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On the So-Called “Laws of Behavioral Genetics”
2400 words
In the year 2000, psychologist Erik Turkheimer proposed three “laws of behavioral genetics” (LoBG hereafter):
● First Law. All human behavioral traits are heritable.
● Second Law. The effect of being raised in the same family is smaller than the effect of genes.
● Third Law. A substantial portion of the variation in complex human behavioral traits is not accounted for by the effects of genes or families. (Turkheimer, 2000: 160)
In March of 2021, I asked Turkheimer how he defined “law.” He responded: “With tongue in cheek. In fact, it’s a null hypothesis: an expected result when nothing in particular is going on.“
In 2015, Chabris et al (2015) proposed a 4th “law”, that a typical behavioral trait is associated with many variants which each explain a small amount of behavioral variability. They state that the “4th law” explains the failure of candidate gene studies and also the need for higher sample sizes in GWA studies. (It seems they are not aware that larger sample sizes increase the probability of spurious correlations—which is all GWA studies are; Claude and Longo, 2016; Richardson, 2017; Richardson and Jones, 2019) Nice ad hoc hypothesis to save their thinking.
One huge proponent of the LoBG is JayMan, who has been on a crusade for years pushing this nonsense. He added a “5th law” proposed by Emil Kirkegaard, which states that “All phenotypic relationships are to some degree genetically mediated or confounded.”
But what is a “law” and are these “laws of behavioral genetics” laws in the actual sense? First I will describe what a “law” is and if there even are biological laws. Then I will address each “law” in turn. I will then conclude that the LoBG aren’t real “laws”, they are derived from faulty thinking about the relationship between genes, traits, environment and the system and how the “laws” were derived rest on false assumptions.
What is a law? Are there biological laws?
Laws are “true generalizations that are “purely quantitative” … They have counterfactual force” (Sober, 1993: 458). Philosopher of mind Donald Davidson argued that laws are strict and exceptionless (Davidson, 1970; David-Hillel, 2003). That is, there must be no exceptions for that law. Sober (1993) discusses Rosenberg’s and Beatty’s arguments against laws of biology—where Rosenberg states that the only law in biology is “natural selection.” (See Fodor, 2008 and Fodor and Piattelli-Palmarini, 2009, 2010 for the argument against that claim and for arguments against the existence of laws of selection that can distinguish between causes and correlates of causes.) It has even been remarked that there are “so few” laws in biology (Dhar and Giuliani, 2010; also see Ruse, 1970).
Biology isn’t reducible to chemistry or physics (Marshal, 2021), since there are certain things about biology that neither chemistry or physics have. If there are laws of biology, then they will be found at the level of the organism or its ecology (Rull, 2022). In fact, it seems that although three laws of biology have been proposed (Trevors and Sailer Jr., 2008), they appear to be mere regularities, including McShea and Brandon’s (2010) first law of biology; all “laws of biology” seem to be mere laws of physics (Wayne, 2020). The “special sciences”, it seems, “are not fit for laws” (Kim, 2010). There seem to be, though, no uncontroversial laws or regularities in biology (Hamilton, 2007).
Now that I have described what laws are and have argued that there probably aren’t any biological laws, what does that mean for the LoBG? I will take each “law” in turn.
“Laws” of behavioral genetics
(1) All human behavioral traits are heritable.
JayMan gives derivations for the “laws”, and (1) and (2) have their bases in twin studies. We know that the equal environments assumption is false (Charney, 2012; Joseph, 2014; Joseph et al, 2015), and so if the EEA is false then we must reject genetic claims from twin study proponents. Nevertheless, the claim that these “laws” have any meaning gets pushed around a lot.
When it comes to the first law, the claim is that “ALL human behavioral traits are heritable”—note the emphasis on “ALL.” So this means that if we find only ONE behavioral trait that isn’t heritable, then the first law is false.
Reimann, Schilke, and cook (2017) used a sample of MZ and DZ twins and asked questions related to trust and distrust. They, of course, claim that “MZ and DZ twins share comparable environments in their upbringing“—which is false since MZ twins have more comparable environments. Nevertheless, they conclude that while trust has a heritability or 30%, “ACE analyses revealed that the estimated heritability [for] distrust is 0%.” This,therefore, means, that the “1st law” is false.
This “first law”, the basis of which is twin, family, and adoption studies, is why we have poured countless dollars into this research, and of course people have their careers (in what is clear pseudoscience) to worry about, so they won’t stop these clearly futile attempts in their search for “genes for” behavior.
(2) The effect of being raised in the same family is smaller than genes.
This claim is clearly nonsense, and one reason why is that the first “law” is false. In any case, there is one huge effect on, children’s outcomes due to birth order and how, then, parental attitudes–particularly mothers—affect child outcomes (Lehmann, Nuevo-Chiquero, and Vidal-Fernandez, 2018).
Why would birth order have an effect? Quite simply, the first-born child will get more care and attention than children who are born after, and so variations in parental behavior due to birth order can explain differences in education and life outcomes. They conclude that “broad shifts in parental behavior appear to set later-born children on a lower path for cognitive development and academic achievement, with lasting impact on adult outcomes.” Thus, Murray’s (2002) claim that birth order doesn’t matter and JayMan’s claim that “that the family/rearing environment has no effect on eventual outcomes” is clearly false. Thus, along with this and the falsity of the “1st law”, the “2nd law” is false, too.
(3) A substantial portion of the variation in complex human behavioral traits is not accounted for by the effects of genes or families.
This “law” covers the rest of the variance not covered in the first two “laws.” It was coined due to the fact that the first two “laws” had variance left that wasn’t “explained” by them. So this is basically unique experience. This is what behavioral genetics call “non-shared environment.” Of course, unique experiences (that is, subjective experiences) would definitely “shape who we are”, and part of our unique experiences are cultural. We know that cultural differences can have an impact on psychological traits (Prinz, 2014: 67). So the overall culture would explain why these differences aren’t “accounted for” in the first two “laws.”
Yet, we didn’t need the LoBG for us to know that individual differences are difference-makers for differences in behavior and psychology. So this means that what we choose to do can affect our propensities and then, of course, our behavior. Non-shared environmental effects are specific to the individual, and can include differing life events. That is, they are random. Non-shared environment, then, is parts of the environment that aren’t shared. Going back to Lehmann, Nuevo-Chiquero, and Vidal-Fernandez (2018) above, although children to grow up in the same family under the same household, they are different ages and so they also experience different life events. They also experience the same things differently, due to the subjectivity of experience.
In any case, the dichotomy between shared and non-shared environment is a dichotomy that upholds the behavioral geneticists main tool—the heritability estimate—from which these “laws” derive (from studies of twins, adoptees, and families). So, due to how the law was formulated (since there were still portions “unaccounted for” by the first two “laws”), it doesn’t really matter and since it rests on the first two false “laws”, therefore the third “law” is also false.
(4) Human behavioral traits are associated with many genes of small effect which contribute to a small amount of behavioral variability.
This “law” was formulated by Chabris et al (2015) due to the failure of molecular genetic studies which hoped to find genes with large effects to explain behavior. This “law” also “explains why the results of “candidate-gene” studies, which focus on a handful of genetic variants, usually fail to replicate in independent samples.” What this means to me is simple—it’s an ad-hoc account, meaning it was formulated to save the gene-searching by behavioral geneticists since the candidate gene era was a clear failure, as Jay Joseph noted in his discussion of the” 4th law.”
So here is the time line:
(1) Twin studies show above-0 heritabilities for behavioral traits.
(2) Since twin studies show high heritabilities for behavioral traits, then there must be genes that will be found upon analyzing the genome using more sophisticated methods.
(3) Once we started to peer into the genome after the completion of the human genome project, we then came to find candidate genes associated with behavior. Candidate gene studies “look at the genetic variation associated with disease within a limited number of pre-specified genes“, they refer to genes “believed to be” associated with a trait in question. Kwon and Goat (2000) wrote that “The candidate gene approach is useful for quickly determining the association of a genetic variant with a disorder and for identifying genes of modest effect.” But Sullivan (2020) noted that “Historical candidate gene studies didn’t work, and can’t work.” Charney (2022) noted that the candidate gene era was a “failure” and is now a “cautionary tale.”
Quite clearly, they were wrong then, and the failure of the candidate gene era led to the ad-hoc “4th law.” This has then followed us to the GWAS and PGS era, where it is claimed that we aren’t finding all of the heritability that twin studies say we should find with GWAS, since the traits under review are due to many genes of small effect. It’s literally just a shell game—when one claim is shown to be false, just make a reason why what you thought would be found wasn’t found, and then you can continue to search for genes “for” behavior. But genetic interactions create a “phantom heritability” (Zuk et al, 2011), while behavioral geneticists assume that the interactions are additive. They simply outright ignore interactions, although they pay it lip service.
So why, then, should we believe behavioral geneticists today in 2023 that we need larger and larger samples to find these mythical genes “for” behavior using GWAS? We shouldn’t. They will abandon GWAS and PGS in a few years when the new kid on the block shows up that they can they champion and claim that the mythical genes “for” behavior will finally be found.
(5) All phenotypic relationships are to some degree genetically mediated or confounded.
