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Microbial Intelligence and Intelligent Physiology
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When organisms that we don’t normally signify as ‘intelligent’ do, indeed, show ‘intelligent’ behavior, our definition of the word—what we call ‘intelligent’ behavior—needs to be reevaluated. Bacteria and other microbes can certainly respond to cues from their environments and communicate with each other. So if bacteria can respond to environmental stimulus by having plastic behavior, then they do show a semblance of ‘intelligence’. Just because bacteria don’t talk doesn’t mean that they are not ‘intelligent’ in their own right.
Bacteria respond to cues from their environment, just like any other intelligent organism. That means that they have behavioral plasticity, the ability to change their behavior based on what occurs in their environments. Bacteria have been shown to exhibit behaviors we would call ‘intelligent’, i.e., acquiring information, storage, processing, use of information, perception, learning, memory, and decision-making (Lyon, 2015). It is proposed that “bacteria use their intracellular flexibility, involving signal transduction networks and genomic plasticity, to collectively maintain linguistic communication: self and shared interpretations of chemical cues, exchange of chemical messages (semantic) and dialogues (pragmatic)” (Jacob et al, 2004).
Clearly, bacteria can and do adapt at the phenotypic level, not only the genotypic level as some have asserted in the past. Using this definition of intelligence, that is, being able to perceive, process and integrate information about the state of the environment to change the organism’s behavior is intelligent behavior (Pinto and Mascher, 2016), all organisms, from bacteria to humans and in between are intelligent. If bacteria do show evidence of behavioral plasticity—and they do—then we must look at them as intelligent creatures, as well as come to the realization that all biological organisms are, in their own right, intelligent. Intelligence is not only for any ‘higher’ organisms; so-called ‘lower’ organisms do show behavioral plasticity, meaning they know what is occurring in their environment. Is that not intelligent?
Any organism that can immediately act in a different way when its environment changes can, in my opinion, be said to be intelligent. All biological organisms have this ability to ‘go off of their genetic coding’, if you will, and change their behavior to match what is currently going on in their environment. Furthermore, the number and fraction of single transduction genes can be used as a measure of ‘bacterial IQ’ (Sirota-Mahdi et al, 2010).
This, of course, has implications for our intelligent physiology. Since our physiological systems incorporate the intelligent processes of the intelligent cell, then, on a larger scale, our physiology is also intelligent. Our physiology is constantly responding to cues from the environment, attempting to maintain homeostasis. Since our body has a need to stay in homeostasis, then our physiological systems are indeed intelligent in their own right. They incorporate the processes of the intelligent cell; looking at our physiology in this way, we can see how and why these systems are intelligent.
Further, physiologists have been referring to physiological systems as “homeodynamic”, rather than “homeostatic”, seeing chaotic states as healthy “allowing organisms to respond to circumstances that vary rapidly and unpredictably, again balancing variation and optimization of order with impressive harmony” (Richardson, 2012). If our physiological systems can do this, are they not intelligent? Further, according to physiologist Dennis Noble, “Genes … are purely passive. DNA on its own does absolutely nothing until activated by the rest of the system through transcription factors, markers of one kind or another, interactions with the proteins. So on its own, DNA is not a cause in an active sense. I think it is better described as a passive data base which is used by the organism to enable it to make the proteins that it requires.” So, as you can see, genes are nothing without the intelligent physiology guiding then. This is only possible with physiological systems, and this begins with the intelligent cell—intelligent microbes.
Some people misunderstand what genes are for and what they do in the body. The gene has long been misunderstood. People don’t understand that genes direct the production of proteins. Since physiological systems—at their core—are run by microbes, then the overall physiological system is itself intelligent. Genes, on their own, are not the masters but the servants. Genes do code for proteins that code for traits, but not under their own direction; they are directed by intelligent systems.
Think of how our gut microbiome co-evolved with us. Knowing what we now know about intelligent cells, we can also say that, by proxy, our microbiome is intelligent as well.
Understanding intelligent cells will lead us to understand intelligent physiology then, in turn, lead us to understand how genes are the servants—not the masters as is commonly asserted—of our traits. Physiology is an intelligent system, and since it is intelligent it can then react to cues from the environment, since it is made up of smaller cells, which make up the larger whole of the intelligent physiological system. These intelligent systems that we have evolved are due to the changeability of our environments in our ancestral past. Our physiology then evolved to be homeodynamic, attempting to maintain certain processes. The ever-changing environment that our genus evolved in is the cause for our homeodynamic intelligent physiology, which begins at the smallest levels of the cell.
The intelligent microbes are the smaller part of the larger whole of the intelligent physiological system. Due to this, we can say that at the smallest levels, we are driven by infinitesimally small microbes, which, in a way, guide our behavior. This can definitely be said for our gut microbiome which evolved with us throughout our evolutionary history. Our microbiome, for instance, had to be intelligent and communicate with each other to maintain our normal functioning. Without these intelligent cells, intelligent physiology would not be possible. Without ever-changing dynamic environments, our intelligent physiology and intelligent cells would have never evolved.
Intelligent physiology evolved due to the constant changeability of the new environments that our ancestors found themselves in. If we would have evolved in, say, more stable, unchanging environments, our physiological systems would have never evolved how they did. These intelligent physiological systems can buffer large ranges of physiological deficiencies. The evolvability of these systems due to the changeability of our ancestral environments is the cause of our amazing physiological intelligence, developmental plasticity, and microbial intelligence.
When you think about conception, when a baby is forming in the womb, it becomes easier to see how our physiological systems are intelligent, and how genes are the slaves—not masters—of our development. Intelligence is already in those little cells, it just needs an intelligent physiology for things to be set into motion. This all goes back to the intelligent cells which make up the larger part of intelligent physiology.
Do Physiologists Study General Intelligence?
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The general factor of intelligence (g) is said to be physiological. Jensen (1998: xii) states that “Students in all branches of the behavioral and social sciences, as well as students of human biology and evolution, need to grasp the essential psychometric meaning of g, its basis in genetics and brain physiology, and its broad social significance.” There are, furthermore, “a number of suggestive neurological correlates of g, but as yet these have not been integrated into a coherent neurophysiological theory of g” (Jensen, 1998: 257). I personally don’t care for correlations too much anymore, I’m interested in actual causes. Jensen (1998: 578) also states “Although correlated with g [size of the brain, metabolic rate, nerve conduction velocity, and latency and amplitude of evoked electrical potentials], these physiological variables have not yet provided an integrated explanatory theory.”
This seems suspiciously like Dreary’s (2001: 14) statement that there “is no such thing as a theory of human intelligence differences – not in the way that grown-up sciences like physics or chemistry have theories.” If g is physiological, then where is the explanatory theory? On that same matter, where is the explanatory theory for individual intelligence differences? That’s one thing that needs to be explained, in my opinion. I could muster something up off the top of my head, such as individual differences in glucose metabolism in the brain, comparing both high and low IQ people (Cochran et al, 2006; Jensen, 1998: 137), however, that is still not good enough.
In physiology there is sliding filament theory which explains the mechanism of muscle contraction (Cooke, 2004). Why is there no such theory of why individuals differ in intelligence and why have these “suggestive neurological correlates of g” not been formulated into a coherent neurophysiological theory? There are numerous theories in physiology, but a theory of g or why individuals differ in intelligence is not one of them.
It’s like Darwin only saying “Species change“, and that’s it; no theory of how or why. He’s just stating something obvious. Similarly, saying “Person A is smarter or has a higher IQ than person B” is just an observation; there is no theory of how or why for why individuals differ in intelligence. There are theories for group differences (garbage cold winter theory), but no individual differences in intelligence? Hmmm… Sure it’d be a ‘fact that species change over time’, but without a theory of how or why, how useful is that observation? Similarly, it is true that some people are more intelligent than others (score higher on IQ tests), yet there is no explanatory theory as to why? I believe this ties back to the physiological basis for g: are physiologists studying it, and if not, why?
Reaction time (RT) is one of the most talked about physiological correlates in regards to IQ. However, as a fitness professional, I know that exercise can increase reaction time, especially in those with intellectual disabilities (Yildirim et al, 2001). I am now rethinking the correlate between reaction time and IQ, since it can be trained in children, especially those with intellectual disabilities. Clearly, RT can be trained by exercise, participating in sports, and even by playing video games (Green, 2008). So since RT can be trained, I don’t think it’s a good physiological measure for g.
Individuals do differ in individual physiology, however, I have never heard of a physiologist attempting to rank individuals on different traits, nevermind attempting to say that a higher level of one variable is better than a lower variable, say blood pressure or metabolic rate. In fact, individuals with high blood pressure and metabolic rates would need immediate medical attention.
There are also wide variations in how immune systems act when faced with pathogens, bacteria and viruses. Though, “no one dreams of ranking individual differences on a general scale of immunocompetence” (Richardson, 2017: 166). So if g is physiological then why don’t other physiological traits get placed on a rank order, with physiologists praising certain physiological functions as “better”?
