences the epigenome) further leads to differences in gene expression and behavior since the two are intimately linked as well. Thus, the aetiology of certain behaviors may come down to nutrient deficiencies and complex interactions between the environment, neurotoxins, nutrient deficiencies and genetic factors. Clearly, we can prevent this with preventative nutritional education, and since lower class people are more likely to suffer the most from these problems, the measures targeted to them, if followed through, will lower incidences of crime and antisocial/violent behavior.
Lead has many known neurological effects on the brain (regarding the development of the brain and nervous system) that lead to many deleterious health outcomes and negative outcomes in general. Including (but not limited to) lower IQ, higher rates of crime, higher blood pressure and higher rates of kidney damage, which have permanent, persistent effects (Stewart et al, 2007). Chronic lead exposure, too, can “also lead to decreased fertility, cataracts, nerve disorders, muscle and joint pain, and memory or concentration problems” (Sanders et al, 2009). Lead exposure in vitro, in infancy, and in childhood can also lead to “neuronal death” (Lidsky and Schneider, 2003). While epigenetic inheritance also plays a part (Sen et al, 2015). How do blacks and whites differ in exposure to lead? How much is the difference between the two races in America, and how much would it contribute to crime? On the other hand, China has high rates of lead exposure, but lower rates of crime, so how does this relationship play out with the lead-crime relationship overall? Are the Chinese an outlier or is there something else going on?
The effects of lead on the brain are well known, and numerous amounts of effort have been put into lowering levels of lead in America (Gould, 2009). Higher exposure to lead is also found in poorer, lower class communities (Hood, 2005). So since higher levels of lead exposure are found more often in lower-class communities, then blacks should have higher blood-lead levels than whites. This is what we find.
Blacks had a 27 percent higher concentration of lead in their tibia, while having significantly higher levels of blood lead, “likely because of sustained higher ongoing lead exposure over the decades” (Theppeang et al, 2008). Other data—coming out of Detroit—shows the same relationships (Haar et al, 1979; Talbot, Murphy, and Kuller, 1982; Lead poisoning in children under 6 jumped 28% in Detroit in 2016; also see Maqsood, Stanbury, and Miller, 2017) while lead levels in the water contribute to high levels of blood-lead in Flint, Michigan (Hanna-Attisha et al, 2016; Laidlaw et al, 2016). Cassidy-Bushrow et al (2017) also show that “The disproportionate burden of lead exposure is vertically transmitted (i.e., mother-to-child) to African-American children before they are born and persists into early childhood.”
Children exposed to lead have lower brain volumes as children, specifically in the ventrolateral prefrontal cortex, which is the same region of the brain that is impaired in antisocial and psychotic persons (Cecil et al, 2008). The community that was tested was well within the ‘safe’ range set by the CDC (Raine, 2014: 224), though the CDC says that there is no safe level of lead exposure. There is a large body of studies which show that there is no safe level of lead exposure (Needleman and Landrigan, 2004; Canfield, Jusko, and Kordas, 2005; Barret, 2008; Rossi, 2008; Abelsohn and Sanborn, 2010; Betts, 2012; Flora, Gupta, and Tiwari, 2012; Gidlow, 2015; Lanphear, 2015; Wani, Ara, and Usmani, 2015; Council on Environmental Health, 2016; Hanna-Attisha et al, 2016; Vorvolakos, Aresniou, and Samakouri, 2016; Lanphear, 2017). So the data is clear that there is absolutely no safe level of lead exposure, and even small effects can lead to deleterious outcomes.
Further, one brain study of 532 men who worked in a lead plant showed that those who had higher levels of lead in their bones had smaller brains, even after controlling for confounds like age and education (Stewart et al, 2008). Raine (2014: 224) writes:
The fact that the frontal cortex was particularly reduced is very interesting, given that this brain region is involved in violence. This lead effect was equivalent to five years of premature aging of the brain.
