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Steroids get a bad reputation. It largely comes from movies and people’s anecdotal experiences and repeating stories they hear from the media and other forms of entertainment, usually stating that there is a phenomenon called ‘roid rage’ that makes steroid users violent. Is this true? Are any myths about steroids true, such as a shrunken penis? Are there ways to off-set it? Steroids and their derivatives are off-topic for this blog, but it needs to be stressed that there are a few myths that get pushes about steroids and what it does to behavior, its supposed effects on aggression and so forth.
With about 3 million AAS (ab)users (anabolic-androgenic steroids) in America (El Osta et al, 2016), knowing the effects of steroids and similar drugs such as Winny (a cutting agent) would have positive effects, since, of course, athletes mostly use them.
This is, perhaps, one of the most popular. Though the actual myth is that AAS use causes the penis to shrink (which is not true), in reality, AAS use causes the testicles to shrink by causing the Leydig cells to decrease natural testosterone production which then decreases the firmness and shape of the testicles which then results in a loss of size.
In one study of 772 gay men using 6 gyms between the months of January and February (and you need to think of the type of bias there that those people who are ‘Resolutioners’ would be more likely to go to the gym those months), a questionnaire was given to the men. 15 .2 percent of the men had used, with 11.7 percent of them injecting within the past 12 months. HIV positive men were more likely to have used in the past compared to negative men (probably due to scripts). Fifty-one percent of them reported testicular atrophy, and they were more likely to report suicidal thoughts (Bolding, Sherr, and Elford, 2002). They conclude:
One in seven gay men surveyed in central London gyms in 2000 said they had used steroids in the previous 12 months. HIV positive men were more likely to have used steroids than other men, some therapeutically. Side effects were reported widely and steroid use was associated with having had suicidal thoughts and feeling depressed, although cause and effect could not be established. Our findings suggest that steroid use among gay men may have serious consequences for both physical and mental health.
Of course, those who (ab)use substances have more psychological problems than those who do not. Another study of 203 bodybuilders found that 8 percent (n = 17) found testicular atrophy (for what it’s worth, it was an internet survey of drug utilization) (Perry et al, 2005). Another study found that out of 88 percent of individuals who abused the drug complained of side-effects of AAS use, about 40 percent described testicular atrophy (Evans, 1997), while testicular atrophy was noted in about 50 percent of cases (sample size n = 24) (Darke et al, 2016).
One study of steroid users found that only 17 percent of them had normal sperm levels (Torres-Calleja et al, 2001), this is because exogenous testosterone will result in the atrophy of germinal cells which cause a decrease in spermatogenesis. Though, too, increased AAS (ab)use later into life may lead to infertility later in life. Knuth et al (1989) also studied 41 bodybuilders with an average age of 26.7. They went through a huge laundry list of different types of steroids they have taken over their lives. Nineteen of the men were still using steroids at the time of the investigation (group I), whereas 12 of them (group II) stopped taking steroids 3 months prior, while 10 of them (group III) stopped steroid use 4 to 24 months prior.
They found that only 5 of them had sperm counts below the average of 20 million sperm per square ml, while 24 of the bodybuilders showed these symptoms. No difference between group I and II was noticed and group III (the group that abstained from use for 4 to 24 months) largely had sperm levels in the normal range. So, the data suggests that even in cases of severe decrease of sensitivity to androgens due to AAS (ab)use, spermatogenesis may still continue normally in some men, even when high levels of androgens are administered exogenously, while even after prolonged use it seems it is possible for sperm levels to go back to the normal range (Knuth et al 1989).
Aggression and crime
Now it’s time for the fun part and my reason for writing this article. Does (ab)using steroids cause someone to go into an uncontrollable rage, a la the Incredible Hulk when they inject themselves with testosterone? The media has latched into the mind of many, with films and TV shows showing the insanely aggressive man who has been (ab)using AAS. But how true is this? A few papers have shown that this phenomenon is indeed true (Konacher and Workman, 1989; Pope and Katz, 1994), but how true is it on its own, since AAS (ab)users are known to use multiple substances???
Konacher and Workman (1989) is a case study done on one man who had no criminal history, who began taking AASs three months before he murdered his wife, and they conclude that AAS can be said to be a ‘personality changer’. Piacetino et al (2015) conclude in their review of steroid use and psychopathology in athletes that “AAS use in athletes is associated with mood and anxiety disturbances, as well as reckless behavior, in some predisposed individuals, who are likely to develop various types of psychopathology after long-term exposure to these substances. There is a lack of studies investigating whether the preexistence of psychopathology is likely to induce AAS consumption, but the bulk of available data, combined with animal data, point to the development of specific psycho-pathology, increased aggressiveness, mood destabilization, eating behavior abnormalities, and psychosis after AAS abuse/dependence.” I, too, would add that since most steroid abuse are polysubstance abusers (they use multiple illicit drugs on top of AAS), that the steroids per se are not causing crime or aggressive behavior, it’s the other drugs that the steroid (ab)user is also taking. And there is evidence for this assertion.
Lundholm et al (2015) showed just that: that AAS (ab)use was confounded with other substances used while the individual in question was also taking AAS. They write:
“We found a strong association between self-reported lifetime AAS use and violent offending in a population-based sample of more than 10,000 men aged 20-47 years. However, the association decreased substantially and lost statistical significance after adjusting for other substance abuse. This supports the notion that AAS use in the general population occurs as a component of polysubstance abuse, but argues against its purported role as a primary risk factor for interpersonal violence. Further, adjusting for potential individual-level confounders initially attenuated the association, but did not contribute to any substantial change after controlling for polysubstance abuse.“
Even The National Institute of Health (NIH) writes: “In summary, the extent to which steroid abuse contributes to violence and behavioral disorders is unknown. As with the health complications of steroid abuse, the prevalence of extreme cases of violence and behavioral disorders seems to be low, but it may be underreported or underrecognized.” We don’t know whether steroids cause aggression or more aggressive athletes are more likely to use the substance (Freberg, 2009: 424). Clearly, the claims of steroids causing aggressive behavior and crime are overblown and there has yet to be a scientific consensus on the matter. A great documentary on the matter is Bigger, Stronger, Faster, which goes through the myths of testosterone while chronicling the use of illicit drugs in bodybuilding and powerlifting.
This, too, was even seen in one study where men were administered supraphysiologic doses of testosterone to see its effects on muscle size and strength since it had never been tested; no changes in mood or behavior occurred (Bhasin et al, 1996). Furthermore, injecting individuals with supraphysiological doses of testosterone as high as 200 and 600 mg per week does not cause heightened anger or aggression (Tricker et al, 1996; O’Connor et, 2002). Testosterone is one of the most abused AASs around, and if a heightened level of T doesn’t cause crime, nor can testosterone levels being higher this week compared to last seem to be a trigger for crime, we can safely disregard any claims of ‘roid rage’ since they coincide with other drug use (polysubstance abuse). So since we know that supraphysiologic doses of testosterone don’t cause crime nor aggression, we can say that AAS use, on its own (and even with other drugs) does not cause crime or heightened aggression since aggression elevates testosterone secretion, testosterone doesn’t elevate aggression.
One review also suggests that medical issues associated with AAS (ab)use are exaggerated to deter their use by athletes (Hoffman and Ratamess, 2006). They conclude that “Existing data suggest that in certain circumstances the medical risk associated with anabolic steroid use may have been somewhat exaggerated, possibly to dissuade use in athletes.”
Racial differences in steroid use
Irving et al (2002) found that 2.1 percent of whites used steroids, whereas 7.6 percent of blacks did; 6.1 percent of ‘Hispanics’ use them within the past 12 months, and a whopping 14.1 percent of Hmong Chinese used them; 7.9 percent of ‘other Asians’ used them, and 3,1 percent of ‘Native Americans’ did with 11.3 percent of mixed race people using them within the past 12 months to gain muscle. Middle schoolers were more likely to use than high schoolers, while people from lower SES brackets were more likely to use than people in higher SES brackets.
Stilger and Yesalis (1999: 134) write (emphasis mine):
Of the 873 high school football players participating in the study, 54 (6.3%) reported having used or currently using AAS. Caucasians represented 85% of all subjects in the survey. Nine percent were African-American while the remainder (6%) consisted of Hispanics, Asian, and other. Of the AAS users, 74% were Caucasian, 13% African American, 7% Hispanic, and 3% Asian, x2 (4,854 4) 4.203, p 4 .38. The study also indicated that minorities are twice as likely to use AAS as opposed to Caucasians. Cross tabulated results indicate that 11.2% of all minorities use/used AAS as opposed to 6.5% of all Caucasians (data not displayed).
One study even had whites and blacks reporting the same abuse of steroids in their sample (n = 10,850 ‘Caucasians’ and n = 1,883 black Americans), with blacks reporting, too, lower levels of other drug abuse (Green et al, 2001). Studies indeed find higher rates of drug use for white Americans than other ethnies, in college (McCabe et al, 2007). Black Americans also frequently underreport and lie about their drug use (Ledgerwood et al, 2008; Lu et al, 2001). Blacks are also more likely to go to the ER after abusing drugs than whites (Drug Abuse Warning Network, 2011). Bauman and Ennett (1994) also found that blacks underreport drug use whereas whites overreport.