Richardson (2017: 166-167) writes:
In sum, no physiologist would suggest the following:
(a) that within the normal range of physiological differences, a higher level is better than any others (as is supposed in the construction of IQ tests);
(b) that there is a general index or “quotient” (a la IQ) that could meaningfully describe levels of physiological sufficiency or ability and individual differences in it;
(c) that “normal” variation is associated with genetic variation (except in rare deleterious conditions; and
(d) the genetic causation of such variation can be meaningfully separated from the environmental causes of the variation.
…
A preoccupation with ranking variations, assuming normal distributions, and estimating their heritabilities simply does not figure in the field of physiology in the way that it does in the field of human intelligence. This is in stark contrast with the intensity of the nature-nurture debate in the human cognitive domain. But perhaps ideology has not infiltrated the subject of physiology as much as it has that of human intelligence.
This is all true. I know of no physiologist who would suggest such a thing. So does it make sense to compare g with physiological variables—even when classic physiological variables do not have some kind of rank order? Heritabilities for BMR are between .4 and .8, which is in the same range as the heritability of IQ. Can you imagine any physiologist on earth suggesting a rank order for physiological traits such as BMR or stroke volume? I can’t, and if you knew anything about physiological variables then you wouldn’t either.
In sum, I believe that conflating g with physiology is erroneous; mostly because physiologists don’t rank physiological traits in the same ways that human intelligence researchers do. Our physiology is intelligent in and of itself, and this process begins in the cell—the intelligent cell. Our physiological systems are intelligent—in our bodies are dynamic systems that keenly respond to whatever is going on in the environment (think of how the body always attempts to maintain homeostasis). Physiology deals with the study of living organisms—more to the point, how the systems that run the organisms work.
Looking at physiological variables and attempting to detangle environmental and genetic effects is a daunting task—especially the way our physiological systems run (responding to cues from the environment, attempting to maintain homeostasis). So if general intelligence—g—had a true biological underpinning in the body, and if physiologists did study it, then they would not have a rank ordering for g like psychologists do; it’d just be another human trait to study.
So the answer to the question “Do physiologists study g?” is no, and if they did they would not have the variable on a rank order because physiologists don’t study traits in that manner—if a true biological underpinning for g exists. Physiology is an intelligent and dynamic system in and of itself, and the process begins in the intelligent cell, except it is on a larger scale, with numerous physiological variables working in concert, constantly attempting to stay in homeostasis.
Homo Neanderthalis vs. Homo Sapiens Sapiens: Who is Stronger? Implications for Racial Strength Differences
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Unfortunately, soft tissue does not fossilize (which is a problem for facial reconstructions of hominins; Stephan and Henneberg, 2001; I will cover the recent ‘reconstructions’ of Neanderthals and Nariokotome boy soon). So saying that Neanderthals had X percent of Y fiber type is only conjecture. However, to make inferences on who was stronger, I do not need such data. I only need to look at the morphology of the Neanderthals and Homo sapiens, and from there, inferences can be made as to who was stronger. I will argue that Neanderthals were stronger which is, of course, backed by solid data.
Neanderthals had wider pelves than Homo sapiens. Wider pelves in colder climes are due to adaptations. Although Neanderthals had wider pelves than ours, they had infants around the same size as Homo sapiens, which implies that Neanderthals had the same obstetric difficulties that we do. Neanderthals also had a pelvis that was similar to Heidelbergensis, however, most of the pelvic differences Neanderthals had that were thought to be derived traits are, in fact, ancestral traits—except for the cross-sectional shape of the pubic ramus (Gruss and Schmidt, 2015). Since Neanderthals had wider pelves and most of their pelvis were ancestral traits, then wide pelves may have been a trait of ancestral Homo (Trinkaus, Holliday, and Aurbach, 2014).
Hominins do need wider pelves in colder climates, as it is good for heat retention, however (see East Asians and Northern Europeans). Also, keep in mind that Neanderthals were shorter than us—with the men averaging around 5 feet five inches, and the women averaging about 5 feet, about 5.1 inches shorter than post-WW II Europeans (Helmuth, 1998).
So what does a wider pelvis mean? Since the Neanderthals were shorter than us and also had a wider pelvis, they had a lower center of gravity in comparison to us. Homo sapiens who came Out of Africa, had a narrower pelvis since narrow pelves are better to dissipate heat (Gruss and Schmidt, 2015). Homo sapiens would have been better adapted to endurance running and athleticism, in comparison to the wide-pelved Neanderthals.
People from tropical climates have longer limbs, and are tall and narrow (which is also good for endurance running/sprinting) while people from colder climates are shorter and more ‘compact’ (Lieberman, 2015: 113-114) with a wide pelvis for heat retention (Gruss and Schmidt, 2015). So, clearly, due to the differences in pelvic anatomy between Homo sapiens and Neanderthals,
Furthermore, due to the length of Neanderthal clavicles, it was thought that they had long clavicles which would have impeded strength. However, when the clavicles were reanalyzed it was discovered that when the clavicles were adjusted with the body size of Neanderthals—and not compared with the humeral lengths—Neanderthals had a similar clavicular length, which implies a similar shoulder breadth as well, to Homo sapiens (Trinkaus, Holliday, and Aurbach, 2014). This is another clue that Neanderthals were stronger.
Yet more evidence comes from comparing the bone density of Neanderthal bones to that of Homo sapiens. Denser bones would imply that the body would be able to handle a heavier load, and thusly generate more power. In adolescent humans, muscle power predicts bone strength (Janz et al, 2016). So if the same holds true for Neanderthals—and I don’t see why not—then Neanderthals would have higher muscle power since it predicts bone strength.
Given the “heavy musculature” of Neanderthals, along with high bone robusticity, then they must have had denser bones than Homo sapiens (Friedlander and Jordan, 1994). So since Neanderthals had denser bones, then they had higher muscle power; they had a lower center of gravity due to having a wider pelvis and being shorter than Homo sapiens whose body was heat-adapted. Putting this all together, the picture is now becoming clearer that Neanderthals were, in fact, way stronger than Homo sapiens.
Another cause for these anatomical differences between Neanderthals and Homo sapiens is completely independent of cold weather. Neanderthals had an enlarged thorax (rib cage), which evolved to hold an enlarged liver, which is responsible for metabolizing large amounts of protein. Since protein has the highest thermic effect of food (TEF), then they would have had a higher metabolism due to a higher protein diet which would also have resulted in an enlarged bladder and kidneys which are necessary to remove urea, which possibly would have also contributed to a wider pelvis for Neanderthals (Ben-Dor, Gopher, and Barkai, 2016).
During glacial winters, Neanderthals would have consumed 74-85 percent of their calories from fat, with the rest coming from protein (Ben-Dor, Gopher, and Barkai, 2016). Neanderthals also consumed around 3,360-4,480 kcal per day (Steegman, Cerny, and Holliday, 2002). Let’s assume that Neanderthals averaged 3800 kcal per day. Since the upper limit of protein intake is 3.9 g/bw/day (erectus) and 4.0 g/bw/day for Homo sapiens (Ben-Dor et al, 2011), then Neanderthals would have had a theoretical higher upper limit due to having larger organs, which are useful in processing large amounts of protein. The protein intake for a Neanderthal male was between estimated to be between 985 kcal (low end) to 1170 kcal (high end). It was estimated that Neanderthal males had a protein intake of about 292 grams per day, or 1,170 kcal (Ben-Dor, Gopher, and Holliday, 2016: 370).
Assuming that Neanderthals did not eat carbohydrates during glacial winters (and even if a small amount were eaten, the model would not be affected) and an upper limit of protein intake of 300 grams per day for Neanderthal males, this implies that 74-85 percent of their diet came from animal fat—the rest being protein. Protein is the most thermogenic macro (Corvelli et al, 1997; Eisenstein et al, 2002; Buchholz and Schoeller, 2004; Halton and Hu, 2004; Gillingham et al, 2007; Binns, Grey, and Di Brezzo, 2014). So since Neanderthals ate a large amount of protein, along with their daily activities, they had to have had a high metabolic rate.
To put into perspective how much protein Neanderthals ate, the average American man eats about 100 grams of protein per day. In an analysis of the protein intake of Americans from 2003-2004, it was found that young children ate about 56 grams of protein per day, adults aged 19-30 ate about 91 grams of protein per day, and the elderly ate about 56 grams of protein per day (Fulgoni, 2008). Neanderthals ate about 3 times the amount of protein than we do, which would lead to organ enlargement since larger organs are needed to metabolize said protein as well. Another factor in the increase of metabolism for Neanderthals was the fact that it was, largely, extremely cold. Shivering increases metabolism (Tikuisis, Bell, and Jacobs, 1985; van Ooijen et al, 2005). So the Neanderthal metabolism would have been revved up close to a theoretical maximum capacity.
The high protein intake of Neanderthals is important because high amounts of protein are needed to build muscle. Neanderthals consumed a sufficient amount of kcal, along with 300 grams of protein per day on average for a Neanderthal male, which would have given Neanderthals yet another strength advantage.