So we have good data that the parts of the brain that relate to violent tendencies are reduced in people exposed to more lead had the same smaller parts of the brain, indicating a relationship. But what about antisocial disorders? Are people with higher levels of lead in their blood more likely to be antisocial?
Needleman et al (1996) show that boys who had higher levels of lead in their blood had higher teacher ratings of aggressive and delinquent behavior, along with higher self-reported ratings of aggressive behavior. Even high blood-lead levels later in life is related to crime. One study in Yugoslavia showed that blood lead levels at age three had a stronger relationship with destructive behavior than did prenatal blood lead levels (Wasserman et al, 2008); with this same relationship being seen in America with high blood lead levels correlating with antisocial and aggressive behavior at age 7 and not age 2 (Chen et al 2007).
Nevin (2007) showed a strong relationship between preschool lead exposure and subsequent increases in criminal cases in America, Canada, Britain, France, Australia, Finland, West Germany, and New Zealand. Reyes (2007) also shows that crime increased quicker in states that saw a subsequent large decrease in lead levels, while variations in lead levels within cities correlating with variations in crime rates (Mielke and Zahran, 2012). Nevin (2000) showed a strong relationship between environmental lead levels from 1941 to 1986 and corresponding changes to violent crime twenty-three years later in the United States. Raine (2014: 226) writes (emphasis mine):
So, young children who are most vulnerable to lead absorption go on twenty-three years later to perpetrate adult violence. As lead levels rose throughout the 1950s, 1960s, and 1970s, so too did violence correspondingly rise in the 1970s, 1980s and 1990s. When lead levels fell in the late 1970s and early 1980s, so too did violence fall in the 1990s and the first decade of the twenty-first century. Changes in lead levels explained a full 91 percent of the variance in violent offending—an extremely strong relationship.
From international to national to state to city levels, the lead levels and violence curves match up almost exactly.
But does lead have a causal effect on crime? Due to the deleterious effects it has on the developing brain and nervous system, we should expect to find a relationship, and this relationship should become stronger with higher doses of lead. Fortunately, I am aware of one analysis, a sample that’s 90 percent black, which shows that with every 5 microgram increase in prenatal blood-lead levels, that there was a 40 percent higher risk of arrest (Wright et al, 2008). This makes sense with the deleterious developmental effects of lead; we are aware of how and why people with high levels of lead in their blood show similar brain scans/brain volume in certain parts of the brain in comparison to antisocial/violent people. So this is yet more suggestive evidence for a causal relationship.
Jennifer Doleac discusses three studies that show that blood-lead levels in America need to be addressed, since they are related strongly to negative health outcomes.Aizer and Curry (2017) show that “A one-unit increase in lead increased the probability of suspension from school by 6.4-9.3 percent and the probability of detention by 27-74 percent, though the latter applies only to boys.” They also show that children who live nearer to roads have higher blood-lead levels, since the soil near highways was contaminated decades ago with leaded gasoline. Fiegenbaum and Muller (2016) show that cities’ use of lead pipes increased murder rates between the years o921 and 1936. Finally, Billings and Schnepnel (2017: 4) show that their “results suggest that the effects of high levels of [lead] exposure on antisocial behavior can largely be reversed by intervention—children who test twice over the alert threshold exhibit similar outcomes as children with lower levels of [lead] exposure (BLL<5μg/dL).”
A relationship with lead exposure in vitro and arrests at adulthood. The sample was 90 percent black, with numerous controls. They found that prenatal and post-natal blood-lead exposure was associated with higher arrest rates, along with higher arrest rates for violent acts (Wright et al, 2008). To be specific, for every 5 microgram increase in prenatal blood-lead levels, there was a 40 percent greater risk for arrest. This is direct causal evidence for the lead-causes-crime hypothesis.