So can we really believe the black athletes who state that they do not (ab)use AAS? No, we cannot. Blacks like about any and all drug use, so believing that they are being truthful about AAS (ab)use in this specific instance is not called for.
Like with all things you use and abuse, there are always side-effects. Though, the media furor one hears regarding AAS and testosterone (ab)use are largely blown out of proportion. The risks associated with AAS (ab)use are ‘transient’, and will subside after one discontinues using the drugs. Blacks seem to take more AAS than whites, even if they do lie about any and all drug use. (And other races, too, seem to use it at higher rates than whites.) Steroid use does not seem to be ‘bad’ if one knows what they’re doing and are under Doctor’s supervision, but even then, if you want to know the truth about AAS, then you need to watch the documentary Bigger, Stronger, Faster. I chalk this up to the media themselves demonizing testosterone itself, along with the ‘toxic masculinity’ and the ‘toxic jock effect‘ (Miller, 2009; Miller, 2011). Though, if you dig into the literature yourself you’ll see there is scant evidence for AAS and testosterone (ab)use causing crime, that doesn’t stop papers like those two by Miller talking about the effects of ‘toxic jocks’ and in effect, deriding masculine men and with it the hormone that makes Men men: testosterone. If taken safely, there is nothing wrong with AAS/testosterone use.
(Note: Doctor’s supervision only, etc)
A recent paper was published on the origins of Native Americans titled Terminal Pleistocene Alaskan genome reveals first founding population of Native Americans (Moreno-Mayar et al, 2018). An infant genome was studied and it was found that group of people the infant belonged to was similar to modern Native Americans but not a direct ancestor. The infant’s group and modern Native Americans share the same common ancestors, however. This, of course, supports the hypothesis that Native Americans are descended from Asian migrants.
The infant is also related to both North and South Natives, which implies they’re descended from a single migration. (Though I am aware of a hypothesis that states that there were three waves of migration into the Americas from Beringia, along with back migrations from South America back into Asia.)
Moreno-Mayar et al (2018) write in the abstract: “Our findings further suggest that the far-northern North American presence of northern Native Americans is from a back migration that replaced or absorbed the initial founding population of Ancient Beringians.” And they conclude (pg 5):
The USR1 results provide direct genomic evidence that all Native Americans can be traced back to the same source population from a single Late Pleistocene founding event. Descendants of that population were present in eastern Beringia until at least 11.5 ka. By that time, however, a separate branch of Native Americans had already established itself in unglaciated North America, and diverged into the two basal groups that ultimately became the ancestors of most of the indigenous populations of the Americas.
This is a highly interesting paper which shows that, as we’ve known for decades, that the ancestors of the Native Americans crossed the Bering Land Bridge around 11 kya. Though, my reason for writing this article is not for this very interesting paper, but the ‘conclusions’ that people that people are drawing from it.
Of course, whenever a study like this gets published you get a whole slew of people who read the popular articles on the matter and don’t read the actual journal article. The problem here is that some people took the chance to attempt to say that this paper showed that the origins of Man were in Europe, not Africa as can be seen in the tweet below.
“…represent a growing body of evidence being discovered across the world that suggests the origins of the human race may have been Europe and not Africa as once believed.”
So I read the paper, read it again and even cntrl f’d it and didn’t see the phrase. So where did the phrase come from?
I did some digging and I found the source for the quote, which, of course, was not in the Nature article. The quote in question comes from an article titled Scientists discover DNA proving original Native Americans were White. Oh, wow. Isn’t that interesting? Maybe he read a different paper then I did.
The author stated that the infant was “more closely related to modern white Europeans“, though of course this too wasn’t stated anywhere in the article. He also quoted an evolutionary biologist who stated “This is a new population of Native Americans — the white Native American.” Wow, this is interesting. Now let’s look at what else this author writes:
Working with scientists at the University of Alaska and elsewhere, Willerslev compared the genetic makeup of the baby, named Xach’itee’aanenh t’eede gaay or “sunrise child-girl” by the local community, with genomes from other ancient and modern people. They found that nearly half of the girls DNA came from the ancient North Europeans who lived in what is no Scandinavia. The rest of her genetic makeup was a roughly even mixed of DNA now carried by northern and southern Native Americans. Using evolutionary models, the researchers showed the ancestors of the first Native Americans started to emerge as a distinct population about 35,000 years ago.
Isn’t that weird? This is nowhere in the original article. So I did some digging and what do I find? I found that the author of this article literally plagiarized almost word for word from another article from The Guardian!
Working with scientists at the University of Alaska and elsewhere, Willerslev compared the genetic makeup of the baby, named Xach’itee’aanenh t’eede gaay or “sunrise child-girl” by the local community, with genomes from other ancient and modern people. They found that nearly half of the girls DNA came from the ancient north Eurasians who lived in what is now Siberia. The rest of her genetic makeup was a roughly even mixed of DNA now carried by northern and southern Native Americans.
Using evolutionary models, the researchers showed the ancestors of the first Native Americans started to emerge as a distinct population about 35,000 years ago.
This is not only an example of straight up plagiarism, the author of the other article literally only switched “Siberia” with “Scandinavia” and “ancient north Eurasians” with “ancient North Europeans”. Ancient north Eurasians are NOT WHITE! Where do you gather this from?! There is NO INDICATION that they were ‘ancient north Europeans!
In sum, if you ever see articles like this that purport to show that Native Americans were white European and that it supposedly calls the OoA model into question, always ALWAYS check the claims and don’t fall for plagiarist bullshit. This is truly incredible that not only did the author literally copy and past a full article, he also snipped a few words to fit the narrative he was pushing! I will be notifying the author of the Guardian article of this plagiarism. You can check it out yourself, read the first article cited above then read the Guardian article. Do people really think they can get away with literally plagiarizing and article like that word for word?
This article is on a whole other level compared to the claims that modern Man began in Europe and that a few teeth upend the OoA model. This guy didn’t even read the paper, it seems like he read the Guardian article and then copy and pasted it and changed a few words for his own ‘gain’ to ‘show’ that the first Native Americans were white. There is no way that one can interpret this paper in this manner if they’ve truly read and understood it. Always, always read original journal articles and, if you must read popular science articles then read it from a reputable website, not kooky websites with an agenda to push who literally plagiarize other people’s work. You can tell who’s gullible and who’s not just by what they say about new papers that can possibly be misinterpreted.
Ryan Faulk, like most IQ-ists, believes that the correlation with job performance and IQ somehow is evidence for its validity. He further believes that because self- and peer-ratings correlate with one’s IQ scores that that is further evidence for IQ’s validity.
Well too bad for Faulk, correlations with other tests and other IQ tests lead to circular assumptions. The first problem, as I’ve covered before, is that there is no agreed-upon model or description of IQ/intelligence/’g’ and so therefore we cannot reliably and truthfully state that differences in ‘g’ this supposed ‘mental power’ this ‘strength’ is what causes differences in test scores. Unfortunately for Ryan Faulk and other IQ-ists, again, coming back to our good old friend test construction, it’s no wonder that IQ tests correlate around .5—or so is claimed—with job performance, however IQ test scores correlate at around .5 with school achievement, which is caused by some items containing knowledge that has been learned in school, such as “In what continent is Egypt?” and Who wrote Hamlet?” and “What is the boiling point of water?” As Ken Richardson writes in his 2017 book Genes, Brains, and Human Potential: The Science and Ideology of Intelligence (pg 85):
So it should come as no surprise that performance on them [IQ tests] is associated with school performance. As Robert L. Thorndike and Elizabeth P. Hagen explained in their leading textbook, Educational and Psychological Measurement, “From the very way in which the tests were assembled [such correlation] could hardly be otherwise.”
So, obviously, neither of the two tests determine independently that they measure intelligence, this so-called innate power, and because they’re different versions of the same test there is a moderate correlation between them. This goes back to item analysis and test construction. Is it any wonder, then, why correlations with IQ and achievement increase with age? It’s built into the test! And while Faulk does cite high correlations from one of Schmidt and Hunter’s meta-analyses on the subject, what he doesn’t tell you is that one review found a correlation of .66 between teacher’s assessment and future achievement of their students later in life (higher than the correlation with job performance and IQ) (Hoge and Coladarci, 1989.) They write (pg 303): “The median correlation, 0.66, suggests a moderate to strong correspondence between teacher judgments and student achievement.” This is just like what I quoted the other day in my response to Grey Enlightenment where I quoted Layzer (1972) who wrote:
Admirers of IQ tests usually lay great stress on their predictive power. They marvel that a one-hour test administered to a child at the age of eight can predict with considerable interest whether he will finish college. But as Burt and colleagues have clearly demonstrated, teachers subjective assessments afford even more reliable predictors. This is almost a truism.
So the correlation of .5 between occupation level and IQ is self-fulfilling, which are not independent measures. In regard to the IQ and job performance correlation, which I’ve discussed in the past, studies in the 70s showed much lower correlations, between .2 and .3, which Jensen points out in The g Factor.