I am also assuming that Neanderthals had slow twitch muscle fibers since they have wider pelves, along with evolving in higher latitudes (see Kenyans, East Asians, European muscle fiber distribution), they would have an abundance of type slow twitch muscle fibers, in comparison to fast twitch muscle fibers, however, they also have more slow twitch fibers which Europeans have, while African-Americans (West-African descendants) have a higher amount of fast twitch fibers. (Caesar and Henry, 2015). So now, thinking of everything I explained above and replacing Neanderthals with Europeans and Homo sapiens with Africans, who do you think would be stronger? Clearly, Europeans, which is what I have argued for extensively. African morphology (tall, lanky, high limb ratio) is not conducive to strength; whereas European morphology (wide pelvis, low limb ratio, an abundance of slow twitch fibers) is.
The implications for these anatomic differences between Neanderthals and Homo sapiens and how it translates into racial differences will be explored more in the future. This was just to lay the anatomic and morphologic groundwork in regards to strength and cold weather adaptations. Nevertheless, the evidence that Neanderthals were stronger/more powerful than Europeans stands on solid ground, and the same does hold for the differences in strength between Africans and Europeans. The evolution of racial pelvic variation is extremely important to understand if you want to understand racial differences in sports.
r/K Selection Theory: A Response to Truth-Justice
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After the publishing of the article debunking r/K selection theory last week, I decided to go to a few places and provide the article to a few sites that talk about r/K selection theory and it’s (supposed) application to humans and psychometric qualities. I posted it on a site called ‘truthjustice.net‘, and the owner of the site responded to me:
Phillippe Rushton is not cited a single time in AC’s book. In no way, shape or form does the Theory depend on his opinions.
AC outlines a very coherent theoretical explanation for the differing psychological behavior patterns existing on a bell curve distribution in our population. Especially when it comes to the functioning of the Amygdala for which we have quite a lot of data by now.
Leftists are indeed in favor of early childhood sexualization to increase the quantity of offspring which will inevitably reduce the quality and competitive edge of children. They rank significantly lower on the moral foundations of “loyalty”, “authority” and “purity” as outlined by Jonathan Haidt’s research into moral psychology. Making them more accepting of all sorts of degeneracy, deviancy, and disloyalty to the ingroup.
http://people.stern.nyu.edu/jhaidt/
They desire a redestribution of resources to the less well performing part of our population to reduce competitive stress and advantage while giving far less to charity and being significantly more narcissistic to increase their own reproductive advantage.
https://anepigone.blogspot.com/2008/11/more-income-more-votes-republicans_13.html
Their general mindset becomes more and more nihilistic, atheistic, anarchistic, anti-authority and overall r-selected the further left you go on the bell curve. A denial of these biological realities in our modern age is ridiculous when we can easily measure their psychology and brain functionality in all sorts of ways by now.
Does that now mean that AC is completely right in his opinions on r/K-Selection Theory? No, much more research is necessary to understand the psychological differences between leftists and rightists in full detail.
But the general framework outlined by r/K-Selection Theory very likely applies to the bell curve distribution in psychological behavior patterns we see in our population.
I did respond, however, he removed my comment and banned me after I published my response. My response is here:
“Phillippe Rushton is not cited a single time in AC’s book. In no way, shape or form does the Theory depend on his opinions.”
Meaningless. He uses the r/K continuum so the link in my previous comment is apt.
“AC outlines a very coherent theoretical explanation for the differing psychological behavior patterns existing on a bell curve distribution in our population. Especially when it comes to the functioning of the Amygdala for which we have quite a lot of data by now.”
No, he doesn’t.
1) Psychological traits are not normally distributed,
2) even if r/K were a valid paradigm, it would not pertain to within species variation,
3) it’s just a ‘put these traits on one end that I don’t like and these traits at the other end that I like and that’s my team while the other team has all of the bad traits’ thing,
4) his theory literally rests on the r/K continuum proposed by Pianka. Furthermore, no experimental rationale “was ever given for the assignment of these traits [the r/K traits Pianka inserted into his continuum] to either category” (Graves, 2002: 135), and
5) the r/K paradigm was discredited in the late 70s (see Graves 2002 above for a review)
“Leftists are indeed in favor of early childhood sexualization to increase the quantity of offspring which will inevitably reduce the quality and competitive edge of children. They rank significantly lower on the moral foundations of “loyalty”, “authority” and “purity” as outlined by Jonathan Haidt’s research into moral psychology. Making them more accepting of all sorts of degeneracy, deviancy, and disloyalty to the ingroup.”
I love Haidt. I’ve read his book and all of his papers and articles. So you notice a few things. Then see the (discredited) r/K paradigm. Then you say “oh! liberals are bad and are on the r side while conservatives are K!!”
Let me ask you this: where does alpha-selection fall into this?
“They desire a redestribution of resources to the less well performing part of our population to reduce competitive stress and advantage while giving far less to charity and being significantly more narcissistic to increase their own reproductive advantage.”
Oh.. about that… liberals have fewer children than conservatives. Liberals are also more intelligent than conservatives. So going by Rushton’s r/K model, liberals are K while conservatives are r (conservatives are less intelligent and have more children). So the two cornerstones of the (discredited) r/K continuum show conservatives breeding more and also are less intelligent while it’s the reverse for liberals. So who is ‘r’ and ‘K’ again?
“Their general mindset becomes more and more nihilistic, atheistic, anarchistic, anti-authority and overall r-selected the further left you go on the bell curve. A denial of these biological realities in our modern age is ridiculous when we can easily measure their psychology and brain functionality in all sorts of ways by now.”
‘r’ and ‘K’ are not adjectives (Anderson, 1991: 57).
Why does no one understand r/K selection theory? You are aware that r/K selection theory is density-dependent selection, correct?
“Does that now mean that AC is completely right in his opinions on r/K-Selection Theory? No, much more research is necessary to understand the psychological differences between leftists and rightists in full detail.”
No, he’s horribly wrong with his ‘theory’. I don’t deny psych differences between libs and cons, but to put them on some (discredited) continuum makes no sense in reality.
“But the general framework outlined by r/K-Selection Theory very likely applies to the bell curve distribution in psychological behavior patterns we see in our population.”
No, it doesn’t. Psych traits are not normally distributed (see above). Just like Rushton, AC saw that some things ‘fit’ into this (discredited) continuum. What’s that mean? Absolutely nothing. He doesn’t even cite papers for his assertion; he called Pianka a leftist and said that he tried to sabotage the theory because he thought that it described libs (huh? this makes no sense). AC is a clear ideologue and is steeped in his own political biases as well as wanting to sell more copies of his book. So he will not admit that he is wrong.
Let me ask you a question: where did liberals and conservatives evolve? What selective pressures brought about these psych traits in these two ‘populations’? Are liberals and conservatives local populations?
I’ve also summarily discredited AC and I am waiting on a reply from him (I will be surprised if he replies).
However, unfortunately for AC et al, concerns have been raised “about the use of psychometric indicators of lifestyle and personality as proxies for life history strategy when they have not been validated against objective measures derived from contemporary life history theory and when their status as causes, mediators, or correlates has not been investigated” (Copping, Campbell, and Muncer, 2014). This ends it right here. People don’t understand density-dependent/independent selection since Rushton never talked about it. That, as has been brought up, is a huge flaw in Rushton’s application of r/K theory to the races of Man.
Liberals are, on average, more intelligent than conservatives (Kanazawa, 2010; Kanazawa, 2014) Lower cognitive ability has been linked to greater prejudice through right-wing ideology and low intergroup contact (Hodson and Busseri, 2012), with social conservatives (probably) having lower IQs. There are also three ‘psychological continents’—Europe, Australia, and, Canada and are the liberal countries whereas Southeast Asia, South Asia, South America and Africa contain more conservative countries with all other countries including Russia, the US and Asia in the middle and “In addition, gross domestic product (GDP) per capita, cognitive test performance, and governance indicators were found to be low in the most conservative group and high in the most liberal group” (Stankov and Lee, 2016). Further, economic liberals—as a group—tend to be better educated than Republicans—so intelligence is positively correlated with socially and economically liberal views (Carl, 2014).
There is also a ‘conservative baby boom‘ in the US—which, to the Rushtonites, is ‘r-selected behavior’. Furthermore, women who reported that religion was ‘very important to them’ reported having higher fertility than women who said that it was ‘somewhat important’ or ‘not important’ (Hayford and Morgan, 2008). Liberals are more likely to be atheist (Kanazawa, 2010), while, of course, conservatives are more likely to be religious (Morrison, Duncan, and Parton, 2015; McAdams et al, 2015).
All in all, even if we were to allow the use of liberals and conservatives as local populations, like Rushton’s erroneous use of r/K theory for human races, the use of r/K theory to explain the conservative/liberal divide makes no sense. People don’t know anything about ecology, evolution, or neuroscience. People should really educate themselves on the matters they speak about—I mean a full-on reading into whatever it is you believe. Because people like TIJ and AC are clearly idealogues, pushing a discredited ecological theory and applying it to liberals and conservatives, when the theory was never used that way in the first place.
For anyone who would like a look into the psychological differences between liberals and conservatives, Jonathan Haidt has an outstanding book outlining the differences between the two ideologies called The Righteous Mind: Why Good People are Divided by Politics and Religion. I actually just gave it a second read and I highly, highly recommend it. If you want to understand the true differences between the two ideologies then read that book. Try to always remember and look out for your own biases when it comes to your political beliefs and any other matter.