One study showed that in post-Katrina New Orleans, decreasing lead levels in the soil caused a subsequent decrease in blood lead levels in children (Mielke, Gonzales, and Powell, 2017). Sean Last argues that, while he believes that lead does contribute to crime, that the racial gaps have closed in the recent decades, therefore blood-lead levels cannot be a source of some of the variance in crime between blacks and whites, and even cites the CDC ‘lowering its “safe” values’ for lead, even though there is no such thing as a safe level of lead exposure (references cited above). White, Bonilha, and Ellis Jr., (2015) also show that minorities—blacks in particular—have higher rates of lead in their blood. Either way, Last seems to downplay large differences in lead exposure between whites and blacks at young ages, even though that’s when critical development of the mind/brain and other important functioning occurs. There is no safe level of lead exposure—pre- or post-natal—nor are there safe levels at adulthood. Even a small difference in blood lead levels would have some pretty large effects on criminal behavior.
Sean Last also writes that “Black children had a mean BLL which was 1 ug/dl higher than White children and that this BLL gap shrank to 0.9 ug/dl in samples taken between 2003 and 2006, and to 0.5 ug/dl in samples taken between 2007 and 2010.” Though, still, there are problems here too: “After adjustment, a 1 microgram per deciliter increase in average childhood blood lead level significantly predicts 0.06 (95% confidence interval [CI] = 0.01, 0.12) and 0.09 (95% CI = 0.03, 0.16) SD increases and a 0.37 (95% CI = 0.11, 0.64) point increase in adolescent impulsivity, anxiety or depression, and body mass index, respectively, following ordinary least squares regression. Results following matching and instrumental variable strategies are very similar” (Winter and Sampson, 2017).
Naysayers may point to China and how they have higher levels of blood-lead levels than America (two times higher), but lower rates of crime, some of the lowest in the world. The Hunan province in China has considerably lowered blood-lead levels in recent years, but they are still higher than developed countries (Qiu et al, 2015). One study even shows ridiculously high levels of lead in Chinese children “Results showed that mean blood lead level was 88.3 micro g/L for 3 – 5 year old children living in the cities in China and mean blood lead level of boys (91.1 micro g/L) was higher than that of girls (87.3 micro g/L). Twenty-nine point nine one per cent of the children’s blood lead level exceeded 100 micro g/L” (Qi et al, 2002), while Li et al (2014) found similar levels. Shanghai also has higher levels of blood lead than the rest of the developed world (Cao et al, 2014). Blood lead levels are also higher in Taizhou, China compared to other parts of the country—and the world (Gao et al, 2017). But blood lead levels are decreasing with time, but still higher than other developed countries (He, Wang, and Zhang, 2009).
Furthermore, Chinese women, compared to American women, had two times higher BLL (Wang et al, 2015). With transgenerational epigenetic inheritance playing a part in the inheritance of methylation DNA passed from mother to daughter then to grandchildren (Sen et al, 2015), this is a public health threat to Chinese women and their children. So just by going off of this data, the claim that China is a safe country should be called into question.
Reality seems to tell a different story. It seems that the true crime rate in China is covered up, especially the murder rate:
In Guangzhou, Dr Bakken’s research team found that 97.5 per cent of crime was not reported in the official statistics.
Of 2.5 million cases of crime, in 2015 the police commissioner reported 59,985 — exactly 15 less than his ‘target’ of 60,000, down from 90,000 at the start of his tenure in 2012.
The murder rate in China is around 10,000 per year according to official statistics, 25 per cent less than the rate in Australia per capita.
“I have the internal numbers from the beginning of the millennium, and in 2002 there were 52,500 murders in China,” he said.
Instead of 25 per cent less murder than Australia, Dr Bakken said the real figure was closer to 400 per cent more.”
Guangzhou, for instance, doesn’t keep data for crime committed by migrants, who commit 80 percent of the crime in this province. Out of 2.5 million crimes committed in Guangzhou, only 5,985 crimes were reported in their official statistics, which was 15 crimes away from their target of 6000. Weird… Either way, China doesn’t have a similar murder rate to Switzerland:
The murder rate in China does not equal that of Switzerland, as the Global Times claimed in 2015. It’s higher than anywhere in Europe and similar to that of the US.