This claim is something that comes up a lot—the claim of genetic confounding (and mediation). A confound is a third variable that influences both the dependent and independent variable. The concept of genetic confounding was introduced during the era where it was debated whether or not smoking caused lung cancer (Pingault et al, 2021). (Do note that Ronald Fisher (1957), who was a part of this debate, claimed that smoking and lung cancer were both “influenced by a common cause, in this case individual genotype.“
However, in order for the genetic confounding claim to work, they need to articulate a mechanism that explains the so-called genetic confounding. They need to articulate a genetic mechanism which causally explains X and Y, explains X independent of Y and explains Y independent of X. So for the cop-out genetic confounding claim to hold any water: G confounds X and Y iff there is a genetic mechanism which causally explains X and Y, causally explains X independent of Y and Y independent of X.
Conclusion
The “laws of behavioral genetics” uphold the false dichotomy of genes and environment, nature and nurture. Though, developmental systems theorists have rightly argued that it is a false dichotomy (Homans, 1979; Moore, 2002; Oyama, 2002; Moczek, 2012) and that it is just not biologically plausible (Lewkowicz, 2012). In fact, the h2 statistics assumes that G and E are independent, non-interacting factors, so if the claim is false then—for one of many reasons—we shouldn’t accept their conclusions. The fact that G and E interact means that, of course, we should reject h2 estimates, and along with it, the entire field of behavioral genetics.
Since the EEA is false, h2 equals c2. Furthermore, h2 equals 0. So Polderman’s (2015) meta analysis doesn’t show that for all traits in the analysis that h2 equals 49%. (See Jay Joseph’s critique.) Turkheimer (2000: 160) claimed that the nature-nurture debate is over, since everything is heritable. However, the debate is over because developmental systems approach has upended the false dichotomy of nature vs nurture, since all developmental resources interact and are therefore irreducible to development.
However, for the field to continue to exist, they need to promulgate the false dichotomy, since their heritability estimates depend on it. They also need to hold onto the claim that twin, family and adoption studies can show the “genetic influence” on traits to justify the continued search for genes “for” behavior. Zuk and Spencer (2020) called the nature-nurture “debate” “a zombie idea, one that, no matter how many times we think we have disposed of it, springs back to life.” This is just like Oyama (2000) who compared arguing against gene determinism like battling the undead (Griffiths, 2006).
Jay Joseph proposed a 5th “law” in 2015 where he stated:
Behavior genetic Laws 1-4 should be ignored because they are based on many false assumptions, concepts, and models, on negative gene finding attempts, and on decades of unsubstantiated gene discovery claims.
The “laws” should quite obviously be ignored. Since the whole field of behavioral genetics is based on them, why not abandon the search for “genes for behavior”? At the end of the day, it seems like there are no “laws” of behavioral genetics, since laws are strict and exceptionless. So why do they keep up with their claims that their “laws” tell us anything about human behavior? Clearly, it’s due to the ideology of those who hold that the all-important gene causes traits and behavior, so they will do whatever it takes to “find” them. But in 2023, we know that this claim is straight up false.
Why Purely Physical Things Will Never Be Able to Think: The Irreducibility of Intentionality to Physical States
2600 words
What do “normativity” and “intentionality” mean?
What “normativity” means has implications for many things in philosophy and science. Normativity has been distinguished between “semantic normativity” and “conceptual normativity” (Skorupski, 2007). On the semantic version, “any normative predicate is definitionally reducible to a reason predicate” and on the conceptual version “the sole normative ingredient in any normative concept is the concept of a reason” (Skorupski, 2007). Skorupski rejects the semantic version and holds to the conceptual version. The conceptual version does hold value, so I will be operating on this definition in this article. “Intentionality” is the power of mental states to be “about” things. My mental state right now is to write this article on the normativity of psychological traits, so I have a desire to perform this action, making it normative.
Regarding the mind-body problem, the meaning of normativity entails that what is normative is not reducible to (physical) dispositions. Human psychology is intentional. What is intentional is normative. Intentions are done “on purpose”, that is, they’re done “for a reason.” If something is done for a reason, then there is a goal that the agent desired by performing their action. When someone performs an action, we ask “Why?”, and the answer is they performed the action for a reason. “Why did I go to work?”, because I wanted to make money. “Why did I write down my thoughts?”, because I wanted a written record of what I was thinking at a certain moment in time. So how the normativity of intentionality comes into play here is this—if agents perform actions for reasons, and reasons are due to beliefs, goals, and desires to bring about some end by an agent, then what explains why an agent performed an action is their reason TO perform the action.
When one “does something for a reason”, they intend to “do something”, that is they perform an action “on purpose”, meaning they have a desired outcome that the action they carried out will hopefully, for the agent, manifest in reality. The best example I can think of is murder. Murder is the intentional killing of an individual. For whatever reason, the agent that committed the act of murder has a reason they want the person they killed dead. Contrast this with manslaughter, which is “the unlawful killing of a human being without malice.” There are two kinds of manslaughter, voluntary manslaughter which would happen in the heat of the moment, think a passion killing. The other kind being the unintentional killing of a human being. This distinction between murder and manslaughter is, basically, down to what an agent INTENDS TO DO. Thus, one is a murderer if they set out one night to kill an individual, that is if they plan it out (have a goal to murder); and one commits manslaughter if they did not intend to kill the other individual, let’s say two people have a fight and one punches the other and the hit person hits their head on the curb and dies.
Now that I have successfully stated what normativity means, and have distinguished between intentional and unintentional action (murder and manslaughter), I must discuss the distinction between intentions and dispositions.
The normativity of psychological states
The problem of action is how to distinguish what an agent does for reasons, goals, or desires, and what merely happens to them (Paul, 2021). I have argued before that reasons, goals, beliefs, and desires (what an agent does) make the distinction between antecedent conditions which then cause an agent’s movement but were not consciously done (what happens to them).
We know what intentions are, but what are dispositions? Behavior is dispositional, so Katz’s considerations have value here:
a disposition [is] a pattern of behavior exhibited frequently … in the absence of coercion … constituting a habit of mind under some conscious and voluntary control … intentional and oriented to broad goals” (1993b, 16).
There is a wealth of philosophical literature which argues that intentions are irreducible to dispositions (e.g. Kripke, 1980; Bilgrami, 2005, 2006; also see Weber, 2008). Intentional states are, then, irreducible to physical or functional explanations. It then follows that intentional states can’t be explained/studied by science. If intentional states can’t be explained/studied by science, then intentional states are special, indeed they are unique to agents (minded beings).
In the conclusion to Self-Knowledge and Resentment, Akeel Bilgrami describes his pincer argument using a Fregean extension of Moore’s non-naturalism:
Via a discussion of an imaginary subject wholly lacking agency, it was shown how deeply the very notion of thought or intentionality turns on possessing the point of view of agency, of subjectivity, the point of view of the first, rather than third, person. And it was there shown via an argument owing to a Fregean extension of Moore’s anti-naturalism that such a picture of intentionality required ceasing to see intentional subjects in wholly dispositional terns and, indeed, requires seeing intentional states such as beliefs and desires as themselves normative states or commitments. When so viewed, intentional states are very different from how they appear to a range of philosophers who think of them along normative lines, such as [Donald] Davidson. When so viewed, they are not only irreducible to and non-identical with the physical and causal states of the subjects; they cannot even be clearly assessed to be dependent on such states in the specific ways that philosophers like to capture with such terms as ‘supervenience’. (There are of course all sorts of other dependencies that intentional states have on the states of the central nervous system, which do not amount to anything like the relations that go by the name of ‘supervenience’.) This is because when they are so viewed, they are essentially first-person phenomena, phenomena whose claims to supervenient dependence on third person states such as physical or causal properties are either stateable or deniable. (Therefore, not assesable.) (Bilgrami, 2006: 291-292)
Intentionality is a sufficient and necessary condition for mentality according to Brentano. And intentionality along with normativity are 2 out of 5 of the “marks of the mental” (Pernu, 2017). It can even be said to be the aboutedness of the mind to a thing other than itself. If I talk about something or state that I have a desire to do something, this is the aboutness of intentional states. So mental states that are directed at things are said to be intentional states. Intentionality requires goals, beliefs, and desires, so this designates the intentional stance as one of action, which is distinguished from behavior. Since the mental is normative (Zangwill, 2005), then, since we have the problem of normativity for physicalism, this is yet another reason to reject dualism and to accept some kind of dualism.
Goal-directedness is another mark of intentionality. When one acts intentionally, they act in order to bring about a goal they have in mind about something. Take the example of murder I gave above. Knowing that murder is the intentional killing of a human being, the murderer has the goal in mind to end the life of the other person. They act in accordance with their desired to bring about the goal they have in mind.
Since psychological states are intentional states, and intentional states are normative (Wedgewood, 2007; Kazemi, 2022), then psychological states are normative. Since mental states that have content are normative then we cannot reductively explain mind. Thus, Yoo’s (2004) discussion of the normativity of intentionality holds value:
Thus, the reason why thought and behavior cannot be explained in terms of non-intentional, physical, vocabulary comes down to a certain “normative element” constitutive of our interpretation and attributions of the propositional attitudes. Clearly this normative element plays a pivotal role. But in spite of its significance, it is highly obscure and insufficiently understood. Indeed, there have been no serious attempts to systematically examine what, exactly, the normative element amounts to.