The problem with the so-called validity studies carried out by Schmidt and Hunter, as cited by Ryan Faulk, is that they included numerous other tests that were not IQ tests in their analysis like memory tests, reading tests, the SAT, university admission tests, employment selection tests, and a variety of armed forces tests. “Just calling these “general ability tests,” as Schmidt and Hunter do, is like reducing a diversity of serum counts to a “general. blood test” (Richardson, 2017: 87). Of course the problem with using vastly different tests is that they tap into different abilities and sources of individual differences. The correlation between SAT scores and high school grades is .28 whereas the correlation between both the SAT and high school grades and IQ is about .2. So it’s clearly not testing the same “general ability” that’s being tested.
Furthermore, regarding job performance, it’s based on one measure: supervisor ratings. These ratings are highly subjective and extremely biased with age and halo effects seen with height and facial attractiveness being seen to sway judgments on how well one works. Measures of job performance are unreliable—especially from supervisors—due to the assumptions and biases that go into the measure.
Do IQ tests test neural processes? Not really. One of the most-studied variables is reaction time. The quicker they react to a stimulus, supposedly, the higher their IQ is in average as they are quicker to process information, the story goes. Detterman (1987) notes that other factors other than ‘processing speed’ can explain differences in reaction time, including but not limited to, stress, understanding instructions, motivation to do said task, attention, arousal, sensory acuity, confidence, etc. Khodadadi et al (2014) even write “The relationship between reaction time and IQ is too complicated and reveal a significant correlation depends on various variables (e.g. methodology, data analysis, instrument etc.).” Complex cognition in real life is also completely different than the simple questions asked in the Raven (Richardson and Norgate, 2014).
It is easy to look at the puzzles that make up IQ tests and be convinced that they really do test brain power. But then we ignore the brain power thst nearly everyone displays in their everyday lives. Some psychologists have noticed thst people who stumble over formal tests of cognitive can bangle highly complex problems in their real lives all the time. As Michael Eysenck put it in his well-known book Psychology, “There is an apparent contradiction between our ability to deal effectively with out everyday environment and our failure to perform well on many laboratory reasoning tasks.” We can say the same about IQ tests.
Real-life problems combine many more variables that change over time and interact. It seems that the ability to do pretentious problems in a pencil-and-paper (or computer) format, like IQ test items, is itself a learned, if not-so-complex skill. (Richardson, 2017: 95-96)
Finally, Faulk cites studies showing that how intelligent people and their peers rates themselves and others predicted how well they did on IQ tests. This isn’t surprising. Since they correlate with academic achievement at .5 then if one is good academically then they’d have a high test score more often than not. That friends rate friends high and they end up matching scores is no surprise either as people generally group together with other people like themselves and so therefore will have similar achievements. That is not evidence for test validity though!! See Richardson and Norgate (2015) “In scientific method, generally, we accept external, observable differences as a valid measure of an unseen function when we can mechanistically relate differences in one to diffences in the other …” So even Faulk’s attempt to ‘validate’ IQ tests using peer- and self-ratings of ‘intelligence’ (whatever that is) falls on its face since its not a true measure of validity. It’s not construct validity. (EDIT: Psychological constructs are validated ‘by testing whether they relate to measures of other constructs as specified by theory‘ (Strauss and Smith, 2009). This doesn’t exist for IQ therefore IQ isn’t construct valid.)
In sum, Faulk’s article leaves a ton to be desired and doesn’t outright prove that there is validity to IQ tests because, as I’ve shown in the past, validity for IQ is nonexistent, though some have tried (using correlations with job performance as evidence) but Richardson and Norgate (2015) take down those claims and show that the correlation is between .2 and .3, not the .5+ cited by Hunter and Schmidt in their ‘validation studies’. The criteria laid out by Faulk does not prove that there is true construct validity to IQ tests and due to test construction, we see these correlations with educational achievement.
The word ‘construct’ is defined as “an idea or theory containing various conceptual elements, typically one considered to be subjective and not based on empirical evidence.” Whereas the word ‘validity’ is defined as “the quality of being logically or factually sound; soundness or cogency.” Is there construct validity for IQ tests? Are IQ tests tested against an idea or theory containing various conceptual elements? No, they are not.
Cronbach and Meehl (1955) define construct validity, which they state is “involved whenever a test is to be interpreted as a measure of some attribute or quality which is not “operationally defined.”” Though, the construct validity for IQ tests has been fleeting to investigators. Why? Because there is no theory of individual IQ differences to test IQ tests on. It is even stated that “there is no accepted unit of measurement for constructs and even fairly well-known ones, such as IQ, are open to debate.” The ‘fairly well-known ones’ like IQ are ‘open to debate’ because no such validity exists. The only ‘validity’ that exists for IQ tests is correlations with other tests and attempted correlations with job performance, but I will show that that is not construct validity as is classicly defined.
Construct validity can be easily defined as the ability of a test to measure the concept or construct that it is intended to measure. We know two things about IQ tests: 1) they do not test ‘intelligence’ (but they supposedly do a ‘good enough job’ so that it does not matter) and 2) it does not even test the ‘construct’ that it is intended to measure. For example, the math problem ‘1+1’ is construct valid regarding one’s knowledge and application of that math problem. Construct validity can pretty much be summed up as the proof that it is measuring what the test intends…but where is this proof? It is non-existent.
Richardson (1998: 116) writes:
Psychometrists, in the absence of such theoretical description, simply reduce score differences, blindly to the hypothetical construct of ‘natural ability’. The absence of descriptive precision about those constructs has always made validity estimation difficult. Consequently the crucial construct validity is rarely mentioned in test manuals. Instead, test designers have sought other kinds of evidence about the valdity of their tests.
The validity of new tests is sometimes claimed when performances on them correlate with performances on other, previously accepted, and currently used, tests. This is usually called the criterion validity of tests. The Stanford-Binet and the WISC are often used as the ‘standards’ in this respect. Whereas it may be reassuring to know that the new test appears to be measuring the same thing as an old favourite, the assumption here is that (construct) validity has already been demonstrated in the criterion test.
Some may attempt to say that, for instance, biological construct validity for IQ tests may be ‘brain size’, since brain size is correlated with IQ at .4 (meaning 16 percent of the variance in IQ is explained by brain size). However, for this to be true, someone with a larger brain would always have to be ‘more intelligent’ (whatever that means; score higher on an IQ test) than someone with a smaller brain. This is not true, so therefore brain size is not and should not be used as a measure of construct validity. Nisbett et al (2012: 144) address this:
Overall brain size does not plausibly account for differences in aspects of intelligence because all areas of the brain are not equally important for cognitive functioning.
For example, breathalyzer tests are construct valid. There is a .93 correlation (test-retest) between 1 ml/kg bodyweight of ethanol in 20, healthy male subjects. Furthermore, obtaining BAC through gas chromatography of venous blood, the two readings were highly correlated at .94 and .95 (Landauer, 1972). Landauer (1972: 253) writes “the very high accuracy and validity of breath analysis as a correct estimate of the BAL is clearly shown.” Construct validity exists for ad-libitum taste tests of alcohol in the laboratory (Jones et al, 2016).
There is a casual connection between what one breathes into the breathalyzer and his BAC that comes out of the breathalyzer and how much he had to drink. For example, for a male at a bodyweight of 160 pounds, 4 drinks would have him at a BAC of .09, which would make him unfit to drive. (‘One drink’ being 12 oz of beer, 5 oz of wine, or 1.25 oz of 80 proof liquor.) He drinks more, his BAC reading goes up. Someone is more ‘intelligent’ (scores higher on an IQ test), then what? The correlations obtained from so-called ‘more intelligent people’, like glucose consumption, brain evoked potentials, reaction time, nerve conduction velocity, etc have never been shown to determine higher ‘ability’ to score higher on IQ tests. That, too, would not even be construct validation for IQ tests, since there needs to be a measure showing why person A scored higher than person B, which needs to hold one hundred percent of the time.
Another good example of the construct validity of an unseen construct is white blood cell count. White blood cell count was “associated with current smoking status and COPD severity, and a risk factor for poor lung function, and quality of life, especially in non-currently smoking COPD patients. The WBC count can be used, as an easily measurable COPD biomarker” (Koo et al, 2017). In fact, the PRISA II test has white blood cell count in it, which is a construct valid test. Even elevated white blood cell count strongly predicts all-cause and cardiovascular mortality (Johnson et al, 2005). It is also an independent risk factor for coronary artery disease (Twig et al, 2012).
A good example of tests supposedly testing one thing but testing another is found here:
As an example, think about a general knowledge test of basic algebra. If a test is designed to assess knowledge of facts concerning rate, time, distance, and their interrelationship with one another, but test questions are phrased in long and complex reading passages, then perhaps reading skills are inadvertently being measured instead of factual knowledge of basic algebra.
Numerous constructs have validity—but not IQ tests. It is assumed that they test ‘intelligence’ even though an operational definition of intelligence is hard to come by. This is important, as if there cannot be an agreement on what is being tested, how will there be construct validity for said construct in question?
Richardson (2002) writes that Detterman and Sternberg sent out a questionnaire to a group of theorists which was similar to another questionnaire sent out decades earlier to see if there was an agreement on what ‘intelligence’ is. Twenty-five attributes of intelligence were mentioned. Only 3 were mentioned by more than 25 percent of the respondents, with about half mentioning ‘higher level components’, one quarter mentioned ‘executive processes’ while 29 percent mentioned ‘that which is valued by culture’. About one-third of the attributes were mentioned by less than 10 percent of the respondents with 8 percent of them answering that intelligence is ‘the ability to learn’. So if there is hardly any consensus on what IQ tests measure or what ‘intelligence’ is, then construct validity for IQ seems to be very far in the distance, almost unseeable, because we cannot even define the word, nor actually test it with a test that’s not constructed to fit the constructors’ presupposed notions.