China also ranks highly on the corruption index, higher than the US, which is more evidence indicative of a covered up crime rate. So this is good evidence that, contrary to the claims of people who would attempt to downplay the lead-crime relationship, that these effects are real and that they do matter in regard to crime and murder.
So it’s clear that we can’t trust the official Chinese crime stats since there much of their crime is not reported. Why should we trust crime stats from a corrupt government? The evidence is clear that China has a higher crime—and murder rate—than is seen on the Chinese books.
Lastly, effects of epigenetics can and do have a lasting effect on even the grandchildren of mothers exposed to lead while pregnant (Senut et al, 2012; Sen et al, 2015). Sen et al (2015) showed lead exposure during pregnancy affected the DNA methylation status of the fetal germ cells, which then lead to altered DNA methylation on dried blood spots in the grandchildren of the mother exposed to lead while pregnant.—though it’s indirect evidence. If this is true and holds in larger samples, then this could be big for criminological theory and could be a cause for higher rates of black crime (note: I am not claiming that lead exposure could account for all, or even most of the racial crime disparity. It does account for some, as can be seen by the data compiled here).
In conclusion, the relationship between lead exposure and crime is robust and replicated across many countries and cultures. No safe level of blood lead exists, even so-called trace amounts can have horrible developmental and life outcomes, which include higher rates of criminal activity. There is a clear relationship between lead increases/decreases in populations—even within cities—that then predict crime rates. Some may point to the Chinese as evidence against a strong relationship, though there is strong evidence that the Chinese do not report anywhere near all of their crime data. Epigenetic inheritance, too, can play a role here mostly regarding blacks since they’re more likely to be exposed to high levels of lead in the womb, their infancy, and childhood. This could also exacerbate crime rates, too. The evidence is clear that lead exposure leads to increased criminal activity, and that there is a strong relationship between blood lead levels and crime.
People 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.)
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.)
Testosterone is a fascinating hormone—the most well-known hormone to the lay public. What isn’t well-known to the lay public is how the hormone is produced and the reasons why it gets elevated. I’ve covered racial differences in testosterone in regards to crime, penis size and Rushton’s overall misuse of r/K selection theory. In this article, I will talk about what raises and decreases testosterone, as well as speak about racial differences in testosterone again since it’s such a fun topic to cover.
JP Rushton writes, in his 1995 article titled Race and Crime: An International Dilemma:
One study, published in the 1993 issue of Criminology by Alan Booth and D. Wayne Osgood, showed clear evidence of a testosterone-crime link based on an analysis of 4,462 U.S. military personnel. Other studies have linked testosterone to an aggressive and impulsive personality, to a lack of empathy, and to sexual behavior.
Booth and Osgood (1993: 93) do state that “This pattern of results supports the conclusions that (I) testosterone is one of a larger constellation of factors contributing to a general latent propensity toward deviance and (2) the influence of testosterone on adult deviance is closely tied to social factors.” However, as I have extensively documented, the correlation between testosterone and aggression is extremely low (Archer, 1991; Book et al (2001); Archer, Graham-Kevan and Davies, 2005), and therefore cannot be the cause of crime.
Another reason why testosterone is not the cause of aggression/deviant behavior is due to what times most crimes are committed at. Therefore, testosterone cannot possibly be the cause of crime. I’ve also shown that, contrary to popular belief, blacks don’t have higher levels testosterone than whites, along with the fact that testosterone does not cause prostate cancer, that even if blacks did have these supposed higher levels of the hormone, that it would NOT explain higher rates of crime.
Wu et al (1995) show that Asian Americans had the highest testosterone levels, African Americans were intermediate and European Americans were last, after adjustments for BMI and age were made. Though, I’ve shown in larger samples that, if there is any difference at all (and a lot of studies show no difference), it is a small advantage favoring blacks. We then are faced with the conclusion that this would not explain disease prevalence nor higher rates of crime or aggression.