…
As Davidson points out, the normative element ultimately has its roots in the object of the interpreter’s inquiry, which is another mind. Unlike black holes and quarks, which do not conform to norms, let alone the norms of rationality, a mind, by its very nature, has to conform to the norms of rationality. Otherwise, we are not dealing with a mind, should no or too few norms of rationality apply. Black holes and quarks certainly conform to laws – nomological principles – that support statements like “Light ought to bend in a black hole,” but such uses of “ought” have no normative implications (see Brandom 1994, ch. 1). The mental states that make up a mind, on the other hand, are such that they bear normative relations among each other, since their very contents are individuated by the norms of rationality (which is clearly stated in the third account). And the observer of a person’s mind must discern in the other’s bodily movements and vocal utterances a rational pattern that is itself a pattern to which the observer (attributor, appraiser) must subscribe. Hence, insofar as the norms of rationality are reflexive – they constrain both the mental states of the interpreted mind as well as the process of interpretation engaged by the interpreter herself – this aspect of the normative fully satisfies the third constraint.
Many arguments exist which conclude that the mental cannot be explained in terms of words that refer only to physical properties, and this is one of them. And since the mental is normative, this is yet another reason why there cannot—and indeed why their never will be—reductive explanations of the mental to the physical.
The irreducibility of intentionality
If physicalism is true, then intentionality would reduce, or be identical to, something physical. Then we should have an explanation of intentionality in physical terms. However, I would say this is not possible. (See Heikinheimo’s Rule-Following and the Irreducibility of Intentional States.) It’s not possible because physical systems can’t intend, that is they can’t act intentionally.
The argument is a simple one: Only beings with minds can intend. This is because mind allows a being to think. Since the mind isn’t physical, then it would follow that a physical system can’t intend to do something—since it wouldn’t have the capacity to think. Take an alarm system. The alarm system does not intend to sound alarms when the system is tripped. It’s merely doing what it was designed to do, it’s not intending to carry out the outcome. The alarm system is a physical thing made up of physical parts. So we can then liken this to, say, A.I.. A.I. is made up of physical parts. So A.I. (a computer, a machine) can’t think. However, individual physical parts are mindless and no collection of mindless things counts as a mind. Thus, a mind isn’t a collection of physical parts. Physical systems are ALWAYS a complicated system of parts but the mind isn’t. So it seems to follow that nothing physical can ever have a mind.
Physical parts of the natural world lack intentionality. That is, they aren’t “about” anything. It is impossible for an arrangement of physical particles to be “about” anything—meaning no arrangement of intentionality-less parts will ever count as having a mind. So a mind can’t be an arrangement of physical particles, since individual particles are mindless. Since mind is necessary for intentionality, it follows that whatever doesn’t have a mind cannot intend to do anything, like nonhuman animals. It is human psychology that is normative, and since the normative ingredient for any normative concept is the concept of reason, and only beings with minds can have reasons to act, then human psychology would thusly be irreducible to anything physical. Indeed, physicalism is incompatible with intentionality (Johns, 2020). The problem of intentionality is therefore yet another kill-shot for physicalism. It is therefore impossible for intentional states (i.e. cognition) to be reduced to, or explained by, physicalist theories/physical things.
This is similar to Lynn Baker’s (1981) argument in Why Computers Can’t Act (note how in her conclusion she talks about language—the same would therefore hold for nonhuman animals):
P1: In order to be an agent, an entity must be able to formulate intentions.
P2: In order to formulate intentions, an entity must have an irreducible first-person perspective.
P3: Machines lack an irreducible first-person perspective.
C: Therefore, machines are not agents.…
So machines cannot engage in intentional behavior of any kind. For example, they cannot tell lies, since lying involves the intent to deceive; they cannot try to avoid mistakes, since trying to avoid mistakes entails intending to conform to some normative rule. They cannot be malevolent, since having no intentions at all, they can hardly have wicked intentions. And, most significantly, computers cannot use language to make assertions, ask questions, or make promises, etc., since speech acts are but a species of intentional action. Thus, we may conclude that a computer can never have a will of its own.
So PP’s “depression” about ChatGPT “scoring” 11 points on his little (non-construct valid) test is irrelevant. It’s a machine and, as successfully argued, machines will NEVER have the capacity to think/act/intend.
What does this mean for a scientific explanation of human psychology?
The arguments made here point to one conclusion—since intentions don’t reduce to the physical and functional states of humans (like neurophysiology; Rose, 2005), then it is impossible for science to explain intentions, since what is normative isn’t reducible to, or identical with, physical properties. This is another arrow in the quiver of the anti-physicalist/dualist to show that there is something more than the physical—there is an irreducible SELF or MIND and we humans are the only minded beings. Science can’t explain the human mind and, along with it, the intentions that arrive from a deliberating mind. This is also an argument against Benjamin Libet’s experiments in which he concludes that the subjects’ brain activity preceded their actions, that is, it is the brain that initiates action. This view, however, is false, since the (minded) agent is what initiates action. Libet is therefore guilty of the mereological fallacy. Freely-willed processes are therefore not initiated by the brain (Radder and Meynen, 2012).
Elon Musk and Sam Harris have warned of a “robot rebellion” like what occurred in The Terminator. Though, since what I’ve argued here is true—that purely physical things lack minds, that is they can’t intend or think—then such worries should rightly stay in the realm of sci-fi. The implication is clear—since purely physical things cannot intend, and humans can intend, then there is an irreducible SELF or MIND which allows us to intend. The claim, then, that the human brain is a computer is clearly false. It then follows that humans aren’t purely physical; there is a mental and physical aspect to humans—that is, there are two substances that make us up, the mental and the physical, and it is clear that M (the mental) is irreducible to P (the physical). Sentient machines are, luckily, a myth. It’s just not possible for scientists to imbue a machine with a mind since machines are purely physical and minds aren’t. John Searle’ s Chinese Room Argument, too, is an argument against strong A.I.. Machines will never become conscious since consciousness isn’t physical.
This is yet another argument against the scientific study of the mind/self and, of course, against psychology and hereditarianism. This is then added to the articles that argue against the overall hereditarian program in psychology, and psychology more broadly: Conceptual Arguments Against Hereditarianism; Reductionism, Natural Selection, and Hereditarianism; and Why a Science of the Mind is Impossible. For if the main aspect of IQ test-taking is thinking, thinking is cognition, cognition is intentional and therefore psychological, it follows that since there can be no explanations of intentional states in terms of physical vocabulary, and if cognition—being a psychological trait—is normative, then the conclusion is, again, that hereditarianism and psychology fail their main goal. It is impossible.
Sudden Infant Death Syndrome (SIDS): How A Genetic Determinist Theory Cost Infant Lives
3000 words
Sudden Infant Death Syndrome (SIDS) has a long history—almost as long as human civilization (Raven, 2018). The term was coined in 1969 to bring attention to children who died in the postnatal period (Kinney and Thach, 2012; Duncan and Byard, 2018). About 95 percent of SIDS cases occur within the first 6 months of life, happening around the 4-6 months mark (Fleming, Blair, and Pease, 2015). The syndrome is associated with the sleep period, presumed to have begun with the transition from sleep to waking (Kinney and Thach, 2012) The prone sleeping position, along with smoking, is said to increase the incidence of SIDS (Ramirez, Ramirez, and Anderson, 2018). Due to a campaign in the mid-90s, though (called the back-to-sleep campaign), it has been estimated that SIDS deaths have decreased by 50 percent, saving thousands of infant lives (Kinney and Thach, 2012).
But, those infants who die from SIDS may also have a problem with the part of their brain that controls waking/sleeping:
Infants who die from SIDS may have a problem with the part of the brain that helps control breathing and waking during sleep. If a baby is breathing stale air and not getting enough oxygen, the brain usually triggers the baby to wake up and cry to get more oxygen.
So, if a baby’s brain is not getting enough oxygen, its brain will have it wake up and cry in an attempt to rid itself of “stale oxygen”—this is one other purpose that crying serves—which then gets the baby more oxygen to its brain.
Buchanan (2019) hypothesizes that reduced Co2 is a cause for SIDS—being that Co2 induces arousal from sleep. Buchanan (2019: 4-5) writes:
As can be imagined, acute rises in CO2 levels occur when an individual is unable to expel CO2, such as in the setting of an airway obstruction that might occur when an individual is lying prone in a crib or bed perhaps with a pillow and bedclothes covering the nose and mouth. It has been proposed that such a rise in CO2 would activate arousal circuitry in a normal baby to wake the baby up, cause them to cry out, summoning a caregiver who would come to their aid, and ostensibly correct the airway blockage to allow resumption of normal breathing [16,20,31]. It has been proposed, among other possibilities, that there is an impaired CO2-arousal system in SIDS-susceptible babies such that when they rebreathe CO2 as described above, they do not arouse, and thus do not cry out, and the blockage is not corrected [16,32]. They thus become acidotic and hypoxic and ultimately succumb.