Now, explaining the non-existent validity of IQ tests is very simple: IQ tests are purported to measure ‘g’ (whatever that is) and individual differences in test scores supposedly reflect individual differences in ‘g’. However, we cannot say that it is differences in ‘g’ that cause differences in individual test scores since there is no agreed-upon model or description of ‘g’ (Richardson, 2017: 84). Richardson (2017: 84) writes:
In consequence, all claims about the validity of IQ tests have been based on the assumption that other criteria, such as social rank or educational or occupational acheivement, are also, in effect, measures of intelligence. So tests have been constructed to replicate such ranks, as we have seen. Unfortunately, the logic is then reversed to declare that IQ tests must be measures of intelligence, because they predict school acheivement or future occupational level. This is not proper scientific validation so much as a self-fulfilling ordinance.
Construct validity for IQ does not exist (Richardson and Norgate, 2015), unlike construct validity for breathalyzers (Landauer, 1972) or white blood cell count as a disease proxy (Wu et al, 2013; Shah et al, 2017). So, if construct validity is non-existent, then that means that there is no measure for how well IQ tests measure what it’s ‘purported to measure’, i.e., how ‘intelligent’ one is over another because 1) the definition of ‘intelligence’ is ill-defined and 2) IQ tests are not validated against agreed-upon biological models, though some attempts have been made, though the evidence is inconsistent (Richardson and Norgate, 2015). For there to be true validity, evidence cannot be inconsistent; it needs to measure what it purports to measure 100 percent of the time. IQ tests are not calibrated against biological models, but against correlations with other tests that ‘purport’ to measure ‘intelligence’.
(Note: No, I am not saying that everyone is equal in ‘intelligence’ (whatever that is), nor am I stating that everyone has the same exact capacity. As I pointed out last week, just because I point out flaws in tests, it does not mean that I think that people have ‘equal ability’, and my example of an ‘athletic abilities’ test last week is apt to show that pointing out flawed tests does not mean that I deny individual differences in a ‘thing’ (though athletic abilities tests are much better with no assumptions like IQ tests have.))
Different races have different morphology/somatype. Therefore, we can reason that different races would fare better or worse at a certain lift depending on their limb length, such as leg length, arm length, torso length and so on. How do somatypic differences lead to differences in strength between the races on the Big Four lifts? The four lifts I will cover are bench press, deadlift, squat and overhead press.
East Asians have higher levels of body fat (for instance the Chinese, Wang et al, 2011) and have lower BMIs, yet higher levels of body fat (Wang et al, 1994). This, along with their somatype are part of the reason why they excel in some strength sports. Since East Asians have a smaller stature, averaging about 5 feet 8 inches, with shorter arms and legs. Thinking about how the ancestors of the East Asians evolved, this makes sense: they would have needed to be shorter and have shorter limbs as it is easier to warm a body with a smaller surface area. Therefore, while squatting they have a shorter path to travel with the bar on their back. East Asians would strongly excel at the squat, and if you watch these types of competitions, you’d see them strongly overrepresented—especially the Chinese.
African-Americans are descended from West African slaves, and so they have longer, thinner limbs with lower amounts of body fat on average (especially if they have more African ancestry), which is a classic sign of a mesomorphic phenotype. They do also skew ecto, which is useful in the running competitions they dominate (in the case of West Africans and descendants and certain tribes of Kenyans and Ethiopians). Either way, due to their long limbs and a short torso, they have to travel further with the weight therefore here they suffer and wouldn’t be as strong as people who have a long torso with shorter limbs.
Like East Asians, Europeans have similar morphology—skewing ectomorphic, the somatype that dominates strength competitions. Having a long torso with shorter limbs and more type I than type II fibers, they would then be able to lift more, especially since these competitors keep a high body fat percentage. Again, like with East Asians, there is a biomechanical advantage here and due to their higher levels of body fat and endomorphic somatype along with shorter limbs, they would be able to move more weight on the squat, especially more than African-Americans. Biomechanics is key when it comes to evaluating different groups’ morphology when attempting to see who would be stronger on average.
The deadlift is pretty straightforward: bending down and deadlifting the weight off of the ground. Key anatomic differences between the races dictate who would be better here. East Asians, with shorter limbs and a longer torso the bar has to travel a further path, compared to someone with longer limbs and shorter torso. Though, someone with short limbs and a short torso would also have a biomechanical advantage in pulling, it is nothing like if one has long arms and a short torso.
Here is where they would shine. Their anatomy is perfect for this lift. Since they have longer limbs and a shorter torso, the bar has a shorter path to travel to reach the endpoint of the lift. At the set-up of the lift, they already have a biomechanical advantage and they can generate more power in the lift due to their leverage advantage. The deadlift favors people with a long torso, short femurs, and long arms, and so it would favor African-Americans. (Their long arms off-sets their short torsos, though the bar would still have to travel further, they still would have the ability to move more weight.)
European Americans would have the same biomechanical problems as East Asians, but not as much since they have a taller stature. It is well-known in the world of weightlifting that having shorter, ‘T-rex arms’ impedes strength on the lift, since speaking from an anatomic viewpoint, they are just not built for it. No style of deadlift (the sumo or conventional) suits people with short arms, and so they are already at a biomechanical disadvantage. Relative to African-Americans, European Americans have ‘T-rex arms’ and therefore they would suffer at pulling exercises—deadlift included.
The overhead press is where people with shorter arms would excel. Thus, East Asians would be extremely strong pushers. Say the bar starts at the top of their chest, the path of the bar to the lockout would be shorter than if someone had longer arms. The size of the trapezius muscles also comes into play here, and people with larger trapezius muscles have a stronger press. The East Asians short stature and therefore shorter limbs is perfect for this lift and why they would excel.
African-Americans would suffer at the overhead press for one reason: their long limbs, mainly their arms. The bar has a further path to travel and thus strength would be impeded. Indeed, people not built for pressing have long arms, long torsos, and long legs. Performing the full range of motion, African-Americans would have less strength than East Asians and European Americans.
Again, due to similar morphology as East Asians, they, too, would excel at this lift. Since the lift is completed when the arms lock out, those with shorter arms would be able to move more weight and so what hurts them on the deadlift helps on pressing movements like the overhead press.
Lastly, the bench press. East Asians would excel here as well since they have shorter arms and the bar would have a shorter path to travel. Notice anything with bar movement? That’s a key to see which group would be stronger on average: looking at the average morphology of the races and then thinking about how the lift is performed, you can estimate who would be good at which lift and why. The bench press would favor someone with a shorter stature and arms, and they’d be able to lift more weight. (I personally have long arms compared to my body and my bench press suffers compared to my deadlift.) However, Caruso et al (2012) found that body mass is a more important predictor of who would excel at the bench press. East Asians have a higher body fat percentage, and therefore would be stronger on average in the lift.
Here, too, African-Americans will suffer. Like with the overhead press, the bar has a further path to travel. They also have less body fat on average and that would also have the bar travel more, having the individual put more exertion into the lift compared to someone who had shorter arms. The longer your arms are in a pushing exercise, the further the bar has to travel until lockout. Thus you can see that people with longer arms would suffer in the strength department compared to people with shorter arms, but this is reversed for pulling exercises like the deadlift described above. (There is also a specific longitudinal study on black-white differences in bench press which I will cover in the ‘Objections‘ section.)
Again, like with East Asians due to similar somatype, European Americans, too, would excel at this lift. They are able to generate more pound-for-pound power in the lift. The bar also has a shorter path to travel and since the people who compete in these competitions also have higher levels of body fat, then the bar has less of a distance to travel, thus increasing the amount of force the muscle can generate. Limb size/body mass/somatype predict how races/individuals would do on specific lifts.
One of the main objections that some may have is that one longitudinal study on black and white police officers found that blacks were stronger than whites at the end of the study (Boyce et al, 2014). However, I heavily criticized this paper at the beginning of the year and for good reason: heights of the officers weren’t reported (which is not the fault of the researchers but of an ongoing lawsuit at that department since people complained that they were discriminating against people based on height). The paper is highly flawed, but looking at it on face value someone who does not have the requisite knowledge they would accept the paper’s conclusions at face value. One of the main reasons for my criticism of the paper is that the bench press was tested on a Smith machine, not a barbell bench press. Bench pressing on the Smith machine decreases stability in the biceps brachii (Saterbakken et al, 2011) but there is similar muscle recovery between different bench presses in trained men (Smith, barbell, and dumbbell) (Ferreira et al, 2016). This does not affect my overall critique of Boyce et al (2014) however, since you can move more weight than you would normally be able to, along with the machine being on one plane of motion so everyone has to attempt to get into the same position to do the lift and we know how that is ridiculous due to individual differences in morphology.
