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Action and behavior are distinct concepts, although in common lexicon they are used interchangeably. The two concepts are needed to distinguish what one intends to do and what one reacts to and how they react. In this article, I will explain the distinction between the two and how and why people get it wrong when discussing the two concepts—since using them interchangeably is inaccurate.
Actions are intentional; they are done for reasons (Davidson, 1963). Actions are determined by one’s current intentional state and they then act for reasons. So, in effect, the agent’s intentional states cause the action, but the action is carried out for reasons. Actions are that which is done by an agent, but stated in this way, it could be used interchangeably with behavior. The Wikipedia article on “action” states:
action is an intentional, purposive, conscious and subjectively meaningful activity
So actions are conscious, compared to behaviors which are reflexive and unconscious—not done for reasons.
Davidson (1963: 685) writes:
Whenever someone does something for a reason, therefore, he can be characterized as (a) having some sort of pro attitude toward actions of a certain kind, and (b) believing (or knowing, perceiving, noticing, remembering) that his action is of that kind.
So providing the reason why an agent did A requires naming the pro-attitude—beliefs paired with desires—or the related belief that caused the agent’s action. When I explain behavior, this will become clear.
Behavior is different: behavior is a reaction to a stimulus and this reaction is unconscious. For example, take a doctor’s office visit. Hitting the knee in the right spot causes the knee to jerk up—doctors use this test to test for nerve damage. It tests the L2, L3, and L4 segments of the spinal cord, so if there is no reflex, the doctor knows there is a problem.
This is done without thought—the patient does not think about the reflex. This then shows how and why action and behavior are distinct concepts. Here’s what occurs when the doctor hits the patient’s knee:
When the doctor hits the knee, the patient’s thigh muscle stretches. When the thigh muscle stretches, a signal is then sent along the sensory neuron to the spinal cord where it interacts with a motor neuron which goes to the thigh muscle. The muscle then contracts which causes the reflex. (Recall my article on causes of muscle movement.)
So this, compared to consciously taking a step—consciously jerking your leg in the same way as a doctor expects the patellar reflex—is what distinguishes one from the other—what distinguishes action from behavior. Sure, the behavior of the patellar reflex occurred for a reason—but it was not done consciously by the agent so it is therefore not an action.
Perhaps it would be important at this point to explain the differences between action, conduct, and behavior, because we have used these three terms in the discussion of caring. …
Teleology, the reader is reminded, involves goals or lures that provide the reasons for a person actingin a certain way. It is goals or reasons that establish action from simple behavior. On the other hand the concept of efficient causation is involved in the concept of behavior. Behavior is the result of antecedentconditions. The individual behaves in response to causal stimuli or antecedent conditions. Hence, behavior is a reaction to what already is—the result of a push from the past to do something in the present. In contrast, an action aims at the future. It is motivated by a vision of what can be. (Brencick and Webster, 2000: 147)
This is also another thing that Darwin got wrong. He believed that instincts and reflexes are inherited—this is not wrong since they are behaviors and behaviors are dispositional which means they can be selected. However, he believed that before they were inherited as instincts and reflexes, they were intentional acts. As Badcock (2000: 56) writes in Evolutionary Psychology: A Critical Introduction:
Darwin explicitly states this when he says that ‘it seems probable that some actions, which were at first performed consciously, have become through habit and association converted into relex actions, and are now firmly fixed and inherited.’
This is quite obviously wrong, as I have explained above; instead of “reflexive actions”, Darwin meant “reflexive behaviors”. So, it seems that Darwin did not grasp the distinction between “action” and “behavior” either.
We can then form this simple argument, take cognition:
This is a natural outcome of what has been argued here, due to the distinction between action and behavior. So when we think of “cognition” what comes to mind? Thinking. Thinking is an action—so thinking (cognition) is intentional. Intentionality is “the power of minds and mental states to be about, to represent, or to stand for, things, properties and states of affairs.” So, when we think, our minds/mental states can represent, stand for things, properties and states of affairs. Therefore, cognition is intentional. Since cognition is intentional and behavior is dispositional, it directly follows that cognition cannot be responsible for behavior.
Thinking is a mental activity which results in a thought. So if thinking is a mental activity which results in a thought, what is a thought? A thought is a mental state of considering a particular idea or answer to a question or committing oneself to an idea or answer. These mental states are, or are related to, beliefs. When one considers a particular answer to a question they are paving the way to holding a particular belief; when they commit themselves to an answer they have formulated a new belief.
Beliefs are propositional attitudes: believing p involves adopting the belief attitude to proposition p. So, cognition is thinking: a mental process that results in the formation of a propositional belief. When one acquires a propositional attitude by thinking, a process takes place in stages. Future propositional attitudes are justified on earlier propositional attitudes. So cognition is thinking; thinking is a mental state of considering a particular view (proposition).
Therefore, thinking is an action (since it is intentional) and cannot possibly be a behavior (a disposition). Something can be either an action or a behavior—it cannot be both.
Let’s say that I have the belief that food is downtown. I desire to eat. So I intend to go downtown to get some food. While the cause is the sensation of hunger. This chain shows how actions are intentional—how one intends to act.
Furthermore, using the example I explained above, how a doctor assesses the patellar reflex is a behavior—it is not an action since the agent himself did not cause it. One could say that it is an action for the doctor performing the reflexive test, but it cannot be an action for the agent the test is being done on—it is, therefore, a behavior.
I have explained the difference between action and behavior and how and why they are distinct. I gave an example of action (cognition) and behavior (patellar reflex) and explained how they are distinct. I then gave an argument showing how cognition (an action) cannot possibly be responsible for behavior. I showed how Darwin believed (falsely) that actions could eventually become behaviors. Darwin pretty much stated “Actions can be selected and eventually become behaviors.” This is nonsense. Actions, by virtue of being intentional, cannot be selected, even if they are done over and over again, they do not eventually become behaviors. On the other hand, behavior, by virtue of being dispositional, can be selected. In any case, I have definitively shown that the two concepts are distinct and that it is nonsense to conflate the terms.
In 2012, biologist Hippokratis Kiaris published a book titled Genes, Polymorphisms, and the Making of Societies: How Genetic Behavioral Traits Influence Human Cultures. His main point is that “the presence of different genes in the corresponding people has actually dictated the acquisition of these distinct cultural and historical lines, and that an alternative outcome might be unlikely” (Kiaris, 2012: 9). This is a book that I have not seen discussed in any HBD blog, and based on the premise of the book (how it purports to explain behavioral/societal outcomes between Eastern and Western society) you would think it would be. The book is short, and he speaks with a lot of determinist language. (It’s worth noting he does not discuss IQ at all.)
In the book, he discusses how genes “affect” and “dictate” behavior which then affects “collective decisions and actions” while also stating that it is “conceivable” that history, and what affects human decision-making and reactions, are also “affected by the genetic identity of the people involved” (Kiaris, 2012: 11). Kiaris argues that genetic differences between Easterners and Westerners are driven by “specific environmental conditions that apparently drove the selection of specific alleles in certain populations, which in turn developed particular cultural attitudes and norms” (Kiaris, 2012: 91).
Kiaris attempts to explain the societal differences between the peoples who adopted Platonic thought and those who adopted Confucian thought. He argues that differences between Eastern and Western societies “are not random and stochastic” but are “dictated—or if this is too strong an argument, they are influenced considerably—by the genes that these people carry.” So, Kiaris says, “what we view as a choice is rather the complex and collective outcome of the influence of people’s specific genes combined with the effects of their specific environment … [which] makes the probability for rendering a certain choice distinct between different populations” (Kiaris, 2012: 50).