So, if a babe’s airway gets blocked, for instance by a pillow or toy, they wake, cry out for attention and their caregiver comes to solve the problem or they change their laying position. But in SIDS cases, this does not occur. Why? Buchanan argues that those who succumb to sudden deaths like SIDS have screwy serotonin receptors—they ensure that blood oxygen and CO2 levels are healthy. But some of these infants may have brains that don’t allow them to detect the CO2 and blood oxygen levels—when the body may be suffocating. SIDS victims are usually found face-down in their cribs. But, there are no biomarkers for SIDS (Haynes, 2018). The SIDS diagnosis is only given after all other causes of death are ruled out—this is why SIDS is so mysterious. Genetic mutations have been posited as a cause (Männikkö et al, 2018), as has a pregnant mother smoking during pregancy, leading to a doubled risk of SIDS (Anderson et al, 2019).
But the best prevention against SIDS is nonprone sleeping—having the baby sleep on its back. The efficacy of this approach since the 1990ss has been noted (Gibson et al, 1992; de Luca and Hinide, 2016) while “Achieving recommended prenatal care and infant vaccinations, as well as reductions in maternal tobacco and substance use, has the potential to further reduce rates of SIDS and should be given as much attention as safe sleep advice in SIDS risk reduction campaigns” (Hauck and Tanabe, 2017: e289). The back-to-sleep program, though, has been associated with a decrease in motor development from the infant sending time in the supine position along with the strong possibility of developing plagiocephaly—which causes a “flat head” due to being placed in similar positions while the infant’s skull is soft and still developing (Miller et al, 2011). It has also been estimated that if it was known that the advice to place infants on their stomachs to sleep led to SIDS, then we “might have prevented over 10 000 infant deaths in the UK and at least 50 000 in Europe, the USA, and Australasia” (Gilbert et al, 2005: 884).
But the history of SIDS in America is a lot more sinister—rather than children dying from ‘natural causes’ (SIDS), in the 1970s, it was hypothesized by one SIDS researcher that SIDS was ‘genetic’ and ‘transmissible’ on the basis of one family who, unfortunately, had experienced this tragedy more than once.
This leads us to the story of Waneta Hoyt, who is the subject of this article.
Hoyt and Steinschneider: Genes vs environment
Horrible tragedies befell a woman from New York named Waneta Hoyt—five of her children had mysteriously died due to SIDS between the years of 1965-1971.
Waneta killed her first child, Eric who was three-months-old. SIDS is a diagnosis that is arrived at through a process of elimination—rule out all other causes at a young age (under 1) and the cause is then SIDS. But, the thing is, when an autopsy is performed on the infant, there is no difference between what would be said to be SIDS deaths and a light smothering.
After Waneta murdered her first child, she was cold and distant but it was not noticed. It was reported that she would never hold her children as a loving mother would, keeping them quite far from her. But it wasn’t until three years later that she, again, murdered. But this time it was two of her children—her two-year-old son and six-week-old daughter. The murders that Waneta were committing were wrongfully diagnosed as being due to SIDS.
This caught the attention of renowned SIDS researcher Alfred Steinschneider who had a clinic in which he specialized in caring for infants who were thought to be high-risk for SIDS. Steinschneider wanted to watch Waneta’s fourth child in his sleeping ward, in an attempt to prevent what he thought was due to SIDS. So, when he heard of Waneta’s story, he reached out to her to monitor her daughter, Molly.
The nurses at Steinschneider’s clinic, though, became suspicious of Waneta when she was at the clinic since she was cold and distant to Molly—she would not show her any affection. Steinschneider’s nurses emphatically told Steinschneider that it was Waneta who was murdering her children. Steinschneider shot back, and sent Molly home anyway. In an interview on the television program Deadly Women called Mothers Who Kill, one of the nurses who watched Molly before she was discharged by Steinschneider said:
And then about a quarter to eleven when we were getting ready to go off duty I said ‘Joyce, what do you think, do you think she’s still alive?’ Of course when I came on duty the next day she was dead.
This is wonderfully noted by Firstman and Talman in their book on Waneta’s case The Death of Innocents (1996):
Forty-eight hours later, on Thursday, June 4, Steinschneider scheduled Molly for her third discharge. By now, the nurses were speaking more openly about their suspicions. “I just know something’s going to happen,” Corrine Dower said to Thelma. “One of these times she’s going to do it.” Corrine was scornful of Steinschneider. “If he had any brains at all he would have seen that she didn’t want the baby,” she would say years later. “You can tell in the grocery store if a person cares about their child. We were just disgusted with Steinschneider.” (book excerpt from How Two Baby Deaths Led to a Misguided SIDS Theory)
Presumably, since this was Waneta’s fourth time experiencing the tragedy of SIDS, Steinschneider did not think that Waneta could be involved—but his nurses knew the truth. It was when Waneta had her fifth child that Steinschneider thought he would make his breakthrough in his research. Steinschneider was so convinced that the baby’s were dying due to SIDS, and he thought that if he could monitor Waneta’s new baby as much as possible, that he may figure out why babies die from SIDS.
Steinschneider believes that SIDS is hereditary—passed on through genes. The fifth child was watched at Steinschneider’s clinic and when Steinschneider discharged him—in an attempt to prove his theory—his nurses protested. Then, shortly after, Waneta called Steinschneider saying that it had happened again—her fifth child had mysteriously died.
After the death of Waneta’s fifth child, Steinschneider published his paper Prolonged Apnea and the Sudden Infant Death Syndrome: Clinical and Laboratory Observations arguing that SIDS was caused largely by hereditary sleep apnea (Steinschneider, 1972). By 1997, Steinschneider’s paper was the most-cited paper in the SIDS literature (Bergman, 1997). It was due to Steinschneider’s research, though, that parents began using sleep monitors to monitor their children’s sleep so they could be alerted in case their child had sleep apnea.
Steinschneider cared more about his research and theory of SIDS and sleep apnea over what was striking him right in the face—Waneta was responsible for the deaths of her five children. Steinschneider’s 1972 paper was cited and used for 22 years, until it was found upon an in-depth look into Steinschneider’s paper that what was clear to Steinschneider’s nurses and not him was true—Waneta was responsible for the deaths of her children. Steinschneider’s paper, in any case, concluded that SIDS is a genetic disorder and it was thusly inherited. And Waneta’s case, it seems, lent credence to his hypothesis. Steinschneider gave Waneta the perfect alibi—her woes were caused by a genetic disease and there was nothing that could have been done to prevent it.
Waneta was convicted in 1995 of five counts of murder and sentenced to 75 years in prison—therefore refuting Steinschneider’s theory. Three years after her sentence, though, Waneta died in prison of cancer. The case of Waneta Hoyt allowed mothers to kill their children in this specific way (a light smothering) for almost a quarter of a century.
Hickey, O’Brien, and Lighty (1996) write:
Norton saw history repeating itself in the reluctance of many factors to face the fact that some deaths attributed to SIDS were homicides. She agreed with the bulk of SIDS research, which pointed to apnea, or the cessation of breathing, as the final pathway to death. But there were many causes of apnea, not all of them natural. An adult could place a hand or a pillow over an infant’s nose and mouth and stop the child from breathing. The pressure needed to smother an infant often left no telltale signs, Norton explained.
“There is no way for the pathologist at autopsy to distinguish between homicidal smothering and SIDS,” she concluded.
Norton worried that homicides were being passed off as SIDS because many doctors held the erroneous belief that SIDS ran in families. They ignored large-scale studies that had shown no genetic tendency toward SIDS. Flouting conventional wisdom, Norton warned that the sudden, unexplained death of a SIDS victim’s sibling should be treated as a possible homicide.
When Waneta was convicted, letters to the editor were sent about Steinschneider’s paper. The short correction to the paper chronicles, interestingly, a letter to the editor of the journal Pediatrics, who published the Steinschneider paper
“But the paper indicated a more sinister possibility to Dr. John F. Hick of Minnesota. In a letter to the journal, he wrote that the case offered “circumstantial evidence suggesting a critical role for the mother in the death of her children.” (See below.)
But his warning was dismissed, until Mr. Fitzpatrick read the paper 15 years later.
“The medical records described two happy, healthy, perfectly normal kids,” he said. “It convinced me that these children were murdered.”
Hick’s letter to Pediatrics says:
In reporting two siblings who succumbed to “sudden infant death syndrome,” Steinschneider exposes an unparalleled family chronicle of infant death.’ Of five children, four died in early infancy and the other died without explanation at age 28 months. Prolonged apnea is proposed as the common denominator in the deaths, yet the author leaves many questions relevant to the fate of these children unanswered.
In her signed confession, Waneta said that she smothered her five children because their screaming made her “feel useless”, though Waneta later stated that she only said that to stop the police from questioning her. Steinschneider, like another motivated-reasoner J.P. Rushton, ignored data that did not fit his theory of sleep-apnea-induced-SIDS—specifically how Waneta acted around her children while at his clinic and the thoughts of his own nursing staff telling him not to discharge the Hoyt infants.
Waneta recalled her strangling of her children—specifically Julie:
”They just kept crying and crying. . . . I just picked up Julie and I put her into my arm, in between my arm and my neck like this . . . and I just kept squeezing and squeezing and squeezing.”