For instance, if you see yourself frantically attempting to gather support for a contention in a debate, then that’s the backfire effect in action (Nyhan and Reifler, 2012), and if you have a knowledge of the cognitive bias, you can better take steps to avoid such a heavy-handed bias. This, obviously, occurred with TIJ. The response above is airtight. If this ‘continuum’ did exist, then it’s completely reversed with liberals having fewer children and generally being more intelligent with the reverse for conservatives. So liberals would be K and conservatives would be r (following Rushton’s interpretation of the theory which is where the use of the continuum comes from).
Marching Up the ‘Evolutionary Tree’?
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There are numerous misconceptions about evolution. One of the largest, in my opinion, is that there is some sort of intrinsic ‘progress’ to evolution. This is inferred from the fact that the first life—bacteria—are simpler and less ‘complex’ than so-called ‘higher’ organisms. This notion is still pushed by some, despite the fact that it is a discredited concept.
The concept of scala naturae was first proposed by Aristotle (Hodos, 2009; Werth, 2012; Diogo, Ziermann, and Linde-Medina, 2014). This notion was held until Darwin’s landmark book On the Origin of Species (Darwin, 1859) when Darwin proposed the theory of evolution by natural selection. However, the notion of the scala naturae is still entrenched in modern-day thought, from the layman all the way to educated scientists. This notion is wrong.
Neuroscientist Herculano-Houzel writes on page 94 of her book The Human Advantage A New Understanding of How Our Brain Became Remarkable:
Moreover, evolution is not synonmous with progress, but simply change over time. And humans aren’t even the youngest, most recently evolved species. For example, more than 500 new species of cichlid fish in Lake Victoria, the youngest of the great African Lakes, have appeared since it filled with water some 14,500 years ago.
When people think of ‘progression up this evolutionary tree’ they look at Man as the ultimate culmination of the evolutionary process—as if every event that occurred before the Dawn of Man was setting the stage for us to be here. This, of course, goes back to the scala naturae concept. The ‘lower’ animals are the ones that are less ‘complex’ than the ‘higher’ animals. The notion that there was a ‘march of progress’ towards Man is erroneous (see Gould, 1989: 27-45 for a review).
Indeed, even Darwin himself didn’t believe in some ‘straight line’ to the evolutionary process. In one of his notebooks, he drew a ‘coral of life’ (seen below):
Notice how there are no ‘lower’ or ‘higher’ organisms and each branch branches off to the side, with no way of denoting which organism has ‘progressed’ more?
The scala naturae proposes that inanimate objects, to plants, to animals can all be placed somewhere on this ladder of ‘progress’, which eventually culminate with Man at the top—as if we are the ultimate culmination of evolutionary history and time—like we were preordained to be here. The scala naturae is still with us today. Why should we view humans as ‘higher than’ other organisms? It doesn’t make sense. It’s clearly steeped in a large anthropometric bias.
Indeed, the scala naturae is so entrenched in our minds that modern-day biologists still use terms that would denote ‘higher’ and ‘lower’, the scala naturae. Rigato and Minelli (2013) data mined 67,413 biological articles published between the years 2005 and 2010 looking for signs of pre-evolutionary language (e.g., lower vs. higher vertebrates and lower vs. higher plants). Of the 67,413 article that were mined for data, 1,287 (1.91%) returned positive hits for scala naturae language. Shockingly, the journal Molecular Biology and Evolution had frequent scala naturae language (6.14 %) along with the journal Bioessays (5.6%) and the Annual Review of Ecology, Evolution, and Systematics (4.82%). Clearly, misconceptions about the nature of evolution can still persist in the modern-day amongst experts (that doesn’t mean that the notion of the scala naturae is correct since specialists still use some of the terminology, however). In terms of scala naturae thinking by country, Russia topped the list followed by Japan, Germany, Israel, and France.
This notion of ‘progress’ to evolution—that there is some sort of scala naturae with has ‘primitive’ organisms on the bottom with ‘advanced’ organisms at the top is wrong. When comparing organisms, the comparison isn’t between which organism is more ‘primitive’ or ‘advanced’. The comparison is between ancestral and derived, so the only meaningful comparison is to say that organism A is more like the common ancestor (ancestral) while organism B has derived traits in comparison to the common ancestor (Gregory, 2008).
It is further assumed that earlier organisms are more ‘primitive’ than organisms that are younger. This is false. Once organisms diverge from a common ancestor, they both share a mixture of ancestral and derived traits; ancestral and derived organisms share a mix of ancestral and derived traits from said common ancestor (Crisp and Cook, 2005: 122). Furthermore, ‘early’ does not denote ‘primitiveness’ (Gould, 1997: 36). So to say that, for instance, ‘this organism on this tree did less/no branching than others and is therefore primitive’ is incorrect. It is fallacious to make a comparison between ‘primitive’ and ‘advanced’ organisms. For instance, one may look at a phylogeny and see a straight line and assume that no change has occurred. This is wrong.
The terminology ‘driven’ and ‘passive’ is used to denote trends in complexity. Is the trend driven or passive? Large amounts of research has been done into this matter (Gould, 1996; McShea, 1996) with no clear-cut answer. What is increasing? Complexity? The thing about ‘complexity’ (whatever that is) is that it may be a trend, but it is not an inevitability (Werth, 2012: 2135). Since life began at the left wall—where no organism can get any simpler—there was only one way to go: up. Any organism that arises in between the left and right walls can either become more or less complex depending on what is needed in that particular ecosystem.
Gould (1996) speaks of a drunkard leaving a bar. The drunkard leans on the bar wall (the left wall of complexity) and continuously stumbles toward the gutter (the right wall of complexity). The drunkard may go back and forth, touching the bar wall all the while getting closer to the gutter which each stumble. The drunkard will—eventually—end up in the gutter. Now we can look at the right wall of complexity as us humans and the left wall as bacteria. Any organism caught in the middle of the walls can either get less or more complex, but no simpler than the left wall—where life began. Some may say that this denotes ‘progress’, however, since life began constrained at the left wall, there was no way to go but ‘up’.
McShea (1994: 1761) notes:
If such a trend in primates exists and it is driven, that is, if the trend is a direct result of concerted forces acting on most lineages across the intelligence spectrum, then the inference is justified. But if it is passive, that is, forces act only on lineages at the low-intelligence end, then most lineages will have no increasing tendency. In that case, most primate species—especially those out on the right tail of the distribution like ours—would be just as likely to lose intelligence as to gain it in subsequent evolution (if they change at all).
Are there any instances like this in our genus? Of course there are, with the most famous (and most studied) being Homo floresiensis. I’ve written twice before about how the evolution of floresiensis proves that 1) evolution is not progress and 2) large brains need high-quality energy and without that brain size—and body size—will shrink. Indeed, a new paper on the evolution of floresiensis lends credence to the idea that floresiensis is a derived form of erectus (Diniz-Filho and Raia, 2017). Their analysis lends credence to the support that floresiensis is derived from erectus and not habilis. No matter which hominin floresiensis evolved from, this shows how critical the quality of energy is for maintaining a large brain and body size and, without large amounts of high-quality energy then reductions in brain and body size will persist. This, yet again, lends more credence to my argument of non-progressive evolution.
Now, I must talk about the scala naturae and its involvement in attempting to figure out the evolution of the human brain. Does the supposed increase in brain size denote ‘progress’ in evolution? No, it does not.
Brains are made from metabolically expensive tissue; that is, the larger a brain is the more kcal are needed to power it. Brains and the tissue that compose it (along with other bodily structures) are so expensive that there is a trade-off between elaborate defense mechanisms and brain size—as EQ decreases, defense mechanisms get more elaborate and vice-versa (Stankowich and Romero, 2017). So organisms don’t need intelligence—and [sometimes] the larger brain that comes with it—if they have evolved elaborate defense mechanisms to where they don’t need a large brain to survive.
The increase in brain size over the past few million years in our genus Homo is pointed at as proof that evolution is ‘progressive’, however that is literally only one metric and any wild swings in environment can and will select for smaller brains. The point is that increases in brain size are due to local change, so therefore trends in the opposite direction can and do occur.
The terms ‘higher and lower’ in regards to the scala naturae have been discredited (Diogo, Ziermann, and Linde-Medina, 2014: 18). Indeed, when we believe that things may go our way when, say, we are testing ourselves compared to other animals we will invoke the scala naturae. But what if we humans are not the ‘best’ at any given task tested? Eleven animal species (including human infants) were tested to analyze color processing speed. First came honeybees, then fish, then birds and lastly human infants. Of course this contradicted the scala naturae concept, and some people even argued that learning speed is not a useful measure of intelligence (Chittka et al, 2012)! This scala naturae thinking would have us believe that we should be on top of the learning speed ‘pyramid’, yet when it’s found that we are not then we say that learning speed is not a useful measure of intelligence? Can you see the huge bias there?
Above is a figure from Mashour and Alkire (2013) which shows the evolution of the brain through the lens of the scala naturae concept on the left and the modern theory on the right. Clearly, with the modern theory, there is no such ‘progress’ or ‘inherent advancement’ from fish culminating to the brain of Man.