The first thing that Kiaris discusses (behavior wise) is DRD4. This allele has been associated with miles migrated from Africa (with a correlation of .85) along with novelty-seeking and hyperactivity (which may cause the association found with DRD4 frequency and miles migrated from Africa (Chen et al, 1999). Kiaris notes, of course, that the DRD4 alleles are unevenly distributed across the globe, with people who have migrated further from Africa having a higher frequency of these alleles. Europeans were more likely to have the “novelty-seeking” DRD7 compared to Asian populations (Chang et al, 1996). But, Kiaris (2012: 68) wisely writes (emphasis mine):
Whether these differences [in DRD alleles] represent the collective and cumulative result of selective pressure or they are due to founder effects related to the genetic composition of the early populations that inhabited the corresponding areas remains elusive and is actually impossible to prove or disprove with certainty.
Kiaris then discusses differences between Eastern and Western societies and how we might understand these differences between societies as regards novelty-seeking and the DRD4-7 distribution across the globe. Westerners are more individualistic and this concept of individuality is actually a cornerstone of Western civilization. The “increased excitability and attraction to extravagance” of Westerners, according to Kiaris, is linked to this novelty-seeking behavior which is also related to individualism “and the tendency to constantly seek for means to obtain satisfaction” (Kiaris, 2012: 68). We know that Westerners do not shy away from exploration; after all, the West discovered the East and not vice versa.
Easterners, on the other hand, are more passive and have “an attitude that reflects a certain degree of stoicism and makes life within larger—and likely collectivistic—groups of people more convenient“. Easterners, compared to Westerners, take things “the way they are” which “probably reflects their belief that there is not much one can or should do to change them. This is probably the reason that these people appear rigid against life and loyal, a fact that is also reflected historically in their relatively high political stability” (Kiaris, 2012: 68-69).
Kiaris describes DRD4 as a “prototype Westerner’s gene” (pg 83), stating that the 7R allele of this gene is found more frequently in Europeans compares to Asians. The gene has been associated with increased novelty-seeking, exploratory activity and human migrations, along with liberal ideology. These, of course, are cornerstones of Western civilization and thought, and so, Kiaris argues that the higher frequency of this allele in Europeans—in part—explains certain societal differences between the East and West. Kiaris (2012: 83) then makes a bold claim:
All these features [novelty-seeking, exploratory activity and migration] indeed tend to characterize Westerners and the culutral norms they developed, posing the intriguing possibility that DRD4 can actually represent a single gene that can “predispose” for what we understand as the stereotypic Western-type behavior. Thus, we could imagine that an individual beating the 7-repeat allele functions more efficiently in Western society while the one without this allele would probably be better suited to a society with Eastern-like structure. Alternatively, we could propose that a society with more individuals bearing the 7-repeat allele is more likely to have followed historical lines and choices more typical of a Western society, while a population with a lower number (or deficient as it is the actual case with Easterners) of individuals with the 7-repeat allele would more likely attend to the collective historical outcome of Eaasterners.
Kiaris (2012: 84) is, importantly, skeptical that having a high number of “novelty-seekers” and “explorers” would lead to higher scientific achievement. This is because “attempts to extrapolate from individual characteristics to those of a group of people and societies possess certain dangers and conceptual limitations.”
Kiaris (2012: 86) says that “collectivistic behavior … is related to the activity of serotonin.” He then goes on to cite a few instances of other polymorphisms which are associated with collective behavior as well. Goldman et al (2010) show ethnic differences in the l and s alleles (from Kiaris, 2012: 86):
It should also be noted that populations (Easterners) that had a higher frequency of the s allele had a lower prevalence of depression than Westerners. So Western societies are more likely to “suffer more frequently from various manifestations of depression and general mood disorders than those of Eastern cultures (Chiao & Blizinsky, 2010)” (Kiaris, 2012: 89).
As can be seen from the table above, Westerners are more likely to have the l allele than Easterners, which should subsequently predict higher levels of happiness in Western compared to Eastern populations. However, “happiness” is, in many ways, subjective; so how would one find an objective way to measure “happiness” cross-culturally? However, Kiaris (2012: 94) writes: “Intuitively speaking, though, I have to admit that I would rather expect Asians to be happier, in general, than Westerners. I cannot support this by specific arguments, but I think the reason for that is related to the individualistic approach of life that the people possess in Western societies: By operating under individualistic norms, it is unavoidably stressful, a condition that operates at the expense of the perception of individuals’ happiness.”
Kiaris discusses catechol-O-methyltransferase (COMT), which is an enzyme responsible for the inactivation of catecholamines. Catecholamines are the hormones dopamine, adrenaline, and noradrenaline. These hormones regulate the “fight or flight” function (Goldstein, 2011). So since catecholamines play a regulatory role in the “fight or flight” mechanism, increased COMT activity results in lower dopamine levels, which is then associated with better performance.
“Warriors” and “worriers” are intrinsically linked to the “fight or flight” mechanism. A “warrior” is someone who performs better under stress, achieves maximal performance despite threat and pain, and is more likely to act efficiently in a threatening environment. A “worrier” is “someone that has an advantage in memory and attention tasks, is more exploratory and efficient in complex environments, but who exhibits worse performance under stressful conditions (Stein et al., 2006)” (Kiaris, 2012: 102).
Kiaris (2012: 107) states that “at the level of society, it can be argued that the specific Met-bearing COMT allele contributes to the buildup of Western individualism. Opposed to this, Easterners’ increased frequency of the Val-bearing “altruistic” allele fits quite well with the construction of a collectivistic society: You have to be an altruist at some degree in order to understand the benefits of collectivism. By being a pure individualist, you only understand “good” as defined and reflected by your sole existence.”
So, Kiaris’ whole point is thus: there are differences in polymorphic genes between Easterners and Westerners (and are unevenly distributed) and that differences in these polymorphisms (DRD4, HTT, MAOA, and COMT) explain behavioral differences between behaviors in Eastern and Western societies. So the genetic polymorphisms associated with “Western behavior” (DRD4) are associated with increased novelty-seeking, tendency for financial risk-taking, distance of OoA migration, and liberal ideology. Numerous different MAOA and 5-HTT polymorphisms are associated with collectivism (e.g., Way and Lieberman, 2006 for MAOA and collectivism). The polymorphism in COMT more likely to be found in Westerners predisposes for “worrier’s behavior”. Furthermore, certain polymorphisms of the CHRNB3 gene are more common in all of the populations that migrated out of Africa, which predisposed for leaders—and not follower—behavior.
|Novelty seeking||DRD4||7-repeat novelty seeking allele more common in the West|
|Migration||DRD4||7-repeat allele is associated with distance from Africa migration|
|Nomads/settlers||DRD4||7-repeat allele is associated with nomadic life|
|Political ideology||DRD4||7-repeat allele is more common in liberals|
|Financial risk taking||DRD4||7-repeat allele is more common in risk takers|
|Individualism/Collectivism||HTT||s allele (collectivistic) of 5-HTT is more common in the East|
|Happiness||HTT||l allele has higher prevalence in individuals happy with their life|
|Individualism/Collectivism||MAOA||3-repeat allele (collectivistic) more common in the East)|
|Warrior/Worrier||COMT||A-allele (worrier) more common in the West|
|Altruism||COMT||G-allele (warrior) associated with altruism|
|Leader/Follower||CHRBN3||A-allele (leader) more common in populations Out-of-Africa|
The table above is from Kiaris (2012: 117) who lays out the genes/polymorphisms discussed in his book—what supposedly shows how and why Eastern and Western societies are so different.
Kiaris (2012: 141) then makes a bold claim: “Since we know now that at least a fraction (and likely more than that) of our behavior is due to our genes“, actually “we” don’t “know” this “now”.
The takeaways from the book are: (1) populations differ genetically; (2) since populations differ genetically, then genetic differences correlated with behavior should show frequency differences between populations; (3) since these populations show both behavioral/societal differences and they also differ in genetic polymorphisms which are then associated with that behavior, then those polymorphisms are, in part, a cause of that society and the behavior found in it; (4) therefore, differences in Eastern and Western societies are explained by (some) of these polymorphisms discussed.