Steinschneider’s testimony during Waneta’s trial, however, is very interesting. Reported by the New York Times, Steinschneider attempted to defend his patient Waneta against claims that she had murdered her children:
Autopsies were done,” he said, speaking of Molly. “They could not find a known cause of death.”
This, Dr. Steinschneider said, “by definition” is SIDS.
But under intense cross-examination. Dr. Steinschneider conceded that he could not remember — and did not record — crucial details from the medical histories of the two infants, whom he had hospitalized for observation soon after birth. In each case, the parents had reported that the baby was having difficulty breathing and that its older siblings had died mysteriously.
The doctor also acknowledged concluding that Molly and Noah had died of SIDS without knowing how thoroughly the authorities had probed the “death scene” for evidence of other causes, including murder.
It is said—even by the prosecutor on her case—that Waneta suffered from Munchausen by proxy (Firstman and Talan, 1996)—which is the intentional cause of illness, usually on children, in order for the mother to elicit sympathy for others (Gehlawat et al, 2015). In cases like this, mothers who have the Munchausen syndrome will suffocate their children and then rush them to the hospital—they get the satisfaction of inflicting pain and then the satisfaction of getting cared for for the so-called mysterious death of their baby. One study of 51 sleep apnea monitorings found that about 40 percent of the program treated infants who had apnea that seemed to be induced by the parent; this was inferred from the fact that once the infants were admitted to the hospital, the doctors found no signs of apnea (Light and Sheridan, 1990).
One doctor even took it upon himself to place cameras in his practice in order to monitor parents that were suspected of abusing their children. Thirty-nine infants were monitored—thirty-three infants were being abused by their parents, what’s more is that some of the infants in this study who were identified in the video also had a sibling who mysteriously died from SIDS (Southall et al, 1997). What the study shows is that these parents were suffocating their children, causing their breathing problems and that they most likely have gotten away with infanticide before. Another case involved a mother taking her daughter to eleven different hospitals, but none of them found anything wrong with the girl and she ended up dying under suspicious circumstances (Hassler, Zamorski, and Weirich, 2007).
Conclusion
We now know that Steinschneider ignored contrary evidence to his theory of genetically-induced sleep apnea causing SIDS which apparently ran in families, and since he brushed off his nursing staff telling him that Waneta was acting strangely around her two children that he had admitted into his clinic, he could have saved their lives. But Steinschneider’s genetic determinist theory was more important than seeing what was clear as day to his staff and even others who read his 1972 paper—a mother was strangling her own infants.
SIDS has a long history, dating back to biblical times. But, in the modern-era, erroneous theories on the causes of SIDS were pushed while other, more obvious causes were disregarded in favor of a grand genetic theory of SIDS causation. Waneta and Steinschneider both helped each other out: Steinschneider (unknowingly) helped Waneta evade detection for 22 years while Waneta lent credence to the hypothesis that Steinschneider was developing. The fact that, at the time of their first meeting, three of Waneta’s children had died in almost the same fashion pointed to a genetic, inherited cause in Steinschneider’s eyes.
At the time of publication of The Death of Innocents, Steinschneider still continues to defend his now-discredited theory and still lobbies for the use of infant sleep monitors. Of course, since he testified FOR Waneta, despite the mounting evidence against her, he could be seen as an accomplice, however weakly. But this case shows one thing that should be well-known—researchers become attached to their pet hypotheses/theories and will ignore contrary evidence if it is brought to their attention. Firstman and Talman estimate that between 5 and 10 percent of SIDS cases are actually homicides. (But see Milroy and Kepron, 2017.)
Steinschneider created the SIDS disease on the basis of Waneta’s story—and a multi-million dollar industry then appeared due to his paper—it’s all to save infants, buy these sleep apnea monitors. But there were two children that Steinschneider did not—could not—save: He could have saved those babies, if not for his genetic determinist beliefs on SIDS causation. Had Steinshneider looked at the more obvious answer to the problem which was right in front of his face, he may have seen that Waneta suffered from Munchausen by Proxy, and, as evidenced from the references above, those who suffer from the disease act out exactly how Waneta did—by strangling their children with the cause of death being blamed on SIDS.
The Hoyt-Steinschneider case is a warning—don’t jump so quickly to implicate heredity in the ontology of X, especially when other, more obvious, tells are right there in front of you.
Does Playing Violent Video Games Lead to Violent Behavior?
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President Trump was quoted the other day saying “We have to look at the Internet because a lot of bad things are happening to young kids and young minds and their minds are being formed,” Trump said, according to a pool report, “and we have to do something about maybe what they’re seeing and how they’re seeing it. And also video games. I’m hearing more and more people say the level of violence on video games is really shaping young people’s thoughts.” But outside of broad assertions like this—that playing violent video games cause violent behavior—does it stack up to what the scientific literature says about it? In short, no, it does not. (A lot of publication bias exists in this debate, too.) Why do people think that violent video games cause violent behavior? Mostly due to the APA and their broad claims with little evidence.
Just doing a cursory Google search of ‘violence in video games pubmed‘ brings up 9 journal articles, so let’s take a look at a few of those.
The first article is titled The Effect of Online Violent Video Games on Levels of Aggression by Hollingdale and Greitemeyer (2014). They took 101 participants and randomized them to one of four experimental conditions: neutral, offline; neutral online; (Little Big Planet 2) violent offline; and violent online video games (Call of Duty: Modern Warfare). After they played said games, they answered a questionnaire and then measured aggression using the hot sauce paradigm (Lieberman et al, 1999) to measure aggressive behavior. Hollingdale and Greitemeyer (2014) conclude that “this study has identified that increases in aggression are not more pronounced when playing a violent video game online in comparison to playing a neutral video game online.”
Staude-Muller (2011) finds that “it was not the consumption of violent video games but rather an uncontrolled pattern of video game use that was associated with increasing aggressive tendencies.” Przybylski, Ryan, and Rigby (2009) found that enjoyment, value, and desire to play in the future were strongly related to competence in the game. Players who were high in trait aggression, though, were more likely to prefer violent games, even though it didn’t add to their enjoyment of the game, while violent content lent little overall variance to the satisfactions previously cited.
Tear and Nielsen (2013) failed to find evidence that violent video game playing leads to a decrease in pro-social behavior (Szycik et al, 2017 also show that video games do not affect empathy). Gentile et al (2014) show that “habitual violent VGP increases long-term AB [aggressive behavior] by producing general changes in ACs [aggressive cognitions], and this occurs regardless of sex, age, initial aggressiveness, and parental involvement. These robust effects support the long-term predictions of social-cognitive theories of aggression and confirm that these effects generalize across culture.” The APA (2015) even states that “scientific research has demonstrated an association between violent video game use and both increases in aggressive behavior, aggressive affect, aggressive cognitions and decreases in prosocial behavior, empathy, and moral engagement.” How true is all of this, though? Does playing violent video games truly increase aggression/aggressive behavior? Does it have an effect on violence in America and shootings overall?
No.
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?)
Sex Differences in Aggressive Behavior and Testosterone
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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.)
MAOA, Race, and Crime: A Simple Relationship?
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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.
Responses to The Alternative Hypothesis and Robert Lindsay on Testosterone
2300 words
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)
Artificially increasing the amount of testosterone in a person’s blood has been shown to lead to increases in their level of aggression (Burnham 2007; Kouri et al. 1995).
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.
Why Testosterone Does Not Cause Crime
Testosterone and Aggressive Behavior
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.
Robert Lindsay
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).
Gapstur et al (2002) help my argument, not yours.
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.
Wu et al (1995) show that Asians have the highest testosterone levels. Evidence is also mixed here as well. See above on AR sensitivity.
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.)
The Androgen Receptor and “masculinization”
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.
Conclusion
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.
Why Testosterone Does Not Cause Crime
Testosterone and Aggressive Behavior
Race, Testosterone, and Prostate Cancer
Population variation in endocrine function—Race/History/Evolution Notes
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.
The ENA Theory: On Testosterone and Aggressive Behavior by Race/Ethnicity
3250 words
A commenter by the name of bbloggz alerted me to a new paper by Lee Ellis published this year titled Race/ethnicity and criminal behavior: Neurohormonal influences in which Ellis (2017) proposed his theory of ENA (evolutionary neuroandrogenic theory) and applied it to racial/ethnic differences in crime. On the face, his theory is solid and it has great explanatory power for the differences in crime rates between men and women, however, there are numerous holes in the application of the theory in regards to racial/ethnic differences in crime.
In part I, he talks about racial differences in crime. No one denies that, so on to part II.
In part II he talks about environmental causes for the racial discrepancies, that include economic racial disparities, racism and societal discrimination and subordination, a subculture of violence (I’ve been entertaining the honor culture hypothesis for a few months; Mazur (2016) drives a hard argument showing that similarly aged blacks with some college had lower levels of testosterone than blacks with less than high school education which fits the hypothesis of honor culture. Though Ellis’ ENA theory may account for this, I will address this below). However, if the environment that increases testosterone is ameliorated (i.e., honor culture environments), then there should be a subsequent decrease in testosterone and crime, although I do believe that testosterone has an extremely weak association with crime, nowhere near high enough to account for racial differences in crime, the culture of honor could explain a good amount of the crime gap between blacks and whites.