Modern theories of the scala naturae include John Bonner’s assertion that animals found in lower strat are ‘lower’ whereas those found in the higher strata are ‘higher’. This erroneous assumption made by Bonner, however, is corrected in subsequent publications (see Randomness in Evolution, Bonner, 2013). He stresses, as can be seen by the title of the book, that evolution is random and possibly non-drive (i.e., passive, see McShea, 1994, Gould, 1996) (Diogo, Ziermann, and Linde-Medina, 2014: 3). Furthermore, there is “no general trend to increase the number of muscles at the nodes leading to hominoids and to modern humans. That is, with respect to the muscles in the regions we have investigated, although modern humans accumulated more evolutionary transitions than the other primates included in our cladistic study, these evolutionary transitions did not result in more muscles, or more muscle components (Diogo & Wood, 2011, 2012a,b; Diogo et al., 2013b)” (Diogo, Ziermann, and Linde-Medina, 2014: 18). So looking at this one facet of hominin evolution (muscles), there is no general increase in the number of muscles at the nodes leading to our genus.
Next, one Dale Russel (who I have written about at length) needs to be addressed again. Russel asserts that had the dinosaurs not gone extinct, that one species of dinosaur, the troodon, would have evolved human-like bipedalism, a large brain among other traits. This is horribly incorrect. In his book (Russel, 1989) he denotes ever-increasing complexity, which, as I have noted, is due to the beginnings of life at the left wall of complexity. The behaviors of most dinosaurs which were inferred from skeletal morphology and trackways “may not have lain much outside the observed range in ectothermic crocodilians” (Hopson, 1977: 444), along with most dinosaur endocasts showing not showing a tendency for increased brain size (Hopson, 1977: 443). Further, since dinosaurs were tied to the sun their behavior was restricted, they needed to avoid getting too hot or cold and couldn’t explore and understand the world, and in turn wouldn’t have been able to evolve large brains—nevermind human-like intelligence (Skoyles and Sagan, 2002: 12). Russell’s contentions are moot.
On that same note, E.O. Wilson, author of the 1975 book Sociobiology asserts that evolution must be progressive (I will cover Wilson’s views on evolutionary progress in depth in the future) since life started prokaryotes with no nucleus, to eukaryotes with nucleus and mitochondria, then multi-cellular organisms with complex organs like eyes and brains and finally the emergence of the human mind (Rushton, 1997: 293). This, too, can be explained by life beginning at the left wall and having nowhere to go ‘but up’.
This finally brings me to JP Rushton who attempted to revive the scala naturae concept by (wrongfully) applying r/K selection theory to human races. Rushton argues that since Mongoloids are the ‘newest’ race that they are then the most ‘progressed’ and thusly are a pinnacle of evolution of Man. However, as anyone who understands evolution knows, evolution through natural selection is local change, not progress.
This notion of evolutionary progress, the scala naturae, and the ‘march up the evolutionary tree’ are all large misconceptions about the nature of evolution. This misconception arises due to only looking at the right tail of the variation. Of course, if you only looked at the right tail, you would assume that evolution is ‘progressive’, that there was a ‘march’ from simple to complex organisms. Why focus only on the complex end of the distribution of life? Because looking at the whole of life, bacteria is the mode (Gould, 1996; 1997). We are currently living in the age of the bacteria. That is the mode of all life, and that is why there is no ‘progress’ to evolution, nor any ‘march up an evolutionary tree’, because evolution through natural selection is local change, not progress.
Saying that evolution is progress doesn’t allow us to appreciate the full house of variation (Gould, 1996). Bacteria rule the earth, and will do so until the Sun explodes. What does that tell you about any ‘progress’ to life? Aboslutely nothing because bacteria have remained the most numerous lifeforms on the planet since life began.
r/K Selection Theory: A Response to Anonymous Conservative
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I knew the article about r/K selection would stir a bit of debate. Anonymous Conservative has replied to both articles that were published the other day. However, he seems confused. He doesn’t talk about r/K selection theory in terms of density-dependence/independence. That’s what r/K theory was based on before it was discredited for age-specific mortality (Reznick et al, 2002). The theory was discredited decades ago. This article will be a response to him. How can you use age-specific mortality for your theory?
Combining all African and all European populations probably dulls the degree to which certain populations are r and K.
Combining the ethnies of all three populations makes no sense if you’re attempting to infer how behavior X evolved in ecosystem Y using r/K selection theory. To conduct such a study, you would need to study the races in the ecosystem that the selection was hypothesized to have occurred. r/K selection is—as I’ve already brought up—proven false. I will get to that below.
If r/K selection did apply to humans, then since Africans have been in their habitat—according to Rushton—for 140ky and Mongoloids have been in their habitat for 40ky, then Africans would have had more opportunity to approach the environmental carrying capacity while Mongoloids who migrated into novel environments (cold weather, as mentioned above) would experience r-selected traits since they are in a novel environment (r pressure) and facing cold weather (another r pressure). Per Rushton’s own arguments—along with how r/K theory was really used—Africans are K and Mongoloids are r.
Take the most r populations in Africa and you would also see highly obvious differences deviating from normal human behavior.
Which populations in Africa are ‘the most r’? What is ‘normal human behavior’?
Goal number one should be to get people forced to acknowledge that some humans are exhibiting the r-strategy compared to others.
If this were the case, then Mongoloids would be r while Africans would be K—if r/K selection theory weren’t discredited and if human races qualified as local populations. This, of course, comes from Rushton own words, who asserts that Mongoloids have cold-weather adaptations. So if Mongoloids have cold-weather adaptations and cold weather is an agent of r-selection as described previously, then Mongoloids are r-selected. This argument comes straight from Rushton’s own theory. Furthermore, Africans would be K-selected since endemic disease is an agent of K-selection. This is simple enough to understand, especially if you read a few papers on r/K selection.
I get the impression the author is a pot-stirrer ginning up debate, which I can respect. But I would counter that I think this argument requires a slightly more complex view on a few points, and it seeks to cite the established literature on r/K a little too much.
Citing papers is what’s needed when discussing scientific matters. If your arguments are not backed by scientific papers then your argument is pretty much moot.
Most of the literature on r/K is incredibly shallow in its analyses. I suspect nobody really cared about the theory on an emotional level, so nobody really bothered to look too closely at it, or tried to understand why some arguments would seemingly violate simple common sense. One person would assert things that would make no sense in certain contexts, and nobody would ever try to highlight the complexity required for a fuller understanding of the issue. It is either that, or the more powerful minds gravitated somewhere else in the sciences with more practical application.
This looks pretty clear-cut to me. r/K selection theory has been extensively tested and falsified. Of course people cared about it, it dominated biology and ecology literature for about twenty years after Pianka’s (1970) paper where he proposed his now debunked ‘r/K continuum’. As I have said, Pianka gave no experimental rationale on why he chose the traits he did for the continuum (Graves, 2002: 135). This is simple enough to understand on its own.
As an example, the author cites papers that say drought is an r-selective pressure. Drought can be r or K, depending on the abilities of the organisms confronted with it. Mice will die in a drought, and have short enough life cycles to reproduce in the wet periods following it. So with mice, after the drought, there will be free resources and that makes drought a huge r-selection pressure.
But suppose you have an organism with the intelligence to envision how to survive the drought, and which thinks in terms of long time frames. Now that drought will cull the relatively r-selected individuals who are designed to exploit a glut with no thought of the future, while favoring those who planned for the drought and stockpiled water, or organized a way to acquire it. Is the drought still an r-selective pressure? Being human, with a high IQ and an ability to plan for the future changes a lot of these rules.
Drought is an agent of r-selection. How about earthquakes and volcanic eruptions? Are those agents of K-selection as well if you can ‘plan for the future changes’? Provide references for your assertion or your claim is unfounded.
On the issue of colder climates being K, the author cites research which makes the case that cold climates kill back the population in the winter, and then allow explosive growth in the summer, and thus are r-selecting.
This will be true in things like insects with short lifespans and no ability to plan for the winter. But in humans, this will favor those who can defer pleasures in the summer, looking forward to the winter and sacrificing by setting aside resources to get themselves through the colder period. It will also favor groups which can work together in pursuit of common goals.
You don’t get it. Mongoloids being r-selected is straight from Rushton. He asserts that they have cold-adaptations. Cold adaptations are due to cold weather. Cold weather is an agent of r-selection (temperature extreme). If cold weather is an agent of r-selection and Mongoloids further migrated into a novel environment (another agent of r-selection), then, per Rushton’s own words, Mongoloids are r-selected. Conversely, Rushton describes endemic disease and drought in Africa (without references), but let’s assume it’s true. As described above, drought is an agent of r (see the table from Anderson above) while endemic disease is an agent of K-selection.
Endemic (native) disease is an agent of K-selection. Since the disease is constant, then the population under that agent of K-selection can prepare ahead for disease. Indeed, in Africa, measures can be taken to reduce the number of those infected with malaria, such as mothers shielding their babies from mosquitoes, to even herbal remedies which have been in use for thousands of years (Wilcox and Bodecker, 2004). If endemic disease is constant (and it is) and Africans are under that constant pressure, then they will be K-selected.