Some may point to hand-grip tests, which I have written about in the past, and state that ‘blacks are stronger’ based on hand-grip tests. Just by looking at the raw numbers you’d say that blacks had a stronger grip. However, to get an idea of the strength differences pound-for-pound there is a simple formula: weight lifted/bodyweight=how strong one is pound-for-pound on a certain exercise. So using the values from Araujo et al (2010), for blacks we have a grip strength of 89.826 with an average weight of 193 pounds. Therefore pound-for-pound strength comes out to .456. On the other hand, for Europeans, they had an average grip strength of 88.528 pounds with an average weight of 196 pounds, so their pound-for-pound grip strength is about .452, which, just like African-Americans is almost half of their body weight. One must also keep in mind that these hand-grip studies are done on older populations. I have yet to come across any studies on younger populations that use the big four lifts described in this article and seeing who is stronger, so inferences are all that we have.
Further, Thorpe et al (2016) also show how there is an association between household income and grip-strength—people who live in homes with higher incomes have a stronger grip, with blacks having a stronger grip than whites. Thorpe et al (2016) showed that black women had a stronger grip strength than white women, whereas for black men they only had a stronger grip than white men at the highest SES percentile. This could imply nutrient deficiencies driving down their ability for increases grip strength, which is a viable hypothesis. Although Thorpe et al (2016) showed that black men had a stronger grip strength, these results conflict with Haas, Krueger, and Rohlfson (2012) though the disparities can be explained by the age of both cohorts.
Nevertheless, grip strength—as well as overall strength—is related to a higher life expectancy (Ruiz et al, 2008; Volkalis, Haille, and Meisinger, 2015). If blacks were stronger—and this is being debated with studies like hand-grip—then we should expect to see black men living longer than white men, however, we see the opposite. Black men die earlier than white men, and it just so happens that the diseases that are correlated with strength and mortality are diseases that blacks are more likely to get over whites. One should think about this if they’re entertaining the idea that blacks have an inherent strength advantage over whites.
Others may argue that since chimpanzees have a higher proportion of type II fibers and that’s one reason why they are stronger than us by 1.35 times (O’Neill et al, 2017) and have the ability to rip our faces off. Of course, other factors are at play here other than the chimps’ fast twitch fiber content. Of course, one must also think of the chimpanzee’s way smaller stature when discussing their overall strength. It’s not just their type II fibers, but how much smaller they are which gives them the ability to generate more force pound-for-pound in comparison to humans. So this is a bad example to attempt to show that blacks are stronger than whites based solely on the composition of the muscle fibers.
Finally, back in July I argued that Neanderthals would be stronger than Homo sapiens due to their morphology and a wide waist. This, of course, has implications for strength differences between the races. People with a wider waist would have the ability to generate more power. Blacks have a higher center of gravity due to longer limbs whereas whites and Asians have lower centers of gravity due to a longer torso. Along with climatic conditions, the Neanderthal diet also contributed to their wide waist and thorax, which would then help with strength. Therefore, this has implications for racial differences in strength. We can replace Europeans with Neanderthals and Homo sapiens with Africans and the relationship would still hold. This is yet more proof that blacks are not stronger than whites. This article also contributes to the argument I laid out in my article on how racial differences in muscle fiber typing predict differences in elite sporting competition. Morphology/somatype is the final piece of the puzzle; without the correct morphology, it’d be really hard for someone to become an elite athlete in a certain field if they do not have the correct morphology.
Looking at the big four lifts, the advantage goes to European Americans and East Asians. This is due to their average somatype and morphology. The only lift that Africans would excel at is the deadlift and this is due to their morphology—mainly their long arms. People with longer arms excel at pulling exercises whereas people with shorter arms excel at pushing exercises. Hand-grip strength studies show blacks having a higher grip strength than whites, however in one study if you see who is stronger pound-for-pound, the differences are insignificant. The longitudinal bench press study is highly flawed due to numerous confounds and is therefore unacceptable to assess strength and race. The fact that chimpanzees have a higher proportion of type II fibers compared to humans is also irrelevant. Chimpanzees have a smaller stature and they can, therefore, generate way more power pound-for-pound. Attempting to replace Africans with chimpanzees in this scenario doesn’t make sense because Africans have longer limbs than Europeans and would, therefore, generate less force pound-for-pound. Overall strength is related to mortality; stronger people live longer and have fewer maladies than weaker people. This too lends credence to my argument that whites are stronger than blacks.
American Renaissance published an article the other day titled “Is ‘Racism’ Killing Black People?” and, for the most part, I largely agree with it. However, there are a few faults in it that I need to address.
First, off, as the article rightly noted, it’s not only perceived ‘racism’ that is the cause for these health disparities, but stress from other blacks as well. Gregory Hood (the author of the AmRen article) cites a new study showing that blacks who move out of the ‘hood’ see a subsequent decrease in BP (Kershaw et al, 2017). They followed 2,290 people 974 were men and 1,306 were women. This is data collected from the CARDIA study which has helped us to understand racial disparities in all types of different health outcomes. Blacks who lived in high segregation neighborhoods had higher levels of SBP (systolic blood pressure), and saw a decrease in their SBP when they moved to less segregated neighborhoods. The authors conclude that “policies that reduce segregation may have meaningful health benefits.” What kind of policies will ‘reduce segregation’? Most races/ethnic groups group together in an area, so I don’t see how this would happen.
In regards to the argument on black maternal mortality and ‘racism’, I think it’s much more nuanced. Black women are 2 to 6 times more likely to die giving birth than white women; while the leading causes of maternal death in black women is pregnancy-induced hypertension, and embolism (Chang et al, 2003), though reasons for the mortality rate are not explainable at present (Flanders-Stepans, 2002). Further, in regards to preeclampasia, women who get pregnant at younger ages are more likely to acquire the disease while pregnant, and blacks and other non-whites are more likely to get pregnant at younger ages than whites (Main et al, 2015).
However, there are ways to reduce maternal mortality in black women. In a RCT undertaken between the years of 1990-2011 in Memphis, Tennesee, black women were followed with their live-in children and placed into one of four groups: “treatment 1 (transportation for prenatal care [n = 166]), treatment 2 (transportation plus developmental screening for infants and toddlers [n = 514]), treatment 3 (transportation plus prenatal/postpartum home visiting [n = 230]), and treatment 4 (transportation, screening, and prenatal, postpartum, and infant/toddler home visiting [n = 228])” (Olds et al, 2014). They conclude that pre- and post-natal care greatly reduces maternal/infant mortality in black women, “living in highly disadvantaged settings.”
Further, the racial disparity in post-term neonates is largely driven by “CHD among term infants with US-born mothers is driven predominately by the postneonatal survival disadvantage of African-American infants” (Collins et al, 2017). Though, as can be seen in the study by Olds et al (2014), pre- and post-natal care can greatly reduce both infant and maternal mortality.
Stress can also be measured in pregnant women by measuring the level of blood cortisol (Gillespie et al, 2017). They show that, independent of adulthood stress, stress during childhood may shape birth timing, with cortisol being the biological mediator. This may be an explanation for what Gregory Hood notes. He states in his article that there has to be an explanation for why black women birth earlier, and while I am sympathetic to biological models ala Rushton (1997), Gillespie et al (2017) drive a hard argument that stress during childhood using cortisol as a biological mediator makes a lot of sense.
There are a few studies that attest to pre- and post-natal care having a large effect on the morality of black women, and that having the carers being black women seems to have a positive effect (Guerra-Reyes and Hamilton, 2017). They conclude that “Recognition, support, and increasing the number of African-American midwives and birth assistants is vital in tackling health inequalities.” In regards to infant mortality rate (IMR), 18 states will achieve racial equality by 2050 if current trends from 1999-2013 hold (Joedrecka et al, 2017).
Now for the main reason I decided to write this: the ‘Hispanic’ paradox. This paradox is that for the past twenty years, ‘Hispanics’ with low SES have similar or better health outcomes than whites (Franzini, Ribble, and Keddie, 2001). However, more recent analyses show that the ‘Hispanic’ paradox does not exist, mostly due to methodological problems and migrant selectivity (Crimmins et al, 2007; Teruya and Bazargan-Hezeji, 2013) and was not noticed in Chile either (Cabiesies, Tunstall, and Pickett, 2013). There is no migrant selectivity in regards to smoking, however (Fenelon, 2013, 2016).
Studies which advocate the validity of the Immigrant Paradox are countered by those which report specific, negative physical and mental health outcomes, and higher rates of substance use, especially among immigrant adolescents. Findings may also be compromised by fundamental methodological concerns such as migrant health selectivity, and approaches that consider only selectively healthy groups. Moreover, the Immigrant Paradox’s benefits do not appear to extend evenly and consistently to all races, ethnicities and subgroups. Similarly, the Hispanic Paradox does not protect consistently across all Latino ethnicities, age groups and genders, with Puerto Ricans and Cubans in particular found to enjoy fewer health advantages.
This is good evidence that the people who migrate to America are healthier, and that the symptoms of low SES show in their children, but not in them because they are a self-selected population. There is no ‘Hispanic’ paradox (Smith and Bradshaw, 2006; Schoenthaler, 2016). Even a new meta-analysis on this ‘paradox’ states “Immigrant children and youth suffer from an immigrant mortality disadvantage” (Shor, Roelfs, and Vamg, 2017).