Ellis also speaks about the general stress/strain explanation, stating that blacks have higher rates of self-esteem and Asians the lowest, with that mirroring their crime rates. This could be seen as yet another case for the culture of honor in that blacks with a high self-esteem would feel the need to protect their ‘name’ or whatever the case may be and feel the need for physical altercation based on their culture.
In part III, Ellis then describes his ENA theory, which I don’t disagree with on its face as it’s a great theory with good explanatory power but there are some pretty large holes that he rightly addresses. He states that, as I have argued in the past, females selected men for higher rates of testosterone and that high rates of testosterone masculinize the brain, changing it from its ‘default feminine state’ and that the more androgens the brain is exposed to, the more likely it is for that individual to commit crime.
Strength
Ellis cites a study by Goodpaster et al (2006) in which he measured the races on the isokinetic dynamometry, pretty much a leg extension. However, one huge confound is that participants who did not return for follow-up were more likely to be black, obese and had more chronic disease (something that I have noted before in an article on racial grip strength). I really hate these study designs, but alas, it’s the best we have to go off of and there are a lot of holes in them that must be addressed. Though I applaud the researchers’ use of the DXA scan (regular readers may recall my criticisms on using calipers to assess body fat in the bench press study, which was highly flawed itself; Boyce et al, 2014) to assess body fat as it is the gold standard in the field.
Ellis (2017: 40) writes: “as brain exposure to testosterone surges at puberty, the prenatally-programmed motivation to strive for resources, status, and mating opportunities will begin to fully activate.” This is true on the face, however as I have noted the correlation between physical aggression and testosterone although positive is low at .14 (Archer, 1991; Book et al, 2001). Testosterone, as I have extensively documented, does cause social dominance and confidence which do not lead to aggression. However, when other factors are coupled with high testosterone (as noted by Mazur, 2016), high rates of crime may occur and this may explain why blacks commit crime; a mix of low IQ, high testosterone and low educational achievement making a life of crime ‘the smart way’ to live seeing as, as Ellis points out, and that intelligent individuals find legal ways to get resources while less intelligent individuals use illegal ways.
ENA theory may explain racial differences in crime
In part IV he attempts to show how his ENA theory may explain racial differences in crime—with testosterone sitting at the top of his pyramid. However, there are numerous erroneous assumptions and he does rightly point out that more research needs to be done on most of these variables and does not draw any conclusions that are not warranted based on the data he does cite. He cites one study in which testosterone levels were measured in the amniotic fluid of the fetus. The sample was 59 percent white and due to this, the researchers lumped blacks, ‘Hispanics’ and Native Americans together which showed no significant difference in prenatal testosterone levels (Martel and Roberts, 2014).
Umbilical cord and testosterone exposure
Ellis then talks about testosterone in the umbilical cord, and if the babe is exposed to higher levels of testosterone in vitro, then this should account for racial/ethnic differences in crime. However, the study he cited (Argus-Collins et al, 2012) showed no difference in testosterone in the umbilical cord while Rohrmann et al (2009) found no difference in testosterone between blacks and whites but found higher rates of SHBG (sex hormone-binding globulin) which binds to testosterone and makes it unable to leave the blood which largely makes testosterone unable to affect organ development. Thusly, if the finding of higher levels of SHBG in black babes is true, then they would be exposed to less androgenic hormones such as testosterone which, again, goes against the ENA theory.
He also cites two more studies showing that Asian babes have higher levels of umbilical cord testosterone than whites (Chinese babes were tested) (Lagiou et al, 2011; Troisi et al, 2008). This, again, goes against his theory as he rightly noted.
Circulating testosterone
Next he talks about circulating differences in testosterone between blacks and whites. He rightly notes that testosterone must be assayed in the morning within an hour after waking as that’s when levels will be highest, yet cites Ross et al (1986) where assay times were all over the place and thusly testosterone cannot be said to be higher in blacks and whites based on that study and should be discarded when talking about racial differences in testosterone due to assay time being between 10 am and 3 pm. He also cites his study on testosterone differences (Eliss and Nyborg, 1993), but, however, just as Ross et al (1986) did not have a control for WC (waist circumference) Ellis and Nyborg (1993) did not either, so just like the other study that gets cited to show that there is a racial difference in testosterone, they are pretty hugely flawed and should not be used in discussion when discussing racial differences in testosterone. Why do I not see these types of critiques for Ross et al (1986) in major papers? It troubles me…
He also seems to complain that Lopez et al (2013) controlled for physical activity (which increases testosterone) and percent body fat (which, at high levels, decreases testosterone). These variables, as I have noted, need to be controlled for. Testosterone varies and fluctuated by age; WC and BMI vary and fluctuate by age. So how does it make sense to control for one variable that has hormone levels fluctuate by age and not another? Ellis also cites studies showing that older East Asian men had higher levels of testosterone (Wu et al, 1995). Nevertheless, there is no consensus; some studies show Chinese babes have higher levels of testosterone than whites and some studies show that whites babes have higher levels of testosterone than Chinese babes. Indeed, this meta-analysis by Ethnicmuse shows that Asians have the highest levels, followed by Africans then Europeans, so this needs to be explained to save the theory that testosterone is the cause of black overrepresentation of violence (as well as what I showed that testosterone is important for vital functioning and is not the boogeyman the media makes it out to be).
Bone density and crime
Nevertheless, the next variable Ellis talks about is bone density and its relationship to crime. Some studies find that blacks are taller than whites while other show no difference. Whites are also substantially taller than Asian males. Blacks have greater bone density than the other three races, but according to Ellis, this measure has not been shown to have a relationship to crime as of yet.
Penis size, race and crime
Now on to penis size. In two articles, I have shown that there is no evidence for the assertion that blacks have larger penises than whites. However, states that penis length was associated with higher levels of testosterone in Egyptian babes. He states that self-reported penis size correlates with self-reports of violent delinquency (Ellis and Das, 2012). Ellis’ main citations for the claim that blacks have larger penises than other races comes from Nobile (1982), the Kinsey report, and Rushton and Boagert (1987) (see here for a critique of Rushton and Boagert, 1987), though he does cite a study stating that blacks had a longer penis than whites (blacks averaging 5.77 inches while whites averaged 5.53 inches). An HBDer may go “Ahah! Evidence for Rushton’s theory!”, yet they should note that the difference is not statistically significant; just because there is a small difference in one study also doesn’t mean anything for the totality of evidence on penis size and race—that there is no statistical difference!
He then cites Lynn’s (2013) paper which was based on an Internet survey and thus, self-reports are over-measured. He also cites Templer’s (2002) book Is Size Important?, which, of course, is on my list of books to read. Nevertheless, the ‘evidence’ that blacks average larger penises than whites is extremely dubious, it’s pretty conclusive that the races don’t differ in penis size. For further reading, read The Pseudoscience of Race Differences in Penis Size, and read all of Ethnicmuses’ posts on penis size here. It’s conclusive that there is no statistical difference—if that—and any studies showing a difference are horribly flawed.
2d/4d ratio and race
Then he talks about 2d/4d ratio, which supposedly signifies higher levels of androgen exposure in vitro (Manning et al, 2008) however these results have been challenged and have not been replicated (Koehler, Simmons, and Rhodes, 2004; Yan et al, 2008, Medland et al, 2010). Even then, Ellis states that in a large analysis of 250,000 respondents, Asians had the lowest 2d/4d ratio, which if the hypothesis of in vitro hormones affecting digit length is to be believed, they have higher levels of testosterone than whites (the other samples had small ns, around 100).
Prostate-specific antigens, race, and prostate cancer
He then talks about PSA (prostate-specific antigen) rates between the races. Blacks are two times more likely to get prostate cancer, which has been blamed on testosterone. However, I’ve compiled good evidence that the difference comes down to the environment, i.e., diet. Even then, there is no evidence that testosterone causes prostate cancer as seen in two large meta-analyses (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even then, rates of PCa (prostate cancer) are on the rise in East Asia (Kimura, 2012; Chen et al, 2015; Zhu et al, 2015) which is due to the introduction of our Western diet. I will cover the increases in PCa rates in East Asia in a future article.
CAG repeats
He then reviews the evidence of CAG repeats. There is, however, no evidence that the number of CAG repeats influences sensitivity to testosterone. However, intra-racially, lower amounts of CAG repeats are associated with higher spermatozoa counts—but blacks don’t have higher levels of spermatozoa (Mendiola et al, 2011; Redmon et al, 2013). Blacks do have shorter CAG repeats, and this is consistent with the racial crime gap of blacks > whites > Asians. However, looking at the whole of the evidence, there is no good reason to assume that this has an effect on racial crime rates.
Intelligence and education
Next he talks about racial differences in intelligence and education, which have been well-established. Blacks did have higher rates of learning disabilities than whites who had higher levels of learning disabilities then Asians in a few studies, but other studies show whites and South Asians having different rates, for instance. He then talks about brain size and criminality, stating that the head size of males convicted for violent crimes did not differ from males who committed non-violent crimes (Ikaheimo et al, 2007). I won’t bore anyone with talking about what we know already: that the races differ in average brain size. However, a link between brain size and criminality—to the best of my knowledge—has yet to been discovered. IQ is implicated in crime, so I do assume that brain size is as well (no matter if the correlation is .24 or not; Pietschnig et al, 2015).