Do groups not work together in Africa to reach common goals? In the Pleistocene as well? Citations? Think before you write (and cite), because hunting bands in our species began with Homo erectus. The capacity for endurance running evolved in erectus which can be seen with the beginnings of our modern pelvis as well as the evolution of the gluteus maximus (Lieberman et al, 2006). So how can you assert that working together to reach common goals only occurred where it was cold—as if tropical environments don’t have their own challenges which require foresight and planning? Think about human evolution and how modern human cognition evolved in Africa.
This will be true of most hardships to some degree. Where they kill back the population massively and randomly, and then allow explosive regrowth, they are r-pressures. But where they are challenges that select for those who can prepare and overcome them, they will tend to favor K, even if they may, strictly by the numbers, appear to be r.
How can you prepare and overcome a violent winter storm, volcanic eruption, earthquake, and drought (which vary wildly)? At a certain point, you can be the smartest one around but one would still succumb to the elements.
He also speaks of aggression. There the question is, is aggression borne of a competitive psychology that embraces risk innately because it evolved to embrace risk in a competitive environment where resources are scarce, or is aggression an opportunistic seizure of free resources from the weak and helpless.
A criminal who sees an old lady and pushes her to the ground to steal her purse is not the same as a Marine who proceeds to selflessly storm enemy lines and kill fifteen men with his bare hands simply to try and save his fellow Marines in battle. The criminal will seek out the weak and vulnerable to victimize safely for personal gain, while the Marine would find that in conflict with his nature. The Marine will sacrifice himself for his group and nothing more, while the criminal would view that as pointless and stupid. Those are two vastly different forms of aggression.
Aggression and violence can be principled and daring, or opportunistic and cowardly. Each is driven by a different psychology, and you can see this difference extend to sexual drive, promiscuity, and even rearing investments. I think there needs to be a difference cited there. One aggressive psychology is r and one is K. One is designed to take free resources in a world with no consequences, while the other is programmed to fight with anyone to try and get a share of scarce resources, because if they didn’t they would starve.
I speak of aggression in regards to testosterone and Richard Lynn’s claims that gonadotropin levels and testosterone lend further support for Rushton’s theory. However, I’ve falsified Ross et al (1986) numerous times. Further, the correlation between testosterone and physical aggression is a pitiful .08 (Archer, Graham-Kevan, and Lowe 2005). The point is that testosterone is not related to aggression, nor crime. Furthermore, the time of day that crime is committed at the highest rates for teens (3 pm) and adults (10 pm) discredit the testosterone-causing-crime theory since testosterone levels are highest at 8 am and lower at 8 pm. You did not address my arguments on testosterone—try again.
Then there is disease. Disease can be r or K, depending on epidemiology. If a disease is sexually transmitted, it is going to take out those with a high sex drive, promiscuity, and reduced disgust. That doesn’t means the disease is K-selecting, so much as it preferentially kills those with an r-selected psychology, and fosters the rise of K.
What about if a disease is endemic? Endemic disease (Rushton’s assertion) is an agent of K, this is not up for discussion. Endemic disease reduces carrying capacity and thusly is an agent of K-selection.
This is simple enough to understand, especially if you understand r/K selection theory.
On the other hand, if a disease infects and kills randomly, such as one transmitted by mosquito, then it will open up free resources by killing the population back below the carrying capacity. That will favor the rise of the r-selected psychologies.
Nope.
I have found the vast majority are written by individuals looking to create quick rules of thumb for much more complex variables that can only be looked at in the context of the mechanisms they are a part of. In many cases, I see authors claiming something is always r or K, when the truth is they are more often the opposite for reasons which the authors seem strangely blind to.
The vast majority of what was written about r/K in its heyday was written by biologists and ecologists. Why reduce a complex biological system interacting with its almost equally complex environment down to a discredited theory? It doesn’t make sense to reduce what organisms do to some ‘simple model’ when the real world—and by proxy ecological theories—are much more complex than a ‘simple model’.
r and K are simple adaptation to either free or limited resource availabilities. To understand how the environment affects the evolution of r and K psychologies, you have to understand that those adaptations to free or limited resources imbue certain psychological predispositions. Once imbued, all other selective pressures have to be examined with an eye to how they either confer advantage or disadvantage on those who express those psychological traits.
r/K selection theory is based on density-dependence and density-independence. As a matter of fact, searching for ‘density-dependent‘ brings up no hits and for ‘density-independent‘, the only hit is for your response to my article. Which makes me believe that you don’t understand r/K selection theory since it’s based on density-dependence and density-independence. It’s also impossible to predict which life history traits will be favored by selection unless you know which particular ecological factors influence life history traits as well as needing a model as to how they function (Anderson, 1991). Rushton did neither, and so he was wrong with his application of r/K to human races.
A sexually transmitted disease that savages a population will open up resource availability and reduce the population well below the carrying capacity, and thus could be mistaken for an r-selecting pressure. But if it wipes out every promiscuous r-strategist, and leaves behind only the monogamous K-strategists, then it is not an r-selective pressure at all. It is favoring the K-psychology, even as from a raw numerical standpoint it would appear an r-pressure.
Which STD? Which population(s)? Source? Even then, STDs such as chancroid (in the US and Europe) were endemic in the early 20th century (Aral, Fenton, and Holmes, 2007). Which populations are you describing? An event like that would be part of the density-dependence aspect of what r/K described. The population would dip and then go right back to environmental carrying capacity (K).
It is necessary—for a K-selected history—to have some sort of density-dependent pressure. Density-dependent pressures are things such as endemic disease in Africa—which is necessary for a K-selected history since density-dependent natural selection occurs at or close to the environmental carrying capacity (Anderson, 1991: 58). If you truly understood r/K selection theory, you’d understand how it’s based on density dependence. You’d understand that ‘r’ and ‘K’ are not adjectives.
(Indeed, I suspect a golden age in the context of human history will be found to often be such an unusual circumstance, where a population is K-ified, even as it is placed in an r-selected environment of free resource availability. The opposite, an r-ified population placed in a grossly overpopulated environment of shortage will be found to reliably be Hell on earth. Guess which one we have coming.)
You should learn about what r/K selection really is (it is density-dependent selection).
The complete absence of that type of detailed understanding of the effects of selective pressures in the literature about r/K Selection Theory is why I don’t waste extensive time here quoting the source texts on the subject. Most seem strangely shallow in their analyses.
It is detailed, see the table above. Where does alpha-selection fit into your theory? Are conservatives alpha-selected? Not speaking about alpha-selection throws a wrench into the theory. The r/K continuum doesn’t even exist!
I am amused to see the author mention r/K Selection Theory has been linked to ideology, without any mention of where. My greatest hope has always been that r/K Theory would become so ever present in the dialog that nobody would remember where it first arose. When that happens, r/K will be everywhere, and nobody will have any idea who to blame.
Well, the ‘one’s to blame’ would be the originators of the theory, MacArthur and Wilson. But r/K selection is a dead concept in biology and population ecology. Don’t worry, r/K selection is dead and isn’t coming back. I’ve shown how it’s a discredited model.
In regards to r/K being falsified, when the theory was tested, key life history variables did not conform to the predictions of the theory (Graves, 2002: 137). People should stop pushing discredited theories.
By the way, in regards to the one comment that was left, why breakdown complex biological interactions with the environment into something so simple? Can you explain to me how and why complex biological systems interacting with their environment can be broken down ‘simply’? You, as well, have no idea what r/K selection is either.
Anonymous Conservative should try to be aware of his political biases. That much is clear. Although, now I know what will happen. We will see a case of the backfire effect where these corrections will increase his misconceptions of r/K selection theory (Nyhan and Reifler, 2012). Everyone should try keep this quote in mind at all times:
When you are studying any matter, or considering any philosophy, ask yourself only what are the facts and what is the truth that the facts bear out. Never let yourself be diverted either by what you wish to believe, or by what you think would have beneficent social effects if it were believed. But look only, and solely, at what are the facts. That is the intellectual thing that I should wish to say. —Bertrand Russel, 1959
E.O. Wilson on Rushton’s r/K Theory and More on Endemic Disease
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I thought I’d address what E.O. Wilson’s thoughts on Rushton’s theory and clarify some things on endemic disease and cold winter and how they relate to this r/K paradigm. Proponents of Rushton may look to it and say ‘Well, E.O. Wilson said X, so therefore the reason why it’s not accepted is Y!” However, this comes from a faulty misunderstanding of what Wilson said.
I think Phil is an honest and capable researcher. The basic reasoning by Rushton is solid evolutionary reasoning; that is, it is logically sound. If he had seen some apparent geographic variation for a non-human species – a species of sparrow or sparrow hawk, for example – no one would have batted an eye. … when it comes to [human] racial differences, especially in the inflamed situation in this country, special safeguards and conventions need to be developed.
This little blurb does not address anything, really. Yes, it does address the fact that people attacked Rushton for his research on human racial differences. What it does not address is Rushton’s incorrect application of the theory, as covered yesterday. So, bringing up Wilson’s thoughts on Rushton and the controversy surrounding his theory is a moot point.