Now for a simple rebuttal of the book:
“B iff G” (behavior B is possible if and only if a specific genotype G is instantiated) or “if G, then necessarily B” (genotype G is a sufficient cause for behavior B). Both claims are false; genes are neither a sufficient or necessary cause for any behavior. Genes are, of course, a necessary pre-condition for behavior, but they are not needed for a specific behavior to be instantiated; genes can be said to be difference makers (Sterelny and Kitcher, 1988) (but see Godfrey-Smith and Lewontin, 1993 for a response). These claims cannot be substantiated; therefore, the claims that “if G, then necessarily B” and “B iff G” are false, it cannot be shown that genes are difference makers in regard to behavior, nor can it be shown that particular genes or whatnot.
I’m surprised that I have not come across a book like this sooner; you would expect that there would be a lot more written on this. This book is short, it discusses some good resources, but the conclusions that Kiaris draws, in my opinion, will not come to pass because genes are not neccesary nor sufficient cause of any type of behavior, nor can it be shown that genes are causes of any behavior B. Behavioral differences between Eastern and Western societies, logically, cannot come down to differences in genes, since they are neither necessary nor sufficient causes of behavior (genes are neccessary pre-conditions for behavior, since without genes there is no organism, but genes cannot explain behavior).
Kiaris attempts to show how and why Eastern and Western societies became so different, how and why Western societies are dominated by “Aristotle’s reason and logic”, while Eastern lines of thought “has been dominated by Confucious’s harmony, collectivism, and context dependency” (Kiaris, 2012: 9). While the book is well-written and researched (he talks about nothing new if you’re familiar with the literature), Kiaris fails to prove his ultimate point: that differences in genetic polymorphisms between individuals in different societies explain how and why the societies in question are so different. Though, it is not logically possible for genes to be a necessary nor sufficient cause for any behavior. Kiaris talks like a determinist, since he says that “the presence of different genes in the corresponding people has actually dictated the acquisition of these distinct cultural and historical lines, and that an alternative outcome might be unlikely” (Kiaris, 2012: 9), though that is just wishful thinking: if we were able to start history over again, things would occur differently, “the presence of different genes in the corresponding people” be dammed, since genes do not cause behavior.
President Trump was quoted the other day saying “We have to look at the Internet because a lot of bad things are happening to young kids and young minds and their minds are being formed,” Trump said, according to a pool report, “and we have to do something about maybe what they’re seeing and how they’re seeing it. And also video games. I’m hearing more and more people say the level of violence on video games is really shaping young people’s thoughts.” But outside of broad assertions like this—that playing violent video games cause violent behavior—does it stack up to what the scientific literature says about it? In short, no, it does not. (A lot of publication bias exists in this debate, too.) Why do people think that violent video games cause violent behavior? Mostly due to the APA and their broad claims with little evidence.
Just doing a cursory Google search of ‘violence in video games pubmed‘ brings up 9 journal articles, so let’s take a look at a few of those.
The first article is titled The Effect of Online Violent Video Games on Levels of Aggression by Hollingdale and Greitemeyer (2014). They took 101 participants and randomized them to one of four experimental conditions: neutral, offline; neutral online; (Little Big Planet 2) violent offline; and violent online video games (Call of Duty: Modern Warfare). After they played said games, they answered a questionnaire and then measured aggression using the hot sauce paradigm (Lieberman et al, 1999) to measure aggressive behavior. Hollingdale and Greitemeyer (2014) conclude that “this study has identified that increases in aggression are not more pronounced when playing a violent video game online in comparison to playing a neutral video game online.”
Staude-Muller (2011) finds that “it was not the consumption of violent video games but rather an uncontrolled pattern of video game use that was associated with increasing aggressive tendencies.” Przybylski, Ryan, and Rigby (2009) found that enjoyment, value, and desire to play in the future were strongly related to competence in the game. Players who were high in trait aggression, though, were more likely to prefer violent games, even though it didn’t add to their enjoyment of the game, while violent content lent little overall variance to the satisfactions previously cited.
Tear and Nielsen (2013) failed to find evidence that violent video game playing leads to a decrease in pro-social behavior (Szycik et al, 2017 also show that video games do not affect empathy). Gentile et al (2014) show that “habitual violent VGP increases long-term AB [aggressive behavior] by producing general changes in ACs [aggressive cognitions], and this occurs regardless of sex, age, initial aggressiveness, and parental involvement. These robust effects support the long-term predictions of social-cognitive theories of aggression and confirm that these effects generalize across culture.” The APA (2015) even states that “scientific research has demonstrated an association between violent video game use and both increases in aggressive behavior, aggressive affect, aggressive cognitions and decreases in prosocial behavior, empathy, and moral engagement.” How true is all of this, though? Does playing violent video games truly increase aggression/aggressive behavior? Does it have an effect on violence in America and shootings overall?
Whitney (2015) states that the video-games-cause-violence paradigm has “weak support” (pg 11) and that, pretty much, we should be cautious before taking this “weak support” as conclusive. He concludes that there is not enough evidence to establish a truly causal connection between violent video game playing and violent and aggressive behavior. Cunningham, Engelstatter, and Ward (2016) tracked the sale of violent video games and criminal offenses after those games were sold. They found that violent crime actually decreased the weeks following the release of a violent game. Of course, this does not rule out any longer-term effects of violent game-playing, but in the short term, this is good evidence against the case of violent games causing violence. (Also see the PsychologyToday article on the matter.)
We seem to have a few problems here, though. How are we to untangle the effects of movies and other forms of violent media that children consume? You can’t. So the researcher(s) must assume that video games and only video games cause this type of aggression. I don’t even see how one can logically state that out of all other types of media that violent video games—and not violent movies, cartoons, TV shows etc—cause aggression/violent behavior.
Back in 2011, the Supreme Court case Brown vs. Entertainment Merchants Association concluding that since the effects on violent/aggressive behavior were so small and couldn’t be untangled from other so-called effects from other violent types of media. Ferguson (2015) found that violent video game playing had little effect on children’s mood, aggression levels, pro-social behavior or grades. He also found publication bias in this literature (Ferguson, 2017). Contrary to what those say about video games causing violence/aggressive behavior, video game playing was associated with a decrease in youth crime (Ferguson, 2014; Markey, Markey, and French, 2015 which is in line with Cunningham, Engelstatter, and Ward, 2016). You can read more about this in Ferguson’s article for The Conversation, along with his and others’ responses to the APA who state that violent video games cause violent behavior (with them stating that the APA is biased). (Also read a letter from 230 researchers on the bias in the APA’s Task Force on Violent Media.)
How would one actually untangle the effects of, say, violent video game playing and the effects of such other ‘problematic’ forms of media that also show aggression/aggressive acts towards others and actually pinpoint that violent video games are the culprit? That’s right, they can’t. How would you realistically control for the fact that the child grows up around—and consumes—so much ‘violent’ media, seeing others become violent around him etc; how can you logically state that the video games are the cause? Some may think it logical that someone who plays a game like, say, Call of Duty for hours on end a day would be more likely to be more violent/aggressive or more likely to commit such atrocities like school shootings. But none of these studies have ever come to the conclusion that violent video games may/will cause someone to kill or go on a shooting spree. It just doesn’t make sense. I can, of course, see the logic in believing that it would lead to aggressive behavior/lack of pro-social behavior (let’s say the kid played a lot of games and had little outside contact with people his age), but of course the literature on this subject should be enough to put claims like this to bed.
It’s just about impossible to untangle the so-called small effects of video games on violent/aggressive behavior from other types of media such as violent cartoons and violent movies. Who’s to say it’s not just the violent video games and not the violent movies and violent cartoons, too, that ’cause’ this type of behavior? It’s logically impossible to distinguish this, so therefore the small relationship between video games and violent behavior should be safely ignored. The media seems to be getting this right, which is a surprise (though I bet if Trump said the opposite—that violent video games didn’t cause violent behavior/shootings—that these same people would be saying that they do), but a broken clock is right twice a day.