Prenatal androgen exposure
Now to wrap things up, the races don’t differ in prenatal androgen exposure, which is critical to the ENA theory; there is a small difference in the umbilical cord favoring blacks, and apparently, that predicts a high rate of crime. However, as noted, blacks have higher levels of SHBG at birth which inhibits the production of testosterone on the organs. Differences in post-pubertal testosterone are small/nonexistent and one should not talk about them when talking about differences in crime or disease acquisition such as PCa. DHT only shows a weak positive correlation with aggression—the same as testosterone (Christiansen and Winkler, 1992; however other studies show that DHT is negatively correlated with measures of physical aggression; Christiansen and Krussmann, 1987; further, DHT is not so evil after all).
Summing it all up
Blacks are not stronger than whites, indeed evidence from the races’ differing somatype, grip strength and leverages all have to do with muscular strength. Furthermore, the study that Ellis cites as ‘proof’ that blacks are stronger than whites is on one measure; an isokinetic dynamometry machine which is pretty much a leg extension. In true tests of strength, whites blow blacks away, which is seen in all major professional competitions all around the world. Blacks do have denser bones which is due to androgen production in vitro, but as of yet, there has been no research done into bone density and criminality.
The races don’t differ on penis size—and if they do it’s by tenths of an inch which is not statisitcally significant and I won’t waste my time addressing it. It seems that most HBDers will see a racial difference of .01 and say “SEE! Rushton’s Rule!” even when it’s just that, a small non-significant difference in said variable. That’s something I’ve encountered a lot in the past and it’s, frankly, a waste of time to converse about things that are not statistically significant. I’ve also rebutted the theory on 2d/4d ration as well. Finally, Asians had a similar level of androgen levels compared to blacks, with whites having the least amount. Along with a hole in the theory for racial differences in androgen causing crime, it’s yet another hole in the theory for racial differences in androgens causing racial differences in penis size and prostate cancer.
On intelligence scores, no one denies that blacks have scored about 1 SD lower than whites for 100 years, no one denies that blacks have a lower educational attainment. In regards to learning disabilities, blacks seem to have the highest rates, followed by Native Americans, than non-Hispanic whites, East Asians and the lowest rates found in South Asians. He states only one study links brain size to criminal behavior and it showed a significant inverse relationship with crime but not other types of offenses.
This is a really good article and I like the theory, but it’s full of huge holes. Most of the variables described by Ellis have been shown to not vary at all or much between the races (re: penis size, testosterone, strength [whites are stronger] prostate cancer caused mainly by diet, 2d/4d ratio [no evidence of it showing a digit ratio difference], and bone density not being studied). Nevertheless, a few of his statements do await testing so I await future studies on the matter. He says that androgen exposure ‘differs by race and ethnicity’, yet the totality of evidence shows ‘not really’ so that cannot be the cause of higher amounts of crime. Ellis talks about a lot of correlates with testosterone, but they do not pass the smell test. Most of it has been rebutted. In fact, one of the central tenets of the ENA theory is that the races should differ in 2d/4d ratio due to exposure of differing levels of the hormone in vitro. Alas, the evidence to date has not shown this—it has in fact shown the opposite.
ENA theory is good in thought, but it really leaves a lot to be desired in regards to explaining racial differences in crime. More research needs to be looked into in regards to intelligence and education and its effect on crime. We can say that low IQ people are more likely to drop out of school and that is why education is related to crime. However, in Mazur (2016) shows that blacks matched for age had lower levels of testosterone if they had some college under their belt. This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have the lowest rate of crime in the worle!
This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have some of the lowest rate of crime in the world (Rushton, 1995)! So this is something that needs to be explained if it is to be shown that testosterone facilitates aggression and therefore, crime.
Conclusion
I’ve shown—extensively—that there is a low positive correlation between testosterone and physical aggression, why testosterone does not cause crime, and have definitively shown that, by showing how flawed the other studies are that purport to show blacks have higher testosterone levels than whites, along with citing large-scale meta-analyses, that whites and blacks either do not differ or the differences is small to explain any so-called differences in disease acquisition or crime. One final statement on the CAG repeats, they are effect by obesity, men who had shorter CAG repeats were more likely to be overweight, which would skew readings (Gustafsen, Wen, and Koppanati, 2003). So depending on the study—and in most of the studies I cite whites have a higher BMI than blacks—BMI and WC should be controlled for due to the depression of testosterone.
It’s pretty conclusive that testosterone itself does not cause crime. Most of the examples cited by Ellis have been definitively refuted, and his other claims lack evidence at the moment. Even then, his theory rests on the 2d/4d ratio and how blacks may have a lower 2d/4d ratio than whites. However, I’ve shown that there is no significant relationship between 2d/4d ratio and traits mediated by testosterone (Kohler, Simmons, and Rhodes, 2004) so that should be enough to put the theory to bed for good.
Race, Testosterone, and Honor Culture
2300 words
Misinformation about testosterone and strength in regards to race is rampant in the HBD-o-sphere. One of the most oft-repeated phrases is that “Blacks have higher levels of testosterone than whites”, even after controlling for numerous confounds. However, the people who believe this literally only cite one singular study with 50 blacks and 50 whites. Looking at more robust data with higher ns shows a completely different story. Tonight I will, again, go through the race/testosterone conundrum (again).
Type I fibers fire first when heavy lifting. Whites have more type I fibers. Powerlifters and Olympic lifters have a greater amount type IIa fibers, with fewer type IIx fibers (like whites). This explains why blacks are hardly represented in powerlifting and strongman competitions.
Somatype, too, also plays a role. Whites are more endo than blacks who are more meso. Endomorphic individuals are stronger, on average, than mesomorphic and ectomorphic individuals.
Blacks have narrower hips and pelves. This morphological trait further explains why blacks dominate sports. Some people may attempt to pick out one variable that I speak about (fiber type, morphology, somatype, fat mass, etc) and attempt to disprove it, thinking that disproving that variable will discredit my whole argument. However, fiber typing is set by the second trimester, with no change in fiber type from age 6 to adulthood (Bell et al, 1980).
It is commonly believed that blacks have higher levels of testosterone than whites. However, this claim is literally based off of one study (Ross et al, 1986) when other studies have shown low to no difference in T levels (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Richard et al 2014). People who still push the “blacks-have-higher-T-card” in the face of this evidence are, clearly, ideologues who want to cushion their beliefs when presented with contradictory evidence (Nyhan and Reifler, 2010).
‘Honor Culture’ and testosterone
In all of my articles on this subject, I have stated—extensively—that testosterone is mediated by the environment. That is, certain social situations can increase testosterone. This is a viewpoint that I’ve emphatically stated. I came across a paper while back that talks about a sociological perspective (I have huge problems with social ‘science’, [more on that soon] but this study was very well done) in regards to the testosterone difference between blacks and whites.
Some people when they read this, however, may go immediately to the part of the paper that says what they want it to say without fully assessing the paper. In this section, I will explain the paper and how it confirms my assertions/arguments.
Mazur (2016) begins the paper talking about ‘honor culture‘, which is a culture where people avoid intentionally offending others while also maintaining a status for not backing down from a confrontation. This theory was proposed by Richard Nisbett in 1993 to explain why the South had higher rates of violence—particularly the Scotch-Irish.
However parsimonious the theory may sound, despite its outstanding explanatory power, it doesn’t hold while analyzing white male homicides in the South. It also doesn’t hold analyzing within-county homicide rates either, since apparently poverty better explains higher homicide rates.
But let’s assume it’s true for blacks. Let’s assume the contention to be true that there is an ‘honor culture’ that people take part in.
Young black men with no education had higher levels of testosterone than educated whites and blacks. Looking at this at face value—literally going right to the section of the paper that says that poor blacks had higher testosterone, nearly 100 ng/ml higher than the mean testosterone of whites. As Mazur (2016) notes, this contradicts his earlier 2009 study in which he found no difference in testosterone between the races.
Note the low testosterone for both races at age 20-29—ranging from about 515 to 425—why such low testosterone levels for young men? Anyway, the cause for the higher levels is due to the type of honor culture that blacks participate in, according to Mazur (which is consistent with the data showing that testosterone rises during conflict/aggressive situations).
Mazur cites Elijah Anderson, saying that most youths have a “code of the streets” they take part in, which have to do with interpersonal communication such as “gait and verbal expressions” to deter aggressive behavior.
Testosterone is not a causal variable in regards to violent behavior. But it does rise during conflicts with others, watching a favorite sports team, asserting dominance, and even how you carry yourself (especially your posture). Since low-class blacks participate in these types of behaviors, then they would have higher levels of testosterone due to needing to “keep their status.”
When testosterone rises in these situations, it increases the response threat in mens’ brains, most notably showing increased activity in the amygdala. Further, dominant behavior and posture also increase testosterone levels. Putting this all together, since blacks with only a high school education have higher testosterone levels and are more likely to participate in honor culture compared to whites and blacks with higher educational achievement, then they would have higher testosterone levels than whites and blacks with a high school education who do not participate in honor culture.