I don’t understand why people cannot just accept that Rushton was wrong with his misuse of the theory. Notice how I never said anything about his data—I only talked about his misuse of the theory. People act as if both his data and theory need to be correct, well, why can’t one be right and the other wrong (the data and the theory)? Because that’s how it is in reality.
Rushton’s data was largely correct, however, his misapplication of r/K theory shows that he just saw, for instance, current TFRs (total fertility rates) and just arbitrarily placed Africans as r and Eurasians as K, when looking at what Rushton said about both environments—tropical and cold—would lead to K selection for the tropics, since Rushton asserts that endemic and infectious disease is a selective agent (with no references) while Asia was ‘unbearably cold (also with no reference). This characterization of Pleiositicine environments as ‘hot and endemic disease’ and ‘unbearably cold’ has literally no basis in reality.
Tropical environments are more challenging than cold/temperate ones (Dobzhansky, 1950: 221). Knowing this, Rushton’s assertion of cold winters selecting for higher levels of intelligence in Eurasians compared to Africans is wrong since life is easy nowhere. This characterization of life being ‘easy’ in tropical environments has no basis in reality. It’s like people assume that in the tropics you can just laze around all day while fruits fall onto your lap and you have to do nothing that’s cognitively demanding. This is not true at all. Just look at how a savanna looks, does that look ‘easy’ to live in?
There are also a few more things I’d like to talk about in regards to Rushton’s theory, mainly on endemic disease and why it is an agent of K-selection; not r. Even then, r characteristics probably wouldn’t be able to evolve in the savanna (Miller, 1991: 670). The thing is, populations that evolve in disease-ridden places are expected to select for high population growth—increasing r. However, populations in other areas would increase K as they would be selected for survival and not disease resistance. So if disease was a main difference in so-called r/K differences between populations, r-selected people would be more disease resistant AND they would live longer lives (Miller, 1991: 672).
Case closed, right? Wrong. Miller (1991) writes: “If differences in disease rates do prove to be part of the explanation, the theory would not be an r vs K selection theory, because resistance to disease and a long life span are considered K characteristics, rather than r characteristics” (pg: 672). It is also doubtful that conditions in Africa are much more variable in comparison to other continents.
Furthermore, if an alien observed us with no prior knowledge of our species and only had Pianka’s (1970) paper to go off of, he would conclude that Mongoloids would be r-selected due to the cold winter temperatures which bring a high mortality rate. This is the direct opposite of what Rushton claimed.
Miller states at the end of the article that these differences between populations clearly need explaining. However, the explanation is not r vs. K selection, as Afrosapiens and I showed yesterday, Rushton reversed r and K for the three races, making Africans r when they really would be K and making Mongoloids K, when in reality they would be r. Miller addresses other possibilities, such as testosterone, citing Ellis and Nyborg (1992) for racial differences in testosterone, however, he notes that the difference is only 3 percent which wouldn’t account for racial differences in behavior. (Also recall my critique of having no measure of central adiposity.) I’ve definitively shown that even if the races did differ largely in testosterone that it would not account for disease acquisition nor higher rates of crime.
from Anderson (1991: 53)
Above are the agents of selection, their defining characteristics, and independent and dependent variables. Notice how for r-selection the typical agents of selection are temperature extremes, drought, and natural disaster. For K-selection, the usual agents of selection are limited food supply, endemic infectious disease, and predation. Alpha-selection selects for competitive ability and is thus closer to K than r. Limited resources that can be collected or guarded such as shelter or food are agents of selection.
Clearly, as you can see, if this theory did apply to the human races, Mongoloids would be r and Africans would be K. Endemic disease is an agent of K-selection, not r. This is because endemic disease usually imposes density-dependent selection while cold winters impose density-independent selection. Furthermore, and perhaps most importantly, intelligence can be selected for due to agents of r- or K-selection! Rushton had no reason to add intelligence as a ‘K trait’, as Pianka did not even add it to his continuum. Further, Pianka gave no experimental rationale as to why he placed those traits on r or K (Graves, 2002: 135)! So due to this, Rushton’s claims are wrong and people should stop pushing his r/K theory.
Clearly, Rushton reversed r and K selection and wrongly applied them to the races of man. The three races he describes are NOT local populations, so any inferences made off of any so-called evolutionary environment are not warranted because he did not use the right variable (r or K) for Africans or Eurasians. However, some people may not want to admit that Rushton—and by extension, them—were wrong so they will attempt whatever kind of mental gymnastics possible to attempt to prove that Rushton was ‘right’. As I’ve already said, I don’t have a problem with Rushton’s data; I have a problem with his misapplication of r/K to humans—which I’ve made a strong case that he was wrong and didn’t know what he was talking about in terms of ecology and evolution.
Rushton’s theory was no longer viable 3 years after it was proposed when Judith Anderson got her hands on it, writing the paper Rushton’s Racial Comparisons: An Ecological Critique of Theory and Method. There is literally no saving his application of r and K to humans because he used it wrong! I don’t care what E.O. Wilson said, because he didn’t address Rushton’s application of r/K to human races. He only said if he noticed this variation between another species that no one would have batted an eye. That says absolutely nothing about Rushton’s erroneous application of r/K selection to the races of man.
I hope any HBDers reading this will stop and think for a moment before stating that Eurasians are K and Africans are r. This canard needs to stop in this sphere and I hope I set the wheels in motion to end it.
r/K Selection Theory: A Response to Rushton
3300 words
by RaceRealist and Afrosapiens
Introduction
Jean Phillipe Rushton (1943-2012) was a British-born Canadian psychologist known for his theories on genetically determined racial differences in cognition and behavior between Africans, Europeans, and East Asians. While marginal among experts, Rushton’s theories are still widely accepted amongst the proponents of eugenics and racialism. This article will focus on Rushton’s Differential K-theory which tries to apply the r/K selection model to racial differences in behavioral traits. To be fair, Rushton wasn’t the only one to use r/K selection as an explanation for psychological differences within humanity. For instance, some have associated the continuum with left-wing vs. right-wing ideologies. And although ecologists (the specialists of ecosystems) find applying r/K selection to humans inappropriate, the behavioral sciences have identified life-history patterns that roughly correspond to the colloquial fast vs. slow life differences in life history. For that reason, Rushton may have accidentally discussed variables and trends that are largely acknowledged by experts but his theory lies on a misunderstanding of core principles of the r/K model as well as using flawed (or non-existent) data.
Agents of selection
To begin, confusion about the modes of selection in an ecological context needs to be cleared up. There are classes of natural selection in ecological theory to be discussed: r-selection where the agent of selection acts in a density-independent way; K-selection where the agent of selection acts in a density-dependent way; and alpha selection which is selection for competitive ability (territoriality, aggression). Typical agents of K-selection include food shortage, endemic and infectious disease, and predation. Typical agents of r-selection temperature extremes, droughts, and natural disasters. Typical agents of alpha-selection are limited resources that can be collected or guarded, examples being shelter and food (Anderson, 1991).
As you can see, the third mode of selection in ecological theory is alpha-selection—which Rushton failed to bring up as a mode of selection to explain racial differences in behavior. He didn’t explain his reasoning as to why he did not include it—especially since alpha-selection is selection for competitive ability. One may wonder why Rushton never integrated alpha-selection into his theory—either he was ignorant to the reality of alpha-selection or it could occur in numerous ecosystems—whether temperate/cold or tropical. The non-application of alpha-selection throws his theory into disarray and should have one questioning Rushton’s use of ecological theory in application to human races.
The Misuse of r/K Theory
Ecoregions
Rushton’s model starts with the erroneous assumption that the populations he describes as humanities three main races qualify as ecological populations. When studying the adaptive strategies of organisms, ecologists only consider species within their evolutionary niche—that is, the location that the adaptation was hypothesized to have occurred. When it comes to humans, this can only be done by studying populations in their ancestral environments. For this reason, Africans, Europeans, Amerindians—any population that is not currently in their ancestral environments—are not suitable populations to study in an evolutionary ecological context. The three populations no longer inhabit the environment that the selection was hypothesized to have occurred, so any conclusions based on observing modern-day populations must be viewed with extreme caution (Anderson, 1991). Even in the Old World, constant gene flow between ecoregions, as well as alterations of the environment due to agriculture and then industrialization, make such a study virtually impossible as it would require ecologists to study only hunter-gatherers that have received no admixture from other areas.
Rushton’s next misuse of the theory is not discussing density-dependence and density-independence and how they relate to agents of selection and the r/K model. K-selection works in a density-dependent way while r-selection works in a density-independent way. Thusly, K-selection is expected to favor genotypes that persist at high densities (increasing K) whereas r-selection favors genotypes that increase more quickly at low densities (increasing r) (Anderson, 1991). Rushton also failed to speak about alpha-selection. Alpha-selection selection for competitive abilities and, like with K-selection, occurs at high population densities, but could also occur with low population densities. Alpha-selection, instead of favoring genotypes that increase at high densities “it favours genotypes that, owing to their negative effects on others, often reduce the growth rate and the maximum population size” (Anderson, 1991: 52).