So Trump’s claim (even if he didn’t outright state it) is wrong, along with anyone else who would want to jump in and attempt to say that video games cause violence. In fact, the literature shows a decrease in violence after games are released (Ferguson, 2014; Markey, Markey, and French, 2015; Cunningham, Engelstatter, and Ward, 2016). The amount of publication bias (also see Copenhaver and Ferguson, 2015 where they show how the APA ignores bias and methodological problems regarding these studies) in this field (Ferguson, 2017) should lead one to question the body of data we currently have, since studies that find an effect are more likely to get published than studies that find no effect.
Video games do not cause violent/aggressive behavior/school shootings. There is literally no evidence that they are linked to the deaths of individuals, and with the small effects noted on violent/aggressive behavior due to violent video game playing, we can disregard those claims. (One thing video games are good for, though, is improving reaction time (Benoit et al, 2017). The literature is strong here; playing these so-called “violent video games” such as Call of Duty improved children’s reaction time, so wouldn’t you say that these ‘violent video games’ have some utility?)
Race, aggression, and prostate cancer are all linked, with some believing that race is the cause of higher testosterone which then causes aggression and higher rates of crime along with maladies such as prostate cancer. These claims have long been put to bed, with a wide range of large analyses.
The testosterone debate regarding prostate cancer has been raging for decades and we have made good strides in understanding the etiology of prostate cancer and how it manifests. The same holds true for aggression. But does testosterone hold the key to understanding aggression, prostate cancer and does race dictate group levels of the hormone which then would explain some of the disparities between groups and individuals of certain groups?
For decades it was believed that heightened levels of testosterone caused prostate cancer. Most of the theories to this day still hold that large amounts of androgens, like testosterone and it’s metabolic byproduct dihydrotestosterone, are the two many factors that drive the proliferation of cells and therefore, if a male is exposed to higher levels of testosterone throughout their lives then they are at a high risk of prostate cancer compared to a man with low testosterone levels, so the story goes.
In 1986 Ronald Ross set out to test a hypothesis: that black males were exposed to more testosterone in the womb and this then drove their higher rates of prostate cancer later in life. He reportedly discovered that blacks, after controlling for confounds, had 15 percent higher testosterone than whites which may be the cause of differential prostate cancer mortality between the two races (Ross et al, 1986) This is told in a 1997 editorial by Hugh McIntosh. First, the fact that black males were supposedly exposed to more testosterone in the womb is brought up. I am aware of one paper discussing higher levels of testosterone in black women compared to white women (Perry et al, 1996). Though, I’ve shown that black women don’t have high levels of testosterone, not higher than white women, anyway (see Mazur, 2016 for discussion). (Yes I changed my view on black women and testosterone, stop saying that they have high levels of testosterone it’s just not true. I see people still link to that article despite the long disclaimer at the top.)
Alvarado (2013) discusses Ross et al (1986), Ellis and Nyborg (1992) (which I also discussed here along with Ross et al) and other papers discussing the supposed higher testosterone of blacks when compared to whites and attempts to use a life history framework to explain higher incidences of prostate cancer in black males. He first notes that nutritional status influences testosterone production which should be no surprise to anyone. He brings up some points I agree with and some I do not. For instance, he states that differences in nutrition could explain differences in testosterone between Western and non-Western people (I agree), but that this has no effect within Western countries (which is incorrect as I’ll get to later).
He also states that ancestry isn’t related to prostate cancer, writing “In summation, ancestry does not adequately explain variation among ethnic groups with higher or lower testosterone levels, nor does it appear to explain variation among ethnic groups with high or low prostate cancer rates. This calls into question the efficacy of a disease model that is unable to predict either deleterious or protective effects.”
He then states that SES is negatively correlated with prostate cancer rates, and that numerous papers show that people with low SES have higher rates of prostate cancer mortality which makes sense, since people in a lower economic class would have less access to and a chance to get good medical care to identify problems such as prostate cancer, including prostate biopsies and checkups to identify the condition.
He finally discusses the challenge hypothesis and prostate cancer risk. He cites studies by Mazur and Booth (who I’ve cited in the past in numerous articles) as evidence that, as most know, black-majority areas have more crime which would then cause higher levels of testosterone production. He cites Mazur’s old papers showing that low-class men, no matter if they’re white or black, had heightened levels of testosterone and that college-educated men did not, which implies that the social environment can and does elevate testosterone levels and can keep them heightened. Alvarado concludes this section writing: “Among Westernized men who have energetic resources to support the metabolic costs associated with elevated testosterone, there is evidence that being exposed to a higher frequency of aggressive challenges can result in chronically elevated testosterone levels. If living in an aggressive social environment contributes to prostate cancer disparities, this has important implications for prevention and risk stratification.” He’s not really wrong but on what he is wrong I will discuss later on this section. It’s false that testosterone causes prostate cancer so some of this thesis is incorrect.
I rebutted Ross et al (1986) December of last year. The study was hugely flawed and, yet, still gets cited to this day including by Alvarado (2013) as the main point of his thesis. However, perhaps most importantly, the assay times were done ‘when it was convenient’ for the students which were between 10 am and 3 pm. To not get any wacky readings one most assay the individuals as close to 8:30 am as possible. Furthermore, they did not control for waist circumference which is another huge confound. Lastly, the sample was extremely small (50 blacks and 50 whites) and done on a nonrepresentative sample (college students). I don’t think anyone can honestly cite this paper as any evidence for blacks having higher levels of testosterone or testosterone causing prostate cancer because it just doesn’t do that. (Read Race, Testosterone and Prostate Cancer for more information.)
What may explain prostate cancer rates if not for differences in testosterone like has been hypothesized for decades? Well, as I have argued, diet explains a lot of the variation between races. The etiology of prostate cancer is not known (ACA, 2016) but we know that it’s not testosterone and that diet plays a large role in its acquisition. Due to their dark skin, they need more sunlight than do whites to synthesize the same amount of vitamin D, and low levels of vitamin D in blacks are strongly related to prostate cancer (Harris, 2006). Murphy et al (2014) even showed, through biopsies, that black American men had higher rates of prostate cancer if they had lower levels of vitamin D. Lower concentrations of vitamin D in blacks compared to whites due to dark pigmentation which causes reduced vitamin D photoproduction and may also account for “much of the unexplained survival disparity after consideration of such factors as SES, state at diagnosis and treatment” (Grant and Peiris, 2012).
As mentioned above, testosterone is assumed to be higher in certain races compared to others (based on flawed studies) which then supposedly exacerbates prostate cancer. However, as can be seen above, a lot of assumptions go into the testosterone-prostate cancer hypothesis which is just false. So if the assumptions are false about testosterone, mainly regarding racial differences in the hormone and then what the hormone actually does, then most of their claims can be disregarded.
Perhaps the biggest problem is that Ross et al is a 32-year-old paper (which still gets cited favorably despite its huge flaws) while our understanding of the hormone and its physiology has made considerable progress in that time frame. So it’s in fact not so weird to see papers like this that say “Prostate cancer appears to be unrelated related to endogenous testosterone levels” (Boyle et al, 2016). Other papers also show the same thing, that testosterone is not related to prostate cancer (Stattin et al, 2004; Michaud, Billups, and Partin, 2015). This kills a lot of theories and hypotheses, especially regarding racial differences in prostate cancer acquisition and mortality. So, what this shows is that even if blacks did have 15 percent higher serum testosterone than whites as Ross et al, Rushton, Lynn, Templer, et al believed then it wouldn’t cause higher levels of prostate cancer (nor aggression, which I’ll get into later).
How high is testosterone in black males compared to white males? People may attempt to cite papers like the 32-year-old paper by Ross et al, though as I’ve discussed numerous times the paper is highly flawed and should therefore not be cited. Either way, levels are not as high as people believe and meta-analyses and actual nationally representative samples (not convenience college samples) show low to no difference, and even the low difference wouldn’t explain any health disparities.