Testosterone, contrary to Rushton’s (1999) assertion, is not a ‘master switch’. Rushton, of course, cites Ross et al (1986) which I’ve tirelessly rebutted. Assay times were all over the place (between 10 am and 3 pm) with testosterone levels being highest at 8 am. The most important physiological variable in Rushton’s model is testosterone, and without his highly selected studies, his narrative falls apart. Testosterone doesn’t cause crime, aggression, nor prostate cancer.
The most important take away is this: Rushton’s r/K theory hinges on 1) blacks having higher levels of testosterone than whites and 2) that these higher levels of testosterone then influence higher levels of aggression which lead to crime and then prostate cancer. Even then, Sridhar et al (2010) meta-analyzed 17 articles which talk about racial differences in prostate cancer survival rates. They state in their conclusion that “there are no differences between African American and Whites in survival from prostate cancer.” Zagars et al (1998) show that there were no significant racial differences in serum testosterone. Furthermore, when matched for major prognostic factors “the outcome for clinically local–regional prostate cancer does not depend on race (6,7,14–19). Moreover there appear to be no racial differences in the response of advanced prostate cancer to androgen ablation (29,47). Our study provides further evidence that racial differences in disease outcome are absent for clinically localized prostate cancer” (Zagars et al, 1998: 521). So it seems that these two studies also provide further support that Rushton et al were wrong in regards to prostate cancer mortality as well.
Rushton (1997 185) writes:
In any case, socialization cannot account for the early onset of the traits, the speed of dental and other maturational variables, the size of the brain, the number of gametes produced, the physiological differences in testosterone, nor the evidence on cross-cultural consistency.
There are no racial differences in testosterone and if there were, social factors would explain the difference between the races. However, as I’ve noted in the past, testosterone levels are high in young black males with low educational attainment (Mazur, 2016). The higher levels of testosterone in blacks compared to whites (which, if you look at figure 1 the levels are not high at all) is accounted for by honor culture, a social variable. Furthermore, the effects of the environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Environmental factors greatly influence testosterone (Booth et al, 2006), so Rushton stating that “socialization cannot account for the early onset” of “physiological differences in testosterone” is clearly wrong since environmental influences can be seen in infants as well as adults. Testosterone is strongly mediated by the environment; this is not up for debate.
Testosterone is one of many important hormones in the body; the races do not differ in the variable. So, therefore, all of Rushton’s ‘r/K predictions’, which literally hinge on testosterone (Lynn, 1990) fall apart without this ‘master switch’ (Rushton, 1999) driving all of these behaviors. Any theories of crime that include testosterone as a main driver in crime need to be rethunk; numerous studies attest to the fact that testosterone does not cause crime. Racial differences in testosterone only appear in small studies and the studies that do show these differences get touted around all the while, all of the better, larger analyses don’t get talked about because it goes against a certain narrative.
Finally, there is no inevitability of a testosterone decrease in older men. So-called “age-related declines” in the hormone are largely explained by smoking, obesity, chronic disease, marital status, and depression (Shi et al, 2013), and even becoming a father explains lower levels of testosterone (Gray, Yang, and Pope, 2006). On top of that, marriage also reduces testosterone, with men who went from unmarried to married showing a sharp decline in testosterone over a ten-year period (Holmboe et al, 2017). This corroborates numerous other studies showing that marriage lowers testosterone levels in men (Mazur and Michalek, 1998; Nansunga et al, 2014) But some of this decrease may be lessened by frequent sexual intercourse (Gettler et al, 2013). So if you live a healthy lifestyle, the testosterone decrease that plagues most men won’t occur to you. The decreases are due to lifestyle changes; not explicitly tied to age.