Lastly, Gregory Hood brings up stress and suicide, stating that if blacks were really more stressed than whites then blacks would have higher rates of suicide, but some studies show that whites have a higher rate of suicidal ideation, while others do not show this (Perez-Rodriguez et al, 2010). Though, as Balis and Postolache (2010) show, studies show that while there is conflicting evidence in regards to racial/ethnic differences in suicide, whites still attempt it the most. However, suicide for young black Americans is on the rise. Ahmedani et al (2016) show that “Nearly 27% of White individuals made a mental health visit versus less than 20% of Asian, Hawaiian/Pacific Islander, and Black individuals in this period. Within 4 weeks, all visits and mental health visits remained most common for White individuals (67.3% and 47.4%, respectively) and least common among Asian individuals (52.8% and 31.9%, respectively). Within 52-weeks, more than 90% made any visit. Alaskan Native/Native American (81.5%) and White individuals (79.5%) made mental health visits 10–25% more often than other groups.” However, at least in Fulton County, Georgia, black suicide decedents were less likely to report depression than white suicide decedents (Abe et al, 2008).
However, for whites, as noted in this 1982 New York Times article, suicidal feelings “reflects feelings of loneliness and hopelessness, which can be greater factors as one grows older; for instance, after loved ones have died” whereas for older white men, loss of status may be a cause, which would not be that prevalent in lower SES ethnicities. The article seems to implicate loss of status as a main cause for higher rates of suicide in white Americans, and states that as other, lower SES ethnies attain higher status, that suicide rates would rise for them as well.
Another cause could be prescription drugs, for instance in the Northeast which has been hit hard by the opiate/heroin crisis which leads to more white deaths. Robert Putnam puts this on “the links between poverty, hopelessness and health” and states that the suicide rate has declined for two groups, black males and males over the age of 75. Further, “divorce, economic strain, or political repression are often characterized as suicide risks.” Cheng et al (2010) show that “A high level of identification with one’s ethnic group was associated with lower rates of suicide attempts.” So, it seems that if one keeps their status, and has a high level of identification with their ethnic group, whites would then be protected against suicidal ideation. Nonmetropolitan counties also have higher rates of suicide than metropolitan counties (Ivey-Stephenson et al, 2017). People who livee in rural counties are less likely to seek help for mental problems (Carpenter-Song and Snell-Rood, 2016). Whites are also more likely to live in rural areas. This could explain higher rates of suicide in whites, along with loss of status, depression and drug use.
In conclusion, the ‘Hispanic’ paradox doesn’t exist; whites attempt/commit suicide more due to loss of status and since most whites live in rural areas, they do not seek help for their mental health problems which then leads to suicide. In regards to black maternal mortality/infant mortality rates, if they have midwives present during and after the birth, mortality rates have decreased. If these trends continue, there will be racial equality in terms of maternal/infant mortality in 18 states. The AmRen article was good and well written, but there were a few huge flaws. The author assumed that since the ‘Hispanic paradox’ exists, that this should have one disregard the effects of, say, stress on blood pressure in black Americans, as I have discussed in the past. But since the ‘Hispanic’ paradox does not exist, then you cannot say that (perceived) discrimination and ‘racism’ is not a cause for higher rates of mortality in blacks compared to whites.
I was alerted to an article on the website (Ir)”RationalWiki” which in their own words “critique[s] and challenge[s] pseudoscience and the anti-science movement, explore[s] authoritarianism and fundamentalism, and analyze[s] how these subjects are handled in the media.” Unfortunately, it seems like the one who wrote this article (and is still adding to it) just selectively read certain articles and quote mined them.
The article on this website about me is an unfair mischaracterization of my views. Quotes will follow from the article with my comments.
In the opening paragraph they write:
NotPoliticallyCorrect is an Alt-right blog that promotes racialist pseudoscience and white nationalism; the owner posts as RaceRealist using the euphemism “racial realist” coined by the white supremacist J. P. Rushton who is extensively quoted on the blog.
- I’m not alt-right nor am I a white nationalist.
- I don’t promote ‘racialist pseudoscience’ nor do I promote ‘white nationalism’.
- Correct, Rushton did coin the term ‘race realist’, but he was not a ‘white supremacist’.
They continue, quoting an article of mine that I wrote almost two years ago titled Non-Western People are Abnormal to Our Society. I still stand by everything that I wrote in that article.
A racist crank obsessed with controversial topics such as race and IQ and eugenics, RaceRealist argues in a 2016 blog essay “Non-Western People are Abnormal to Our [Western] Societies” and its comments that “MENA” and “SSA’s” (i.e. people from the Middle-East, North Africa and Sub-Saharan Africa) as well as other non-Westerners are somehow abnormal to the US and Europe:
They then quote me:
MENA and SSA people are abnormal to Western societies. It’s clear that, on average, full-on acclimation is not possible.
One only needs to look at what is occurring in Western European countries to see that, on average, this is true.
In the same essay, RaceRealist goes on to post crude racism, such as “Negros” are biologically inferior:
Quoting me writing:
The same can be said for Negros[sic] in America as well. They are deviant, dysfunctional, they cause distress in our country and finally, they pose a danger to us, our families and societies as a whole. Just like those immigrants we have come into our countries who cannot assimilate because it’s not in their biology.
Except everything I wrote here was logically sound (last sentence notwithstanding). Look at the 4 d’s of abnormal psychology (which is the next quote they provide):
The “4 d’s of abnormality” and how they relate to our culture and the current culture/biology of those non-Western immigrants coming into our country is extremely telling. It’s clear that those people cannot assimilate into our societies because of differing biology and differing locations in which they evolved in. We chose our environments based on our biology. Environment increasingly depends on their genes, rather than being the cause of their exogenous behavior.
The 4 d’s of abnormality are deviance, dysfunction, distress and danger. Everything I wrote and then provided examples for in regards to the 4 d’s of abnormality are sound.
You can read my article Diversity in the Social Context for more evidence for this argument.
They then quote my article The Evolution of Jewish Nepotism writing:
RaceRealist is an anti-Semite who dislikes Ashkenazi Jews, accusing them of “derogating other ethnicities”; when discussing Ashkenazi Jews, he bizarrely maintains their higher average IQ is partly a product of “breeding with beautiful Roman women a few thousand years ago”, for which there exists no evidence.
I admit it is conjecture. Evidence exists for Jewish men migrating to Rome to mate with Roman women (Atzmon et al, 2010). I never stated that I ‘dislike Ashkenazi Jews’. In regards to the derogation, it’s true. Close-knit ethnic groups derogate the out-group (Sampasivam et al, 2016). Further, oxytocin promotes human ethnocentrism, which caused in-group favoritism and out-group derogation (Drew et al, 2010). In-groups derogate out-groups. Read the literature.
And the final thing the page shows is my tweet saying that “I finally made it on (Ir)”RationalWiki””:
to which they wrote:
Just because I have the numbers “88” in my handle doesn’t make me “alt-right” nor does it make me a “white nationalist.” I thought about changing it, then I realized that it’s good to weed out the people who aren’t serious about discussion and just look for things to discredit people that are meaningless to the conversation at hand. It tells you a lot about someone when they bring up irrelevant things. I’m not a white nationalist, nor am I an alt-righter. Just because I write about politics rarely and use them as an example (like in my article The Rise of Ethnocentrism and the Alt-Right: The Rebirth of Selfish Genes which I also disavow now that I realize that ‘selfish genes’ are a metaphor; Noble, 2011; Noble, 2013; Noble et al, 2014).
Take a look at the tags it tagged the article with: “Alt-righters, Pseudoscience, Racists, Internet kooks, Psuedoscience promoters, Alt-right, Internet Hate Sites.” Not an alrighter, I don’t push psuedoscience, I’m not a ‘racist’ (whatever that means). If you don’t like what I write, respond to any article you disagree with and explain why with logical, rational arguments. This piece is garbage and mischaracterizes my views using selective quotations (which, even then, failed to prove their point. No, numbers after a username are not evidence).
All in all, this article is garbage. It says that Rushton is ‘extensively quoted’, which is true for what I wrote in the beginning of this blog’s history, but not so for the past, say, 18 months. Rushton has been the target of my attacks on penis size, testosterone, and my personal favorite, r/K selection theory. But sure, go and dig in the archives for old articles to quote mine. This article written about me is dumb, doesn’t characterize my views correctly (calls me a ‘white nationalist’ and ‘alt-righter’). Selectively quote certain articles, assert that Rushton is ‘extensively quoted’ when I hardly discuss him anymore and when I do it’s about testosterone/to rebut him. (Ir)RationalWiki should think about reading a bit of my blog before characterizing me as something I’m not.
For the record, I don’t care about politics. I am not alt-right. I am not a white nationalist. I’m not an anti-semite. This will be updated to cover whatever else they decide to write about me. Hopefully it’s at least a bit closer to reality next time, because this article sucks.
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.
According to a new article published at The Guardian, testosterone does affect human cognition and decision-making. The article, titled, Now we men can blame our hormones: testosterone is trouble, by Phil Daoust, is yet more media sensationalism against testosterone. Daoust’s article is full of assumptions and conclusions that do not follow from an article he cites on testosterone and cognitive reflection and decision making.
The cited article, Single dose testosterone administration impairs cognitive reflection in men, states that endogenous testosterone (testosterone produced in the body) is correlated with physical aggression. However, I’ve shown that this is not true. They conclude overall the exogenous testosterone is related to an increase in irrational thinking and decision-making. Nothing wrong with concluding that from the data. However, Daoust’s interpretation and conclusions he draws from this study are wrong, mostly due to the same old tales and misconceptions about testosterone.