One of the best papers on this matter of racial differences in testosterone is Richard et al (2014). They meta-analyzed 15 studies and concluded that the “racial differences [range] from 2.5 to 4.9 percent” but “this modest difference is unlikely to explain racial differences in disease risk.” This shows that testosterone isn’t as high in blacks as is popularly misconceived, and that, as I will show below, it wouldn’t even cause higher rates of aggression and therefore criminal behavior. (Rohrmann et al 2007 show no difference in testosterone between black and white males in a nationally representative sample after controlling for lifestyle and anthropometric variables. Whereas Mazur, 2009 shows that blacks have higher levels of testosterone due to low marriage rates and lower levels of adiposity, while be found a .39 ng/ml difference between blacks and whites aged 20 to 60. Is this supposed to explain crime, aggression, and prostate cancer?)
However, as I’ve noted last year (and as Alvarado, 2013 did as well), young black males with low education have higher levels of testosterone which is not noticed in black males of the same age group but with more education (Mazur, 2016). Since blacks of a similar age group have lower levels of testosterone but are more highly educated then this is a clue that education drives aggression/testosterone/violent behavior and not that testosterone drives it.
Mazur (2016) also replicated Assari, Caldwell, and Zimmerman’s (2014) finding that “Our model in the male sample suggests that males with higher levels of education has lower aggressive behaviors. Among males, testosterone was not associated with aggressive behaviors.” I know this is hard for many to swallow that testosterone doesn’t lead to aggressive behavior in men, but I’ll cover that in the last and final section.
So it’s clear that the myth that Rushton, Lynn, Templer, Kanazawa, et al pushed regarding hormonal differences between the races are false. It’s also with noting, as I did in my response to Rushton on r/K selection theory, that the r/K model is literally predicated on 1) testosterone differences between races being real and in the direction that Rushton and Lynn want because they cite the highly flawed Ross et al (1986) and 2) testosterone does not cause higher levels of aggression (which I’ll show below) which then lead to higher rates of crime along with higher rates of incarceration.
A blogger who goes by the name of ethnicmuse did an analysis of numerous testosterone papers and he found:
Which, of course, goes against a ton of HBD theory, that is, if testosterone did what HBDers believed it does (it doesn’t). This is what it comes down to: blacks don’t have higher levels of testosterone than whites and testosterone doesn’t cause aggression nor prostate cancer so even if this relationship was in the direction that Rushton et al assert then it still wouldn’t cause any of the explanatory variables they discuss.
Last year Lee Ellis published a paper outlining his ENA theory (Ellis, 2017). I responded to the paper and pointed out what he got right and wrong. He discussed strength (blacks aren’t stronger than whites due to body type and physiology, but excel in other areas); circulating testosterone, umbilical cord testosterone exposure; bone density and crime; penis size, race, and crime (Rushton’s 1997 claims on penis size don’t ‘size up’ to the literature as I’ve shown two times); prostate-specific antigens, race, and prostate cancer; CAG repeats; intelligence and education and ‘intelligence’; and prenatal androgen exposure. His theory has large holes and doesn’t line up in some places, as he himself admits in his paper. He, as expected, cites Ross et al (1986) favorably in his analysis.
Testosterone can’t explain all of these differences, no matter if it’s prenatal androgen exposure or not, and a difference of 2.5 to 4.9 percent between blacks and whites regarding testosterone (Richard et al, 2014) won’t explain differences in crime, aggression, nor prostate cancer.
Other authors have attempted to also implicate testosterone as a major player in a wide range of evolutionary theories (Lynn, 1990; Rushton, 1997; Rushton, 1999; Hart, 2007; Rushton and Templer, 2012; Ellis, 2017). However, as can be seen by digging into this literature, these claims are not true and therefore we can discard the conclusions come to by the aforementioned authors since they’re based on false premises (testosterone being a cause for aggression, crime, and prostate cancer and r/K meaning anything to human races, it doesn’t)
Finally, to conclude this section, does testosterone explain racial differences in crime? No, racial differences in testosterone, however small, cannot be responsible for the crime gap between blacks and whites.
Testosterone and aggression
Testosterone and aggression, are they linked? Can testosterone tell us anything about individual differences in aggressive behavior? Surprisingly for most, the answer seems to be a resounding no. One example is the castration of males. Does it completely take away the urge to act aggressively? No, it does not. What is shown when sex offenders are castrated is that their levels of aggression decrease, but importantly, they do not decrease to 0. Robert Sapolsky writes on page 96 of his book Behave: The Biology of Humans at Our Best and Worst (2017) (pg 96):
… the more experience a male has being aggressive prior to castration, the more aggression continues afterward. In other words, the less his being aggressive in the future requires testosterone and the more it’s a function of social learning.
He also writes (pg 96-97):
On to the next issue that lessens the primacy of testosterone: What do individual levels of testosterone have to do with aggression? If one person higher testosterone levels than another, or higher levels this week than last, are they more likely to be aggressive?
Initially the answer seemed to be yes, as studies showed correlation between individual differences in testosterone levels and levels of aggression. In a typical study, higher testosterone levels would be observed in those male prisoners with higher rates of aggression. But being aggressive stimulates testosterone secretion; no wonder more aggressive individuals had higher levels. Such studies couldn’t disentangle chickens and eggs.
Thus, a better question is whether differences in testosterone levels among individuals predict who will be aggressive. And among birds, fish, mammals, and especially other primates, the answer is generally no. This has been studied extensively in humans, examining a variety of measures of aggression. And the answer is clear. To quote British endocrinologist John Archer in a definitive 2006 review, “There is a weak and inconsistent association between testosterone levels and aggression in [human] adults, and . . . administration of testosterone to volunteers typically does not increase aggression.” The brain doesn’t pay attention to testosterone levels within the normal range.
Thus, aggression is typically more about social learning than about testosterone, differing levels of testosterone generally can’t explain why some individuals are more aggressive than others.
Sapolsky also has a 1997 book of essays on human biology titled The Trouble With Testosterone: And Other Essays On The Biology Of The Human Predicament and he has a really good essay on testosterone titled Will Boys Just Be Boys? where he writes (pg 113 to 114):
Okay, suppose you note a correlation between levels of aggression and levels of testosterone among these normal males. This could be because (a) testosterone elevates aggression; (b) aggression elevates testosterone secretion; (c) neither causes the other. There’s a huge bias to assume option a while b is the answer. Study after study has shown that when you examine testosterone when males are first placed together in the social group, testosterone levels predict nothing about who is going to be aggressive. The subsequent behavioral differences drive the hormonal changes, not the other way around.
Because of a strong bias among certain scientists, it has taken do forever to convince them of this point.
As I said, it takes a lot of work to cure people of that physics envy, and to see interindividual differences in testosterone levels don’t predict subsequent differences in aggressive behavior among individuals. Similarly, fluctuations in testosterone within one individual over time do not predict subsequent changes in the levels of aggression in the one individual—get a hiccup in testosterone secretion one afternoon and that’s not when the guy goes postal.
And on page 115 writes:
You need some testosterone around for normal levels of aggressive behavior—zero levels after castration and down it usually goes; quadruple it (the sort of range generated in weight lifters abusing anabolic steroids), and aggression typically increases. But anywhere from roughly 20 percent of normal to twice normal and it’s all the same; the brain can’t distinguish among this wide range of basically normal values.
Weird…almost as if there is a wide range of ‘normal’ that is ‘built in’ to our homeodynamic physiology…
So here’s the point: differences in testosterone between individuals tell us nothing about individual differences in aggressive behavior; castration and replacement seems to show that, however broadly, testosterone is related to aggression “But that turns out to not be true either, and the implications of this are lost on most people the first thirty times you tell them about it. Which is why you’d better tell them about it thirty-one times, because it’s the most important part of this piece” (Sapolsky, 1997: 115).
Later in the essay, Sapolsky discusses a discusses 5 monkeys that were given time to form a hierarchy of 1 through 5. Number 3 can ‘throw his weight’ around with 4 and 5 but treads carefully around 1 and 2. He then states to take the third-ranking monkey and inject him with a ton of testosterone, and that when you check the behavioral data that he’d then be participating in more aggressive actions than before which would imply that the exogenous testosterone causes participation in more aggressive behavior. But it’s way more nuanced than that.