People are afraid of higher levels of testosterone at a young age and equally as terrified of lowering testosterone levels at an old age. However, I’ve exhasutively shown that testosterone is not the boogeyman, nor the ‘master switch’ (Rushton, 1999) it’s made out to be. There are no ‘genes for’ testosterone; its production is indirect through DNA. Thusly, if you keep an active lifestyle, don’t become obese, and don’t become depressed, you can bypass the so-called testosterone decrease. Fear mongering on both sides of the ‘testosterone curve’ are seriously blown out of proportion. Testosterone doesn’t cause crime, aggression, nor prostate cancer (even then, large meta-analyses show no difference in PCa mortality between blacks and whites).
The fear of the hormone testosterone is due to ignornace of what it does in the body and how it is produced in the body. If people were to understand the hormone, they would not fear it.
The answer to the question of why people are afraid of testosterone is very simple: they do not understand the hormone. People complain about birth rates and spermatogenesis, yet they believe that having high testosterone makes one a ‘savage’ who ‘cannot control their impulses’. However, if you knew anything about the hormone and how it’s vital to normal functioning then you would not say that.
I’ve covered why testosterone does not cause crime by looking at the diurnal variation in the hormone, showing that testosterone levels are highest at 8 am and lowest at 8 pm, while children commit the most crimes at 3 pm and adults at 10 pm. The diurnal variation is key: if testosterone truly did cause crime then rates of crime would be higher in both children and adults in the morning; yet, as can be seen with children, there are increases in amounts of violence committed when they enter school, go to recess, and exit school. This shows why those times are related to the spike in crime in children.
I have wrote a previous article citing a paper by Book et al (2001) in which they meta-analyzed testosterone studies and found that the correlation between testosterone and aggression was .14. However, that estimate is too high since they included 15 studies that should have not been included in the analysis. The true correlation is .08 (Archer, Graham-Kevan, and Davies, 2004). So, clearly, along with the fact that the diurnal variation in testosterone does not correlate with crime spikes, it shows that testosterone has no relationship to the cause of crime; it’s just always at the scene because it prepares the body to deal with a threat. That does not mean that testosterone itself causes crime.
One main reason people fear testosterone and believe that it causes crime and by extension aggressive behavior is because of racial crime disparities. According to the FBI, black Americans by and large commit the most crime, despite being 13 percent of the US population. And since it has been reported that blacks have higher levels of testosterone (Ross et al, 1986; Lynn, 1992; Rushton, 1997; Ellis, 2017), people believe that the supposed higher levels of testosterone that blacks, on average, have circulating in their blood is the ultimate cause of the crime disparities in America between races. Though see above to see why this is not the ultimate cause.
Blacks, contrary to popular belief, don’t have higher levels of testosterone (Gasper et al, 2006; Rohrrman et al, 2007; Lopez et al, 2013; Richard et al, 2014). Even if they did have higher levels, say the 13 percent that is often cited, it would not be the cause of higher rates of crime, nor the cause of higher rates of prostate cancer in blacks compared to whites. What does cause part of the crime differential, in my opinion, is honor culture (Mazur, 2016). The blacks-have-higher-testosterone canard was pushed by Rushton and Lynn to explain both higher rates of prostate cancer and crime in black Americans, however I have shown that high levels of testosterone do not cause prostate cancer (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Looking to testosterone as a ‘master switch’ as Rushton called it is the wrong thing to research because, clearly, the theories of Lynn, Rushton, and Ellis have been rebutted.