Further, as contrary to what I have written in the past (and have since rescinded), there is no indication of higher testosterone levels in black women with low education. It seems this ‘honor culture’ effect on testosterone only holds for black men with only a high school education.
Mazur’s (2016) most significant finding was that black men aged 20-29 with only a high school education had 91 ng/ml higher testosterone than whites. Among older and/or educated men, testosterone did not vary. This indicates that since they have attained higher levels of educational success, there is no need to participate in ‘honor culture’.
This is yet further evidence for my assertion that environmental variables such as posture, dominance, and aggressive behavior raise testosterone levels.
The honor culture hypothesis is found to hold in Brazil in a comparative study of 160 inmates and non-inmates (De Souza et al, 2016). As Mazur (2016) notes, the honor culture hypothesis could explain the high murder rate for black Americans—the need to ‘keep their status’. It’s important to note that this increase in testosterone was not noticed in teenage or female blacks (because they don’t participate in honor culture).
There is a perfectly good environmental—not genetic—reason for this increase in testosterone in young blacks with only a high school education. Now that we know this, back to race and strength.
Mazur (2009) found that black men in the age range of 20-69, they averaged .39 ng/ml higher testosterone than whites, which is partly explained by lower marriage rates and low adiposity. White men are more likely to be obese than black men, since black men with more African ancestry are less likely to be obese. When controlling for BMI, blacks are found to have 2.5-4.9 percent more testosterone than whites (Gapstur et al, 2002, Rohrmann et al, 2007, Richard et al, 2014). There is little evidence for the assertion that blacks have higher levels of testosterone without environmental triggers.
Blacks between the age of 12 and 15 average lower levels of testosterone than whites. However, after the age of 15, “testosterone levels increase rapidly” with blacks having higher peak levels than whites (seen in table 2 below). After adjusting for the usual confounds (BMI, smoking, age, physical activity, and waist circumference), blacks still had higher levels of testosterone—which is attributed to higher levels of lean mass.
As seen above in table 2 from Hu et al (2014), the difference in total testosterone between blacks and whites aged 20-39 was 6.29 ng/ml and 5.04 ng/ml respectively, with free testosterone for whites being 11.50 and 13.56 for blacks and finally bioavailable testosterone for whites and blacks aged 20-39 was 281.23 and 327.18 ng/ml respectively. These small differences in testosterone cannot account for racial disparities in violence nor prostate cancer—since there is no relationship between prostate cancer and testosterone (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).
In regards to Africans, the best studies I can find comparing some African countries with the West study salivary testosterone. However, there is a direct correlation between salivary testosterone and free serum testosterone (Wang et al, 1981; Johnson, Joplin, and Burrin, 1987). Of the studies I could find, Kenyan pastoralists called the Ariaal have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Campbell, Gray, and Ellison, 2006) while men in Zimbabwe had levels “much lower” compared to Western populations (Lukas, Campbell, and Ellison, 2004). Lastly, among men aged 15 to 30, salivary testosterone levels in an American sample was 335 pmol//l compared to 286 pmol/l in men from the Congo (Elisson et al, 2002). Even certain African populations don’t have higher testosterone levels than Western peoples.
Conclusion
The meme that blacks have higher rates of testosterone in comparison to whites needs to be put to rest. This is only seen in blacks who participate in ‘honor culture’, which is an environmental variable. This is in contrast to people who believe that it is genetic in nature—environmental variables can and do drive hormones. Mazur (2016) is proof of that. Mazur (2016) also shows that the honor culture hypothesis doesn’t hold for teens or black males—so they don’t have elevated levels of testosterone. Certain studies of African populations, however, do not show higher levels of testosterone than Western populations.
Looking at the complete literature—rather than a select few studies— we can see that testosterone levels between white and black Americans are not as high as is commonly stated (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). Further, even if blacks did have higher levels of testosterone than whites—across the board (sans honor culture), it still wouldn’t explain higher rates of black violence when compared to whites, nor would it explain higher prostate cancer rates (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).
Only blacks with low educational achievement have higher levels of testosterone—which, even then is not enough to explain higher rates of violence or prostate cancer acquisition. Other factors explain the higher murder rate (i.e., honor culture, which increases testosterone, the environmental trigger matters first and foremost) and violent crime that blacks commit. But attempting to explain it with 30-year-old studies (Ross et al, 1986) and studies that show that environmental factors increase testosterone (Mazur, 2016) don’t lend credence to that hypothesis.
References
Bell, R. D., Macdougall, J. D., Billeter, R., & Howald, H. (1980). Muscle fiber types and morphometric analysis of skeletal muscle in six-year-old children. Medicine & Science in Sports & Exercise,12(1). doi:10.1249/00005768-198021000-00007
Campbell, B., O’rourke, M. T., & Lipson, S. F. (2003). Salivary testosterone and body composition among Ariaal males. American Journal of Human Biology,15(5), 697-708. doi:10.1002/ajhb.10203
Campbell, B. C., Gray, P. B., & Ellison, P. T. (2006). Age-related patterns of body composition and salivary testosterone among Ariaal men of Northern Kenya. Aging Clinical and Experimental Research,18(6), 470-476. doi:10.1007/bf03324846
De Souza, Souza, B. C., Bilsky, W., & Roazzi, A. (2016). The culture of honor as the best explanation for the high rates of criminal homicide in Pernambuco: A comparative study with 160 convicts and non-convicts. Anuario de Psicología Jurídica,26(1), 114-121. doi:10.1016/j.apj.2015.03.001
Ellison, P. T., Bribiescas, R. G., Bentley, G. R., Campbell, B. C., Lipson, S. F., Panter-Brick, C., & Hill, K. (2002). Population variation in age-related decline in male salivary testosterone. Human Reproduction,17(12), 3251-3253. doi:10.1093/humrep/17.12.3251
, , , , , . Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race—the CARDIA male hormone study. Cancer Epidemiol Biomarkers Prev 2002; 11: 1041–7
Hu, H., Odedina, F. T., Reams, R. R., Lissaker, C. T., & Xu, X. (2014). Racial Differences in Age-Related Variations of Testosterone Levels Among US Males: Potential Implications for Prostate Cancer and Personalized Medication. Journal of Racial and Ethnic Health Disparities,2(1), 69-76. doi:10.1007/s40615-014-0049-8
Johnson, S. G., Joplin, G. F., & Burrin, J. M. (1987). Direct assay for testosterone in saliva: Relationship with a direct serum free testosterone assay. Clinica Chimica Acta,163(3), 309-318. doi:10.1016/0009-8981(87)90249-x
Lopez, D. S., Peskoe, S. B., Joshu, C. E., Dobs, A., Feinleib, M., Kanarek, N., . . . Platz, E. A. (2013). Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males. Cancer Causes & Control,24(4), 817-826. doi:10.1007/s10552-013-0154-8
Lukas, W. D., Campbell, B. C., & Ellison, P. T. (2004). Testosterone, aging, and body composition in men from Harare, Zimbabwe. American Journal of Human Biology,16(6), 704-712. doi:10.1002/ajhb.20083
Mazur, A. (2009). The age-testosterone relationship in black, white, and Mexican-American men, and reasons for ethnic differences. The Aging Male,12(2-3), 66-76. doi:10.1080/13685530903071802
Mazur, A. (2016). Testosterone Is High among Young Black Men with Little Education. Frontiers in Sociology,1. doi:10.3389/fsoc.2016.00001
Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633
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Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x
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Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028
Ross R, Bernstein L, Judd H, Hanisch R, Pike M, Henderson B. Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst. 1986 Jan;76(1):45–48
Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572
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Stockholm 5000 BC
by Scott Jameson
350 words
Stockholm Syndrome is when you identify with people who capture and, in some cases, abuse you. I’ve heard two pretty good explanations for this phenomenon. One is that female mammals like powerful male mammals. Makes sense. The other is that abducted people are attempting to maximize their own chances of survival, and perhaps those of any children they already have. Also makes sense. Let me present a third.
Intra-female competition. Imagine that a woman from tribe B is forcibly inducted into tribe A. The women from tribe A know all of the customs of tribe A, speak the language and so on, and they have known the men from tribe A since childhood. All else equal, what does the woman from tribe B have going for her- novelty, perhaps? That’ll wear off pretty quick, likely faster than it takes for her to get familiarized with her new culture. How can she possibly compensate? How can she compete with the women from tribe A for quantity and social status of offspring?
Lots and lots of asabiyah. If she were that much more devoted to her captors, to their religion, and so on, the men may admire her, or perhaps begin to consider her truly one of “their own,” thereby reducing the disadvantage by comparison to the women from tribe A.
All of these line up with the common belief- which I cannot seem to find strong evidence for or against, but here’s a study that mentions a sample of 21 Stockholm cases wherein 18 were women– that women tend to “suffer” from Stockholm Syndrome more often than men.
It’s not a disease in the Darwinian sense, it’s a behavioral response mechanism. The more accurate term is Capture Bonding.
Any one of these three hypotheses may explain it, or perhaps any combination of the three, or maybe something else. You would have to determine selective pressures operating on women currently in a situation wherein capture bonding is common, for example determining which behaviors enabled one war bride to have more children than another. Anybody up for some field work with Boko Haram?
NotPoliticallyCorrect 