So even though small fluctuations in the levels of the hormone don’t seem to matter much, testosterone still causes aggression. But that would be wrong. Check out number 3 more closely. Is he now raining aggression and terror on any and all in the group, frothing in an androgenic glaze of indiscriminate violence. Not at all. He’s still judiciously kowtowing to numbers 1 and 2 but has simply become a total bastard to number 4 and 5. This is critical: testosterone isn’t causing aggression, it’s exaggerating the aggression that’s already there.
The correlation between testosterone and aggression is between .08 and .14 (Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan, and Davies, 2005; Book and Quinsey, 2005). Therefore, along with all of the other evidence provided in this article, it seems that testosterone and aggression have a weak positive correlation, which buttresses the point that aggression concurrent increases in testosterone.
Sapolsky then goes on to discuss the amygdala’s role in fear processing. The amygdala has its influence on aggressive behavior through the stria terminalis, which is a bunch of neuronal connections. How the amygdala influences aggression is simple: bursts of electrical excitation called action potentials go up and down the stria terminalis which changes the hypothalamus. You can then inject testosterone right into the brain and will it cause the same action potentials that surge down the stria terminalis? No, it does not turn on the pathway at all. This only occurs only if the amygdala is already sending aggression-provoking action potentials down the stria terminalis with testosterone increasing the rate of action potentials you’re shortening the rest time between them. So it doesn’t turn on this pathway, it exaggerates the preexisting pattern, which is to say, it’s exaggerating the response to environmental triggers of what caused the amygdala to get excited in the first place.
He ends this essay writing (pg 119):
Testosterone is never going to tell us much about the suburban teenager who, in his after-school chess club, has developed a particularly aggressive style with his bishops. And it certainly isn’t going to tell us much about the teenager in some inner-city hellhole who has taken to mugging people. “Testosterone equals aggression” is inadequate for those who would offer a simple solution to the violent male—just decrease levels of those pesky steroids. And “testosterone equals aggression” is certainly inadequate for those who would offer a simple excuse: Boys will be boys and certain things in nature are inevitable. Violence is more complex than a single hormone. This is endocrinology for the bleeding heart liberal—our behavioral biology is usually meaningless outside of the context of social factors and the environment in which it occurs.
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). This, too, is a large blow for the testosterone-induces-aggression hypothesis. Because aggressive behavior heightens testosterone, testosterone doesn’t heighten aggressive behavior. (This is the causality that has been looked for, and here it is. The causality is not in the other direction.) This tells us that we need to be put into situations for our aggression to rise and along with it, testosterone. I don’t even see how people could think that testosterone could cause aggression. It’s obvious that the environmental trigger needs to be there first in order for the body’s physiology to begin testosterone production in order to prepare for the stimulus that caused the heightened testosterone production. Once the trigger occurs, then it can and does stay heightened, especially in areas where dominance contests would be more likely to occur, which would be low-income areas (Mazur, 2006, 2016).
Lastly, one thing that gets on my nerves that people point to to attempt to show that testosterone and its derivatives cause violence, aggression etc is the myth of “roid rage” which is when an individual objects himself with testosterone, anabolic steroids or another banned substance, and then the individual becomes more aggressive as a result of more free-flowing testosterone in their bloodstream.
The problem here is that people believe what they hear on the media about steroids and testosterone, and they’re largely not true. One large analysis was done to see the effects of steroids and other illicit drug use on behavior, and what was found was that after controlling for other substance use “Our results suggest that it was not lifetime steroid use per se, but rather co-occurrring polysubstance abuse that most parsimoniously explains the relatively strong association of steroid use and interpersonal violence” (Lundholm et al, 2015). So after controlling for other drugs used, men who use steroids do not go to prison and be convicted of violence after other polysubstance use was controlled for, implying that is what’s driving interpersonal violence, not the substance abuse of steroids.
Numerous myths about testosterone have been propagated over the decades, which are still believed in the new millennium despite numerous other studies and arguments to the contrary. As can be seen, the myths that people believe about testosterone are easily debunked. Numerous papers (with better methodology than Ross et al) attest to the fact that testosterone levels aren’t as high as was believed decades ago between the races. Diet can explain a lot of the variation, especially vitamin D intake. Injecting men with supraphysiological doses of testosterone does not heighten anger nor aggression. It does not even heighten prostate cancer severity.
Racial differences in testosterone are also not as high as people would like to believe, there is even an opposite relationship with Asians having higher levels and whites having lower (which wouldn’t, on average, imply femininity) testosterone levels. So as can be seen, the attempted r/K explanations from Rushton et al don’t work out here. They’re just outright wrong on testosterone, as I’ve been arguing for a long while on this blog.
Testosterone doesn’t cause aggression, aggression causes heightened testosterone. It can be seen from studies of men who have been castrated that the more crime they committed before castration, the more crime they will commit after which implies a large effect of social learning on violent behavior. Either way, the alarmist attitudes of people regarding testosterone, as I have argued, are not needed because they’re largely myths.
Many long-time readers may know of the numerous tirades of been on in regards to the “testosterone causes crime and aggression” myth. It’s a fun subject to talk about because the intelligent human physiological system is an amazing system. However, people who are not privy to the literature on testosterone in regards to race, aggression, crime, sex differences etc are only aware of whatever they read in pop science articles. So since they never read the actual papers themselves, they get a clouded view of a subject.
In my last article, I wrote about how there are no “testosterone genes”. In previous articles on the hormone, I have proven that there is no causal link between testosterone and aggression. But when comparing the sexes, how do the results look? Do they look the same with men being more violent while women—who have substantially less testosterone than men—do not have any higher levels of aggression or crime? The most recent study I’m aware of is by Assari, Caldwell, and Zimmerman (2014) titled: Sex Differences in the Association Between Testosterone and Violent Behaviors.
To make a long story short, there was no relationship between testosterone and aggression in men, but a significant relationship between testosterone and aggression in women. This data comes from the Flint Adolescent Study, a longitudinal study conducted between the years of 1994 to 2012. In regards to testosterone collection, saliva was used which has a perfect correlation with circulating testosterone. The eligibility to be included in the testosterone assay was “provided consent for the procedure, not being pregnant, not having anything to eat, drinking nothing except water, and not using tobacco, 1 hour prior to collection” (Assari, Caldwell, and Zimmerman, 2014).
The adolescent who contributed saliva gave a whole slew of demographic factors including SES, demographics, psychological factors, family relations, religion, social relations, behavior, and health. They were aged 14 to 17 years of age. They collected data during face-to-face interviews,
Age and SES were used as control variables in their multivariate analysis. For violent behaviors, the authors write:
Youths were asked how often they had engaged in the following behaviors; ‘had a fight in school’, ‘taken part in a rumble where a group of your friends were against another group’, injured someone badly enough to need bandages or a doctor’, ‘hit a teacher or supervisor at work (work supervisor)’, used a knife or gun or other object (like a club) to get something romantic a person’, ‘carried a knife or razor’, or ‘carried a gun’. All items used a Likert response, ranging from 1 (0 times) to 5 (4 or more times). Responses to each item were averages to calculate the behavior during the last year. Total score was calculated as the average of all items. Higher scores indicated more violent behaviors (a = 0.79). This measure has shown high reliability and validity and it has been used previously in several published reports.
This is a great questionnaire. The only thing I can think of that’s missing is fighting/arguing with parents.
In regards to testosterone assaying, they were assayed after 11 am to “control for changes due to diurnal rhythm” (Assari, Caldwell, and Zimmerman, 2014). I’m iffy on that since testosterone levels are highest at 8 am but whatever. This analysis is robust. Saliva was not taken if the subject had smoked or ingested something other than water or if a subject was pregnant. Assays should be taken as close to 8 am, as that’s when levels are highest. However one study does argue to extend the range to 8 am to 2 pm (Crawford et al, 2015) while other studies show that this only should be the case for older males (Long, Nguyen, and Stevermer, 2015). Even then assays were done at the higher end of the range as stated by Crawford et al (2015), so differences shouldn’t be too much.