People are scared of testosterone because they do not understand the hormone. Indeed, people complain about lower birth rates and lower sperm counts, yet believe that having high testosterone will cause one to be a high T savage. This is seen in the misconception that injecting anabolic steroids causes higher levels of aggression. One study looked at the criminal histories of men who self-reported drug use and steroid use Lundholm et al (2014) who conclude: “We found a strong association between self-reported lifetime AAS use and violent offending in a population-based sample of more than 10,000 men aged 20-47 years. However, the association decreased substantially and lost statistical significance after adjusting for other substance abuse. This supports the notion that AAS use in the general population occurs as a component of polysubstance abuse, but argues against its purported role as a primary risk factor for interpersonal violence. Further, adjusting for potential individual-level confounders initially attenuated the association, but did not contribute to any substantial change after controlling for polysubstance abuse.“
The National Institute of Health (NIH) writes: “In summary, the extent to which steroid abuse contributes to violence and behavioral disorders is unknown. As with the health complications of steroid abuse, the prevalence of extreme cases of violence and behavioral disorders seems to be low, but it may be underreported or underrecognized.” We don’t know whether steroids cause aggression or more aggressive athletes are more likely to use the substance (Freberg, 2009: 424). Clearly, the claims of steroids causing aggressive behavior and crime are overblown and there has yet to be a scientific consensus on the matter. A great documentary on the matter is Bigger, Stronger, Faster, which goes through the myths of testosterone while chronicling the use of illicit drugs in bodybuilding and powerlifting.
People are scared of the hormone testosterone—and by extent anabolic steroids—because they believe the myths of the hulking, high T aggressive man that will fight at the drop of the hat. However, reality is much more nuanced than this simple view and psychosocial factors must also be taken into account. Testosterone is not the ‘master switch’ for crime, nor prostate cancer. This is very simply seen with the diurnal variation of the hormone as well as the peak hours for crime in adolescent and adult populations. The extremely low correlation with aggression and testosterone (.08) shows that aggression is mediated by numerous other variables other than testosterone, and that testosterone alone does not cause aggression, and by extension crime.
People fear things they don’t understand and if people were to truly understand the hormone, I’m sure that these myths pushed by people who are scared of the hormone will no longer persist. Low levels of testosterone are part of the cause of our fertility problems in the West. So does it seem logical to imply that high testosterone is for ‘savages’, when, clearly, high levels of testosterone are needed for spermatogenesis which, in turn, would mean a higher birth rate? Anyone who believes that testosterone causes aggression and crime and that the injection of anabolic steroids causes ‘roid rage’ should do some reading on how the production of the hormone in the body as well as the literature on anabolic steroids. If one wants birth rates to increase in the West, then they must also want testosterone levels to increase as well, since they are intimately linked.
Testosterone does not cause crime and there is no reason to fear the hormone.
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.
Testosterone gets a bad rep. People assume that if one has higher testosterone than average, that they will be a savage, bloodthirsty beast with an insatiable thirst for blood. This, however, is not the case. I’ve documented how testosterone is vital for male functioning, and how higher levels don’t lead to maladies such as prostate cancer. Testosterone is feared for no reason at all. The reason that people are scared of it is that of the anecdotal reports that individual A had higher testosterone when he committed crime B so, therefore, anyone who commits a crime has higher testosterone and that is the ultimate—not proximate—cause of crime. This is erroneous. There is a positive—albeit extremely low—correlation between physical aggression and violence at .14. That’s it. Furthermore, most of these claims of higher levels of testosterone causing violence is extrapolated from animal studies to humans.
Testosterone has been shown to lead to violent and aggressive behavior, largely only in animal studies (Archer, 1991; Book et al, 2001). For years, the relationship between the two variables was thought to be causal, i.e., high levels of testosterone cause violent crimes, which has been called into question over recent years. This is due to how the environment can raise testosterone levels. I have documented how these environmental factors can raise testosterone—and after these events, testosterone stays elevated.
Largely, animal studies are used to infer that high levels of testosterone in and of themselves lead to higher rates of aggression and therefore crime. However, two important meta-analyses show this is not necessarily the case (Archer, 1991; Book et al, 2001). Book et al, 2001 showed that two variables were important in seeing the relationship between aggression and crime—the time of day that the assay was taken and the age of the participant. This effect was seen to be largest in, not unexpectedly, males aged 13-20 (Book et al, 2001: 594). So since age confounds the relationship between aggression and testosterone in males, that is a variable that must also be controlled for (which, in the meta-analyses and other papers I cite on black and white testosterone is controlled for).