This is the largest study of the effect of exogenous testosterone and decision-making and cognition. The authors show that men administered a gel that was rubbed into the upper body that is used for TRT (testosterone replacement therapy) showed “incorrect intuitive answers were more common, and correct answers were less common in the T group, for each of the three CRT questions analyzed separately” (Nave et al, 2017: 8). However, what The Guardian article does not state is that this relationship could be mediated by more than testosterone, such as motivation and arithmetic skills.
Nevertheless, those who rubbed themselves with the testosterone gel answered 20 percent fewer questions correctly. This was attributed to the fact that they were more likely to be anxious and not think about the answer. One of the authors also states that either testosterone inhibits the action of mentally checking your work or it increases the intuitive feeling that you’re definitely right (since those who rubbed themselves with T gel gave more intuitive answers, implying that the testosterone made them go to their first thought in their head). I have no problems with the paper—other than the fact that gel has an inconsistent absorption rate and has high rates of aromatization. The study has a good design and I hope it gets explored more. I do have a problem with Dauost’s interpretation of it, however.
A host of studies have already shown a correlation between elevated testosterone levels and aggression – and now they’re being linked to dumb overconfidence.
The ‘host of studies‘ that ‘have already shown a correlation between elevated testosterone levels and aggression‘ don’t say what you think they do. This is another case of the testosterone sensationalism of the media—talking about a hormone they don’t really know anything about.
That won’t help with the marketing – though it may explain Donald Trump and his half-cocked willy-waggling. Perhaps it’s not the president’s brain that’s running things, but the Leydig cells in his testicles.
Nice shot. This isn’t how it works, though. You can’t generalize a study done on college-aged males to a 71-year-old man.
Women aren’t entirely off the hook – their bodies also produce testosterone, though in smaller quantities, and the Caltech study notes that “it remains to be tested whether the effect is generalisable to females” – but for now at least they now have another way to fight the scourge of mansplaining: “You’re talking out of your nuts.”
Another paragraph showing no understanding, even bringing up the term ‘mansplaining’—whatever that means. This article is, clearly, demonizing high T men, and is a great example of the media bias on testosterone studies that I have brought up in the past.
Better still, with the evils of testosterone firmly established, the world may learn to appreciate older men. Around the age of 30, no longer “young, dumb and full of cum”, we typically find our testosterone levels declining, so that with every day that passes we become less aggressive, more rational and generally nicer.
“The evils of testosterone firmly established“, nice job at hiding your bias. Yes the cited article (Nave et al 2017) does bring up how testosterone is linked to aggression. But, for the millionth time, the correlation between testosterone and aggressive behavior is only .08 (Archer, Graham-Kevan, and Davies, 2005).
Even then, most of the reduction of this ‘evil hormone’ is due to lifestyle changes. It just so happens that around the ages 25-30—when most men notice a decrease in testosterone levels—that men begin to change their lifestyle habits, which involve marriage which decreases testosterone levels (Gray et al, 2002; Burnham et al, 2003; Gray, 2011; Pollet, Cobey, and van der Meij, 2013; Farrelly et al, 2015; Holmboe et al, 2017), having children (Gray et al, 2002; Gray et al, 2006; Gettler et al, 2011) to obesity (Palmer et al, 2012; Mazur et al, 2013; Fui, Dupuis, and Grossman, 2014; Jayaraman, Lent-Schochet, and Pike, 2014; Saxbe et al, 2017) smoking is not clearly related to testosterone (Zhao et al, 2016), and high-carb diets decrease testosterone (Silva, 2014).
So the so-called age-related decline in testosterone is not really age-related at all—it has to do with environmental and social factors which then decreases testosterone (Shi et al, 2013). Why should a man be ‘happy’ that his testosterone levels are decreasing due—largely—to his lifestyle? Low testosterone is related to cardiovascular risk (Maggio and Basaria, 2009), insulin sensitivity (Pitteloud et al, 2005; Grossman et al, 2008), metabolic syndrome (Salam, Kshetrimayum, and Keisam, 2012; Tsuijimora et al, 2013), heart attack (Daka et al, 2015), elevated risk of dementia in older men (Carcaillon et al, 2014), muscle loss (Yuki et al, 2013), and stroke and ischemic attack (Yeap et al, 2009).
So it seems that, contrary to Phil Daoust’s (the author of The Guardian article on testosterone) claims that low testosterone is associated with less aggressive behavior, more rationality and being nicer, in general, are wrong. Low testosterone is associated with numerous maladies, and the Daoust is trying to make low testosterone out to be ‘a good thing’, while demonizing men with higher levels of testosterone with cherry-picked studies and not large meta-analyses like I have cited that show that testosterone has an extremely low correlation with aggressive behavior.
As I have covered in the past, testosterone levels in the West are declining, along with semen count and quality. These things are due, largely in part, to social and environmental factors such as obesity, low activity, and an overall change in lifestyle. One (albeit anecdotal) reason I could conjure up has to do with dominance. Testosterone is the dominance hormone and so if testosterone levels are declining, then that means men must not be showing dominance as much. I would place part of the blame here on feminism and articles like the one reviewed here as part of the problem. So contra the author’s assertion, lower levels of testosterone into old age are not good, since that signifies a change in lifestyle—many of which are in the control of the male in question (I, of course, would not advise anyone to not have children or get married).
Nave et al (2017) lead the way for further research into this phenomenon. If higher doses of exogenous testosterone do indeed inhibit cognitive reflection, then, as the authors note, “The possibility that this widely prescribed treatment has unknown deleterious influences on specific aspects of decision-making should be investigated further and taken into account by users, physicians, and policy makers” (Nave et al, 2017: 11). This is perhaps one of the most important sentences in the whole article. This is about the application of testosterone-infused gel and decision-making. They’re talking about the implications of administering the gel to men and how it affects decision-making and cognitive reflection. This study is NOT generalizable for 1) endogenous testosterone and 2) non-college students. If the author understood the paper and science, he wouldn’t make those assumptions about Trump’s Leydig cells in his testicles “running the show”.
Because of the testosterone fear, good studies like Nave at al (2017) get used for an agenda by people who don’t understand the hormone. People the the Right and Left both have horrible misconceptions about the hormone, and some cannot interpret studies correctly and draw the correct conclusions from them. Testosterone—endogenous or exogenous—does not cause aggression (Batrinos, 2012). This is an established fact. The testosterone decrease between the ages of 25-30 is avoidable if you don’t change to bad habits that decrease testosterone. All in all, the testosterone scare is ridiculous. People are scared of it because they don’t understand it.
Daoust didn’t understand the article he cited and drew false conclusions from his misinterpretations. I would be interested to see how men would fare on a cognitive reflection test after, say, their favorite team scored during a game, and not after being given supraphysiological doses of testosterone gel. Drawing conclusions like Daoust did, however, is wrong and will mislead numerous more people under the guise of science.
I enjoy reading what other bloggers write about testosterone and its supposed link to crime, aggression, and prostate cancer; I used to believe some of the things they did, since I didn’t have a good understanding of the hormone nor its production in the body. However, once you understand how its produced in the body, then what others say about it will seem like bullshit—because it is. I’ve recently read a few articles on testosterone from the HBD-blog-o-sphere and, of course, they have a lot of misconceptions in them—some even using studies I have used myself on this blog to prove my point that testosterone does not cause crime!! Now, I know that most people don’t read studies that are linked, so they would take what it says on face value because, why not, there’s a cite so what he’s saying must be true, right? Wrong. I will begin with reviewing an article by someone at The Alternative Hypothesis and then review one article from Robert Lindsay on testosterone.
The Alternative Hypothesis
Faulk has great stuff here, but the one who wrote this article, Testosterone, Race, and Crime, 1) doesn’t know what he’s talking about and 2) clearly didn’t read the papers he cited. Read this article, you’ll see him make bold claims using studies I have used for my own arguments that testosterone doesn’t cause crime! Let’s take a look.
One factor which explains part of why Blacks have higher than average crime rates is testosterone. Testosterone is known to cause aggression, and Blacks are known to at once have more of it and, for genetic reasons, to be more sensitive to its effects.
- No it doesn’t.
- “Testosterone is known to cause aggression“, but that’s the thing: it’s only known that it ’causes’ aggression, it really doesn’t.
- Evidence is mixed on blacks being “… for genetic reasons … more sensitive to its effects” (Update on Androgen Receptor gene—Race/History/Evolution Notes).
Testosterone activity has been linked many times to aggression and crime. Meta-analyses show that testosterone is correlated with aggression among humans and non human animals (Book, Starzyk, and Quinsey, 2001).
Why doesn’t he say what the correlation is? It’s .14 and this study, while Archer, Graham-Kevan and Davies, (2005) reanalyzed the studies used in the previous analysis and found the correlation to be .08. This is a dishonest statement.
Women who suffer from a disease known as congenital adrenal hyperplasia are exposed to abnormally high amounts of testosterone and are abnormally aggressive.