86.4 percent of the sample was black whereas 13.4 percent were white. 41.2 percent of the subjects had some college education whereas 58.2 percent of the subjects lived with a partner or relative. 21.4 percent of the subjects were unemployed.
The mean age was 20.5 for both men and women, however, which will be a surprise to some, testosterone did not predict aggressive behavior in men but did in women. Testosterone and aggressive behavior were positively correlated, whereas there was a negative correlation between education and testosterone and aggressive behavior. Though education was associated with aggressive behavior in men but not women. So sex and education was associated with aggressive behavior (the sex link being women more privy to aggressive behavior while men are more privy to aggressive behavior due to lack of education). Females who had high levels of education had lower levels of aggressive behavior. Again: testosterone wasn’t associated with violent behavior in men, but it was in women. This is a very important point to note.
This was a community sample, so, of course, there were different results when compared to a laboratory setting, which is not surprising. Laboratory settings are obviously unnatural settings whereas the environment you live in every day obviously is more realistic.
This study does contradict others, in that it shows that there is no association between testosterone and aggression in men. However, still other research shows that testosterone is not linked to aggression or impulsivity, but to sensation-seeking, sexual experience or sociality (Daitzman and Zuckerman, 1980; Zuckerman, 1984). Clearly, testosterone is a beneficial hormone and due to the low correlation of testosterone with aggression (between .08 and .14; Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005). This paper, yet again, buttresses my arguments in regards to testosterone and aggressive behavior.
In regards to the contrast in the literature the authors describe, they write:
One of the many factors that may explain the inconsistency in these findings is the community versus clinical setting, which has been shown to be a determinant of these associations. Literature has previously shown that many of the findings that can be found in clinical samples may not be easily replicated in a community setting (36).
This is like the (in)famous, unreplicable stereotype threat (see Stroessner and Good). It can only be replicated in a lab, not in an actual educational setting. And it also seems that this is the case for testosterone and aggressive behavior.
Just because women have lower testosterone and are less likely to engage in aggressive behavior, that doesn’t mean that a relationship does not exist between females. “It is also plausible to attribute sex differences in the above studies to differential variations in the amount of testosterone among men and women” (Assari, Caldwell, and Zimmerman, 2014). This view supports the case that testosterone is linked to aggression in females, even though their range of testosterone is significantly lower than men’s, while it may also be easier to assay women for testosterone due to less diurnal variation in comparison to men (Book, Starzyk, and Quinsey, 2001).
Assari, Caldwell, and Zimmerman, (2014) also write (which, again, buttresses my arguments):
Age may explain some of the conflicting results across the studies. A meta-analysis of community and selected samples suggested that there might be only low to modest association between testosterone and aggression, with mean weighted correlations ranging from 0.08 to 0.14, in males. Overall, these meta-analyses suggest that the testosterone-aggression association is equally strong in 12 to 21-year-olds, as it is in 22 to 35-year-olds, but that it may be less strong in age groups younger than 12, than in those who are older.
So, testosterone may be associated with aggressive behavior and violence in women but not in men. In men, the significant moderator was education. It’s interesting to note that Mazur (2016) noted that young black males with little education had higher levels of testosterone than age-matched samples of other blacks. This, along with the evidence provided here, may be a clue that if the social environment changes, then so will higher levels of testosterone (as I have argued here).
They, perhaps taking too large of a leap here, argue that “aggressive behaviors may be more social and less biologically based among men” (Assari, Caldwell, and Zimmerman, 2014). Obviously social factors are easier to change than biological ones (in theory), so, they argue, preventative measures may be easier for men than women. More studies need to be done on the complex interactions between sex, testosterone, aggression, biology and the social environment which then shapes the aggressive behaviors of those who live there.
Testosterone and aggression studies are interesting. However, you must know a good amount of the literature to be able to ascertain good studies from the bad, what researchers should and should not have controlled for, time of assay, etc because these variables (some not in the author’s hands, however) can and do lead to false readings if certain variables are not controlled for. All in all, the literature is clearly points to, though other studies contest this at times, the fact that testosterone does not cause aggressive behavior in men. The myth needs to die; the data is piling up for this point of view and those who believe that testosterone causes aggressive behavior and crime (which I have shown it does not, at least for men) will soon be left in the dust as we get a better understanding of this pivotal hormone.
(In case anyone was going to use this as evidence that black women have higher levels of testosterone than white women, don’t do it because it’s not true. You’ll only embarrass yourself like this guy did. Read the comments and see him say that you don’t need scientific measurements, you only need to ‘observe it’ and through ‘observation’ we can deduce that black women have higher levels of testosterone than white women. This is not true. Quoting Mazur, 2016:
The pattern [high testosterone] is not seen among teenage boys or among females.
There is no indication of inordinately high T among young black women with low education.
Whoever still pushes that myth is an idealogue; I have retracted my article ‘Black Women and Testosterone‘, but idealogues just gloss over it and read what they think will bolster their views when I have provided the evidence to the contrary. It pisses me off that people selectively read things then cite my article because they think it will confirm their pre-conceived notions. Well too bad, things don’t work like that.)
Oxytocin (OXT) is known as ‘the love hormone’, since it facilitates bonding from mother to child (Galbally et al, 2011; Feldman and Bakermans-Kranenburg, 2017), facilitates childbirth and breastfeeding (since OXT is released in large amounts after nipple stimulation) (Magon and Kalra, 2011), and increases trust in humans (Kosfeld et al, 2005). It is also implicated in some psychiatric disorders (Marrazziti and Del’Osso, 2008; Cochran et al, 2013). OXT, furthermore, also has endocrine and paracrine roles in male reproduction (Nicholson, 1996; Thackare, Nicholson, and Whittleson, 2006), so it is not strictly ‘a female hormone’ (Saladin, 2010). The hormone induces numerous important behaviors that attach the mother—emotionally speaking—to her new child.
A recent study published back in July titled “Oxytocin-enforced norm compliance reduces xenophobic outgroup rejection” (Marsh et al, 2017), purports to observe that, xenophobic individuals administered a nasal spray with OXT and then shown pro-social behaviors to other ethnies (refugees) show a reduction in xenophobic attitudes. First, I will cover the science aspect of it, then, I will cover the ideological aspect of the paper, and finally will address the societal implications this paper may have in the future. I will conclude with my thoughts on both the science and ideology behind the paper (because, in my opinion, there was a clear ideological drive behind the paper, though, the same holds for most other fields).
In the first experiment, 53 males and 23 females (n=76) were given either the spray with the OXT or a placebo. They were then administered a test that tested how high they scored on a ‘Xenophobia index’. Marsh et al (2017: 9,318) write:
In a separate screening session, we evaluated xenophobia by measuring the attitudes toward refugees based on an adapted assessment instrument developed by Schweitzer and colleagues (33). Adaptions encompassed the wording; for example, “Australian refugee” was replaced by “German refugee.” The assessment instrument contained two inventories, in which participants indicated how strongly they associate refugees with realistic and symbolic threats.
The realistic threat scale items encompass different threat perceptions; for example: “Refugees are not displacing German workers from their jobs” or “Refugees have increased the tax burden on Germans.” Responses were coded on a 10-point Likert scale, ranging from 1 (“I strongly disagree”) to 10 (“I strongly agree”). All items were recoded such that higher values reflected greater feelings of perceived realistic threats. The term Xi index, which we used for subsequent analyses, refers to a subject’s mean score achieved on the realistic threat inventory.
Higher Xi scores imply that an individual is more xenophobic. For experiment 1, they put the subjects into a lecture hall to establish altruistic norms, which enabled reputation pressures if one was seen to not be generous when giving. Marsh et al (2017) discovered that those who donated to refugees donated 19 percent more money. Further, donations to natives or refugees—including outgroup bias—was not dependant on gender. The bias (19 percent more donation) indicated altruistic actions and was lowest in those with high Xi scores.