More interestingly, Book et al (2001) showed that the nature of the measure of aggression (self-reported or behavioral) did not have any effect on the relationship between testosterone and aggression. Since there is no difference between the two measures, then a pencil-and-paper test is a good enough index of measure of aggression, comparable to observing the behavior of the individual studied.
Archer (1991) also showed the same low—but positive—correlations between aggression and testosterone. Of course, as I’ve extensively documented since there is a positive relationship between the two variables does not necessarily mean that high-testosterone men commit more crime—since the outcome of certain situations can increase and decrease testosterone, no causal factors have been detangled. Book et al (2001) confirmed Archer’s (1991) finding that the correlation between violent and aggressive behavior was positive and low at .14.
Valois et al (2017) showed there was a relationship between emotional self-efficacy (ESE) and aggressive and violent behaviors in a statewide sample of high school children in South Carolina (n=3,386). Their results suggested that there was a relationship between carrying a weapon to school within the past 30 days along with being injured with a club, knife or gun in the past 12 months was significantly associated with ESE for specific race and sex groups.
Black girls who reported a low ESE reported carrying a weapon to school 30 days prior to the survey were 3.22 times more than black girls with a high ESE who did not report carrying a weapon to school within the past 30 days prior to the questionnaire. For black boys with low ESE, they were 3.07 times more likely to carry a weapon to school within the past 30 days in comparison to black boys with high ESE who did not carry a weapon to school in the past 30 days. White girls who reported low ESE had the highest chance of bringing a weapon to school in comparison to white girls with low ESE—they were 5.87 times more likely to carry a weapon to school 30 days prior to the survey. Finally, white boys with low ESE were slightly more than 2 times more likely than white boys with high ESE to carry a weapon to school 30 days prior to the survey.
Low ESE in white and black girls is associated with carrying a weapon to school, whereas low ESE for white and black boys is associated with being threatened. Further, their results suggested that carrying a weapon to school was associated with low ESE in black and white girls suggesting that low ESE is both situation-specific and specific to the female sex. The mediator between these things is low ESE—it is different for both black boys and black girls, and when it occurs different courses of action are taken, whether it’s through bringing a weapon to school or being threatened. What this tells me is that black and white boys with low ESE are more likely to be threatened because they are perceived to be more meek, while black and white girls with low ESE that get provoked at school are more likely to bring weapons. So it seems that girls bring weapons when provoked and boys fight.
The two meta-analyses reviewed above show that there is a low positive (.14) correlation between testosterone and aggression (Archer, 1991; Book et al, 2001). Thusly, high levels of testosterone on their own are not sufficient enough to explain high levels of aggression/violence. Further, there are race- and sex-specific differences when one is threatened at high school with black and white boys being more likely to report being threatened more (which implies a higher rate of physical fighting) while black and white girls when threatened brought weapons to school. These race- and sex-specific differences in the course of action taken when they are physically threatened needs to be looked into more.
I’d like to see the difference in testosterone levels for a matched sample of black and white boys from two neighboring districts with different murder rates as a proxy for the amount of violence in the area. I’d bet that the places with a higher murder rate would have children 1) report more violence and instances of bringing weapons to school and 2) report more harm from these encounters—especially if they have low ESE as seen in Valois (2017) and 3) the children in the high schools along with the residents of the area would have higher testosterone than the place with less violence. I would expect these differences to be magnified in the direction of Valois (2017) in that areas with higher murder rates would have black and white girls report bringing weapons to school when threatened whereas black and white boys would report more physical violence.
High testosterone itself is not sufficient enough to explain violence as the correlation is extremely low at .14. Testosterone levels fluctuate depending on the time of day (Brambilla et al, 2009; Long, Nguyen, and Stevermer, 2015) to the time of year (Stanton, Mullette-Gillman, and Huettel, 2011; Demur, Uslu, and Arslun, 2016). How the genders/races react differently when threatened in adolescence is interesting and deserves further study.