Abnormal levels of androgens in the womb for girls with CAH are associated with aggression, while boys with and without CAH are similar in aggression/activity level (Pasterski et al, 2008), yet black women, for instance, don’t have higher levels of testosterone than white women (Mazur, 2016). CAH is just girls showing masculinized behavior; testosterone doesn’t cause the aggression (See Archer, Graham-Kevan and Davies, 2005)
Actually, no. Supraphysiological levels of testosterone administered to men (200 and 600 mg weekly) did not increase aggression or anger (Batrinos, 2012).
Finally, people in prison have higher than average rates of testosterone (Dabbs et al., 2005).
Dabbs et al don’t untangle correlation from causation. Environmental factors can explain higher testosterone levels (Mazur, 2016) in inmates, and even then, some studies show socially dominant and aggressive men have the same levels of testosterone (Ehrenkraz, Bliss, and Sheard, 1974).
Thus, testosterone seems to cause both aggression and crime.
No, it doesn’t.
Furthermore, of the studies I could find on testosterone in Africans, they have lower levels than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006) so, along with the studies and articles cited on testosterone, aggression, and crime, that’s another huge blow to the testosterone/crime/aggression hypothesis.
Richard et al. (2014) meta-analyzed data from 14 separate studies and found that Blacks have higher levels of free floating testosterone in their blood than Whites do.
They showed that blacks had 2.5 to 4.9 percent higher testosterone than whites, which could not explain the higher prostate cancer incidence (which meta-analyses call in to question; Sridhar et al 2010; Zagars et al 1998). That moderate amount would not be enough to cause differences in aggression either.
Exacerbating this problem even further is the fact that Blacks are more likely than Whites to have low repeat versions of the androgen receptor gene. The androgen reception (AR) gene codes for a receptor by the same name which reacts to androgenic hormones such as testosterone. This receptor is a key part of the mechanism by which testosterone has its effects throughout the body and brain.
The rest of the article talks about CAG repeats and aggressive/criminal behavior, but it seems that whites have fewer CAG repeats than blacks.
This one is much more basic, and tiring to rebut but I’ll do it anyway. Lindsay has a whole slew of articles on testosterone on his blog that show he doesn’t understand the hormone, but I’ll just talk about this one for now: Black Males and Testosterone: Evolution and Perspectives.
It was also confirmed by a recent British study (prostate cancer rates are somewhat lower in Black British men because a higher proportion of them have one White parent)
Jones and Chinegwundoh (2014) write: “Caution should be taken prior to the interpretation of these results due to a paucity of research in this area, limited accurate ethnicity data, and lack of age-specific standardisation for comparison. Cultural attitudes towards prostate cancer and health care in general may have a significant impact on these figures, combined with other clinico-pathological associations.”
This finding suggests that the factor(s) responsible for the difference in rates occurs, or first occurs, early in life. Black males are exposed to higher testosterone levels from the very start.
In a study of women in early pregnancy, Ross found that testosterone levels were 50% higher in Black women than in White women (MacIntosh 1997).
I used to believe this, but it’s much more nuanced than that. Black women don’t have higher levels of testosterone than white women (Mazur, 2016; and even then Lindsay fails to point out that this was pregnant women).
According to Ross, his findings are “very consistent with the role of androgens in prostate carcinogenesis and in explaining the racial/ethnic variations in risk” (MacIntosh 1997).
Testosterone has been hypothesized to play a role in the etiology of prostate cancer, because testosterone and its metabolite, dihydrotestosterone, are the principal trophic hormones that regulate growth and function of epithelial prostate tissue.
Testosterone doesn’t cause prostate cancer (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Diet explains any risk that may be there (Hayes et al, 1999; Gupta et al, 2009; Kheirandish and Chinegwundoh, 2011; Williams et al, 2012; Gathirua-Mingwai and Zhang, 2014). However in a small population-based study on blacks and whites from South Carolina, Sanderson et al (2017) “did not find marked differences in lifestyle factors associated with prostate cancer by race.”
Regular exercise, however, can decrease PCa incidence in black men (Moore et al, 2010). A lot of differences can be—albeit, not too largely— ameliorated by environmental interventions such as dieting and exercising.
Many studies have shown that young Black men have higher testosterone than young White men (Ellis & Nyborg 1992; Ross et al. 1992; Tsai et al. 2006).
Ellis and Nyborg (1992) found 3 percent difference. Ross et al (1992) have the same problem as Ross et al (1986), which used University students (~50) for their sample. They’re not representative of the population. Ross et al (1992) also write:
Samples were also collected between 1000 h and 1500 h to avoid confounding
by any diurnal variation in testosterone concentrations.
Testosterone levels should be measured near to 8 am. This has the same time variation too, so I don’t take this study seriously due to that confound. Assays were collected “between” the hours of 10 am and 3 pm, which means it was whenever convenient for the student. No controls on activities, nor attempting to assay at 8 am. People of any racial group could have gone at whatever time in that 5 hour time period and skew the results. Assaying “between” those times completely defeats the purpose of the study.
This advantage [the so-called testosterone advantage] then shrinks and eventually disappears at some point during the 30s (Gapstur et al., 2002).
This makes it very difficult if not impossible to explain differing behavioral variables, including higher rates of crime and aggression, in Black males over the age of 33 on the basis of elevated testosterone levels.
See above where I talk about crime/testosterone/aggression.
Critics say that more recent studies done since the early 2000’s have shown no differences between Black and White testosterone levels. Perhaps they are referring to recent studies that show lower testosterone levels in adult Blacks than in adult Whites. This was the conclusion of one recent study (Alvergne et al. 2009) which found lower T levels in Senegalese men than in Western men. But these Senegalese men were 38.3 years old on average.
Alvergne, Fauri, and Raymond (2009) show that the differences are due to environmental factors:
This study investigated the relationship between mens’ salivary T and the trade-off between mating and parenting efforts in a polygynous population of agriculturists from rural Senegal. The men’s reproductive trade-offs were evaluated by recording (1) their pair-bonding/fatherhood status and (2) their behavioral profile in the allocation of parental care and their marital status (i.e. monogamously married; polygynously married).
They also controlled for age, so his statement “But these Senegalese men were 38.3 years old on average” is useless.
These critics may also be referring to various studies by Sabine Rohrmann which show no significance difference in T levels between Black and White Americans. Age is poorly controlled for in her studies.
That is one study out of many that I reference. Rohrmann et al (2007) controlled for age. I like how he literally only says “age is poorly controlled for in her studies“, because she did control for age.
That study found that more than 25% of the samples for adults between 30 and 39 years were positive for HSV-2. It is likely that those positive samples had been set aside, thus depleting the serum bank of male donors who were not only more polygamous but also more likely to have high T levels. This sample bias was probably worse for African American participants than for Euro-American participants.
Why would they use diseased samples? Do you even think?
Young Black males have higher levels of active testosterone than European and Asian males. Asian levels are about the same as Whites, but a study in Japan with young Japanese men suggested that the Japanese had lower activity of 5-alpha reductase than did U.S. Whites and Blacks (Ross et al 1992). This enzyme metabolizes testosterone into dihydrotestosterone, or DHT, which is at least eight to 10 times more potent than testosterone. So effectively, Asians have the lower testosterone levels than Blacks and Whites. In addition, androgen receptor sensitivity is highest in Black men, intermediate in Whites and lowest in Asians.
Ethnicmuse also showed that, contrary to popular belief, Asians have higher levels of testosterone than Africans who have higher levels of testosterone than Caucasians in his meta-analysis. (Here is his data.)
Let us look at one study (Ross et al 1986) to see what the findings of a typical study looking for testosterone differences between races shows us. This study gives the results of assays of circulating steroid hormone levels in white and black college students in Los Angeles, CA. Mean testosterone levels in Blacks were 19% higher than in Whites, and free testosterone levels were 21% higher. Both these differences were statistically significant.
Assay times between 10 am and 3 pm, unrepresentative sample of college men, didn’t have control for waist circumference. Horribly study.
A 15% difference in circulating testosterone levels could readily explain a twofold difference in prostate cancer risk.
No, it wouldn’t (if it were true).
Higher testosterone levels are linked to violent behavior.
Causation not untangled.
Studies suggest that high testosterone lowers IQ (Ostatnikova et al 2007). Other findings suggest that increased androgen receptor sensitivity and higher sperm counts (markers for increased testosterone) are negatively correlated with intelligence when measured by speed of neuronal transmission and hence general intelligence (g) in a trade-off fashion (Manning 2007).
Who cares about correlations? Causes matter more. High testosterone doesn’t lower IQ. Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut.
Racial differences in testosterone don’t exist/are extremely small in magnitude (as I’ve covered countless times). The one article from TAH literally misrepresents studies/leaves out important figures in the testosterone differences between the two races to push a certain agenda. Though if you read the studies you see something completely different. It’s the same with Lindsay. He misunderstood a few studies to push his agenda about testosterone and crime and prostate cancer. They’re both wrong, though.
Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut. People read and write about things they don’t understand, which is the cause of these misconceptions with the hormone, as well as, of course, misinterpreting studies. Learn about the hormone and you won’t fear it. It doesn’t cause crime, prostate cancer nor aggression; these people who write these articles have one idea in their head and they just go for it. They don’t understand the intricacies of the endocrine system and how sensitive it is to environmental influence. I will cover more articles that others have written on testosterone and aggression to point out what they got wrong.