Experiments 2 and 3 were randomized controlled trials (RCTs) of a random sample of 107 males (mean age of 24). They were administered either the OXT nasal spray or a placebo by a blind researcher. They separated them into high Xi scorers or low Xi scorers (n=53 and n=54 respectively). The OXT administered to low Xi scorers specifically increased altruistic behavior towards the ingroup and outgroup “evident in a 68% (outgroup) and an 81% (ingroup) increase in the donated sums” (Marsh et al, 2017: 9315). However, this effect was not noticed in high Xi scorers, so the researchers wondered if showing pro-social behaviors after being administered OXT would show a change in xenophobic behavior.
So people who scored high on the Xi index and were administered OXT showed no change in altruistic behavior. However, when those who scored high on the XI index were administered OXT and prosocial behavior to the outgroup was seen by those with higher Xi scores, they increased their donations to the outgroup by 74 percent.
Figure 1 shows, clearly, that those who were administered OXT and were exposed to altruistic norms from co-ethnics to the outgroup showed more generosity towards the outgroup than those administered the placebo. It’s also worth noting that these findings (of course) are not generalizable to women.
How does ideology affect this? Of course, both the Right and Left can use this study for their own agendas, but, of course, the Marsh et al (2017) may have biases themselves (everyone has biases, even the most well-known, most respected scientists), so now I will look at the ideology behind this paper through both a Right and Left lens, since political bias permeates our every day lives, and due to this, people won’t be able to think rationally about things, ironically, using their emotions to guide their thought processes/conclusions.
Marsh et al (2017: 9317) write:
The effect of solutions combining selective enhancement of OXT signaling and peer influence would be expected to diminish selfish motives, and thereby increase the ease by which people adapt to rapidly changing social ecosystems. More generally, our results imply that an OXT-enforced social norm adherence could be instrumental in motivating a more generalized acceptance toward ethnic diversity, religious plurality, and cultural differentiation resulting from migration by proposing that interventions to increase altruism are most effective when charitable social cues instill the notion that one’s ingroup shows strong affection for an outgroup. Furthermore, UNESCO has emphasized the importance of developing neurobiologically informed strategies for reducing xenophobic, hostile, and discriminatory attitudes (47). Thus, considering OXT-enforced normative incentives in developing future interventions and policy programs intended to reduce outgroup rejection may be an important step toward making the principle of social inclusion a daily reality in our societies.
This seems pretty bad to me. “If you won’t accept people in your countries, you must take this exogenous OXT while watching your ethnic group show altruistic behavior towards the outgroup so then you too will no longer be a ‘racist’.”
In regard to ref 47, it is a 2001 UNESCO address on ‘racism’. Of course, it begins by stating that “Science – modern genetics in particular – has constantly affirmed the unity of the human species, and denied that the notion of `race’ has any foundation.” This, as regular readers know, is false. Race is a social construct of a biological reality. Self-reported race is a great metric to gauge geographic ancestry (Risch et al, 2002), while Tang et al (2005) showed that self-reported race correlated almost perfectly with geographic ancestry. Though I can forgive this since it is a 2001 address.
Here is the money quote (emphasis mine):
Similarly, respect for others and acceptance of the right to be different should be built in the minds of human beings to replace hostile, discriminatory and xenophobic attitudes.
So it seems that Marsh et al (2017) is the first step in UNESCO’s quest for “[building] the minds of human beings to replace hostile, discriminatory and xenophobic attitudes … I can assure you that UNESCO will work actively to achieve this goal in close cooperation with other UN bodies and specialised agencies, other intergovernmental and nongovernmental organizations and with all interested partners.“. This screams social engineering to me, and it seems that the authors would approve of this, especially if you read the Discussion of the paper. This seems to be whatever the Left thinks would make for a better society, they’ll attempt to enact it. People believe they’re the opposite sex? Give them ‘gender-affirming surgery’ (whatever that means). People are ‘racist’? Better strap them down into a chair and shoot exogenous OXT up their nose while their eyes are forced open while watching videos of prosocial behaviors to the outgroup! The numerous possible scenarios that can be thought up due to this paper are mind boggling. For instance, maybe they can use our Internet history and see who the ‘wrongthinkers’ are to forcibly administer OXT to the ‘racists’. But I thought people should be who they are….?
I’d like to know what the baseline levels of OXT in the subjects were. For instance, did the people who had a high Xi score have higher levels of endogenous OXT? Furthermore, were they around people who did not show altruistic behavior towards ‘refugees’? That, then, would show that higher levels of endogenous OXT combined with non-altruistic behavior would increase ethnocentrism (Dreu et al, 2010). OXT has also been called by journalists ‘the love and trust hormone‘ and ‘the cuddle hormone‘, however, the results of Dreu et al (2010) call this into question showing that the hormone may be a cause of inter-group violence along with outgroup derogation. Dreu et al (2010) also conclude that OXT contributes to prosocial behaviors for the ingroup and facilitates outgroup derogation.
So OXT doesn’t make us prosocial on its own; OXT functions as a way to differentiate the ingroup vs. the outgroup, along with giving the in-group more preferential treatment (though other analyses fail to find that outgroup trust decreases; IJzendoorn and Bakermans-Kranenburg, 2011). Dreu et al (2010) also states that ethnocentrism that’s driven by high levels of endogenous OXT “paves the way for intergroup bias, conflict, and violence.” However, the results of Marsh et al (2017) show that OXT may facilitate prosocial behavior.
This study—especially with the discussion and the authors’ citation of the 2001 UNESCO address about “[building] the minds of human beings” is pretty scary. If you don’t go by what society says is ‘good’ and ‘right’ (whatever that means), you’re a heretic and you must be shown the way—forced OXT and watch the altruistic behavior, you don’t want to be ‘racist’ now, do you? We know that those that run our Western countries would like to make us how they think we should be—non-‘xenophobic’, accepting of migration, and they don’t want use to complain about it. So why not attempt to social engineer the populace into conforming to what the government wants?
Of course, over the past decade or so, mass immigration from outside the West has increased. I won’t go into the causes for that since I don’t discuss politics, however, unchecked immigration—no matter what the ultimate cause is—will change the host society. Go somewhere for X amount of benefits? If enough migration occurs to that nation and the native population is displaced enough, how would those benefits continue if those that migrated still exhibit the same behavior they did in their native countries?
This seems to be the start of “If we don’t like what you think or your beliefs, we will attempt to administer hormones to you and force you to watch this in order to cure you of your unnatural (in our egalitarian society) ‘racism’.” Measures such as this have, as far as I know, been spoken about since the turn of the last millennium and the completion of the Human Genome Project. It seems that as more and more migration occurs to the West, more and more anti-migrant attitudes will be had. The plan here seems to be to socially engineer people to be accepting of their replacement. Why? I thought that people should ‘be themselves’, that’s what they tell transgenders, anyway. Why would ‘racists’ be any different? Oh, because it’s not acceptable in today’s increasingly multi-ethnic society.
I won’t go down the path of the naturalistic fallacy (re: ethnocentrism is good and natural because we evolved that way), however, there is, of course, great adaptive significance to such behavior. If you show more altruistic behavior towards the in-group, you’re more likely to show more altruistic behavior to your family members and thusly have a better chance of protecting co-ethnics.
This is a great example of people attempting to enact policies to socially engineer people, a la Brave New World or 1984. Hormones influence behaviors, yes. Further, watching similar others engage in an action facilitates the possibility that they would also take t at same action. Administering exogenous OXT while seeing that would, according to Marsh et al (2017), cure ‘racism’ and make people happy about being displaced in their own countries. Non-Western people are abnormal to our societies, and when migration occurs to the West, this leads to a decrease in social trust in the native population (Putnam, 2007).
The paper (and its results) seem heavily driven by political bias. Will these political biases doom us to further social engineering through administering the populace with whatever hormones are discovered to do what ‘they‘ (the government) want us to do and how ‘they‘ want us to act? All I know is that it’s pretty scary to hear that this is even being talked about. I hope this never comes to fruition.