The r/K continuum
The r/K continuum—proposed by Pianka (1970)—has been misused over the decades (Boyce, 1984) and that is where Rushton got the continuum and applied it to human racial differences. Different agents of r-selection produce different selection pressures, as does K-selection. However, where Rushton—and most who cite him—go wrong is completely disregarding the agents of selection, along with perhaps the most critical part, reversing r and K in application to human races (if it were applicable to human races, that is), which will be covered below.
Dobzhansky (1950: 221) notes that “Tropical environments provide more evolutionary challenges than do the environments of temperate and cold lands.” It is erroneously assumed that living in colder temperatures is somehow ‘harder’ than it is in Africa. People believe that since food is ‘readily available’, that it must be ‘harder’ to find food in the temperate/Arctic environments so, therefore, selection for high intelligence occurred in Eurasians while Africans have lower intelligence since it’s so ‘easy’ to live in Africa, as well as other tropical environments.
Africans, furthermore, have been in roughly the same environment since the OoA migration occurred (the Ice Age ‘ended’ about 11,700 ya, although we are still in an Ice Age since the planets caps still have ice), and so any assumptions about it being ‘harder’ for the ancestors of Eurasians to survive and pass on their genes is a baseless assumption. Tropical environments that provide more evolutionary challenges than temperate and cold lands whereas the migration that occurred Out of Africa introduced humans to novel environments. As described above, endemic disease is an agent of K-selection whereas migration to novel environments are agents of r-selection. Thus, cold temperatures would be an agent of r-selection, not K-selection as is commonly believed, whereas endemic disease would be an agent of K-selection.
Even though intelligence nor rule-following were not included on the list of variables that Pianka (1970) noted on his r/K continuum, Rushton chose to include the variables anyway, even though selection for intelligence and rule-following can occur due to agents of r- or K-selection (Anderson, 1991: 55; Graves, 2002: 134-144). Pianka (1970) never gave experimental rationalization as to why he placed the traits he did on his continuum (Graves, 2002: 135). This is one critical point that makes his theory unacceptable in application to racial differences in behavior. By Rushton’s own interpretation of the r/K model, Africans would be selected for intelligence while Eurasians would be selected to breed more since novel environments (i.e., colder temperatures) are agents of r-selection, not K. Using the terms r- and K-selection to describe the traits of an organism is inappropriate; Rushton’s application of r/K theory to the traits of the three races, while ignoring that r/K describes a mode of natural selection “indicates circular reasoning rather than support for Rushton’s hypothesis” (Anderson, 1991: 59).
Reznick et al, (2002: 1518) write: “The distinguishing feature of the r- and K-selection paradigm was the focus on density-dependent selection as the important agent of selection on organisms’ life histories. This paradigm was challenged as it became clear that other factors, such as age-specific mortality, could provide a more mechanistic causative link between an environment and an optimal life history (Wilbur et al. 1974, Stearns 1976, 1977). The r- and K-selection paradigm was replaced by new paradigm that focused on age-specific mortality (Stearns 1976, Charlesworth 1980).” r/K selection theory was dropped for the much stronger life-history approach (Graves, 2002)—which uses some elements of r and K, but otherwise those terms are no longer used since other factors are more important as agents of selection, rather than density dependence and independence as was commonly thought.
Simple models?
One of the main reasons that Rushton’s r/K continuum gets pushed is because it’s a ‘simple model’ that so ‘parsimoniously’ explains racial differences. (e.g., cold winters supposedly take more intelligence to survive in and supposedly are an agent of K-selection.) But ecological systems are never simple; there are numerous interactions between the physical environment and the biological system which interact in complex ways.
Rushton’s use of this ‘simple model’—the r/K continuum—and its application to human races are wrong because 1) the three races described are not local populations; 2) the r/K continuum as described by Pianka (1970) is a poor representation of multidimensional ecological processes; and 3) cold weather is normally an agent of r-selection while endemic disease in Africa—as described by Rushton—is an agent of K-selection. Simple models are not always best—especially for organisms as complex as humans—so attempting to reduce complex biological and environmental interactions into a linear continuum is mistaken (Boyce, 1984). The simpler the ecological model, the more complex ecological sophistication is needed to understand and apply said model. So, although Rushton prefers simple models, in this context it is not apt, as complex biological systems interacting with their environments should not be reduced to a ‘simple model’.
Applying r/K to human races
If the r/K model were applicable to humans, then Caucasoids and Mongoloids would be r-selected while Negroids would be K-selected. Endemic and infectious disease—stated by Rushton to be an r-selected pressure—is actually a K-selected pressure. So Negroids would have been subjected to K-selected pressures (disease) and r-selected pressures (drought). Conversely, for Mongoloids, they migrated into colder temperatures which act in a density-independent way—hence, cold winters (temperature extremes) are an agent of r-selection.
Pianka’s (1970) r/K continuum “confuses the underlying pattern of life history variation with density-dependence, a process potentially involved to explain the pattern” (Gaillard et al, 2016). Furthermore, one cannot make assumptions about an organism’s traits and the selection pressures that caused them without studying said organism in their natural habitat. This seems to be impossible since one would need to study non-admixed hunter-gatherer populations that have received no outside contact.
Gonadotropin levels, testosterone, prostate cancer and r/K theory
Numerous attempts have been made to validate Rushton’s r/K theory. One notable paper by Lynn (1990) attempts to integrate gonadotropin levels and testosterone into Rushton’s r/K continuum. Lynn cites studies showing that blacks have higher testosterone than whites who have higher testosterone than Asians. He then implicates higher levels of both testosterone and gonadotropin levels as the cause for the higher incidence of prostate cancer (PCa) in black Americans.
Lynn (1990) asserts that by having fewer children and showing more care, this is shifting to a K strategy. So, according to Lynn, the best way to achieve this would be a reduction in testosterone. However, there is a fault in his argument.
The study he uses for his assertion is Ross et al (1986). He states that the two groups were both “matched for possible environmental factors which might affect testosterone levels” (Lynn, 1990: 1204). However, this is an erroneous assumption. Ross et al (1986) did control for relevant variables, but made two huge errors. They did not control for waist circumference (WC), and, perhaps most importantly, did not assay the subjects in the morning as close to 8 am as possible.
Testosterone levels are highest at 8 am and lowest at 8 pm. When doing a study like this—especially one to identify a cause of a disease with a high mortality rate—all possible confounds must be identified then controlled for—especially confounds that fluctuate with age. The cohort was assayed between the hours of 10 am and 3 pm. Since testosterone assay time was all over the place for both groups, you cannot draw evolutionary hypotheses from the results. Further, the cohort was a sample of 50 black and white college students—a small sample and a non-representative population. So it’s safe to disregard this hypothesis, on the knowledge that blacks don’t have significantly higher testosterone levels than whites.
Another correlate that is used to show that blacks have higher levels of testosterone is the higher rate of crime they commit. However, physical aggression has a low correlation with testosterone (Archer, 1991; Book et al, 2001) and thusly cannot be the cause of crime. Furthermore, the .14 correlation that Book et al, 2001 found was found to be high. Archer, Graham-Kevan, and Lowe (2005) show that even the .14 correlation between testosterone and aggression is high in a reanalysis of Book et al (2001) since they included 15 studies that should have been omitted. The correlation was then reduced by almost half to .08.
Other theories have been developed to attempt to explain the racial crime gap which centers around testosterone (Ellis, 2017), however, the theory has large flaws which the author rightly notes. Exposure to high levels of testosterone in vitro supposedly causes a low 2d/4d ratio and blacks apparently have the lowest (Manning, 2008). Though, larger analyses show that Asians—mainly the Chinese—have a lower digit ratio compared to other ethnicities (Lippa, 2003; Manning et al, 2007).
Testosterone also does not cause PCa (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). The more likely culprit is diet. Less exposure to sunlight along with low vitamin D intake (Harris, 2006; Rostand, 2010) is a large cause for the prostate cancer discrepancy between the races since low vitamin D is linked to aggressive prostate cancer.
Even then, if there were, say, a 19 percent difference in testosterone between white and black Americans as asserted by Rushton and Lynn, it wouldn’t account for the higher rates of crime, nor higher acquisition and mortality from PCa. If their three claims are false (higher levels testosterone in African-Americans, larger penis size, and high levels of testosterone causing PCa), and they are, then this obliterates Rushton’s and Lynn’s theory.
Differential K Theory has, as noted above, has also been associated with a larger penis for black males in comparison to white males who have larger penises than Asian males (Lynn, 2012), which is not true, there is no reliable data and the data that does exist points to no evidence for the assertion. Lynn, (2012) also used data from a website with unverified and nonexistent sources. In a 2015 presentation, Edward Dutton cites studies showing that, again, Negroids have higher levels of testosterone than Caucasoids who have higher levels of testosterone than Mongoloids. Nevertheless, the claims by Dutton have been rebutted by Scott McGreal who showed that population differences in androgen levels don’t mean anything and that they fail to validate the claims of Lynn and Rushton on racial differences in penis size.
r/K selection theory as an attempt at reviving the scala naturae
Finally, to get to the heart of the matter, Rushton’s erroneous attempt to apply r/K selection theory to the human races is an attempt at reviving the scala naturae concept proposed by Aristotle (Hodos, 2009). The scala naturae organizes living and non-living organisms on a scale from ‘highest’ to ‘lowest’. However, these assumptions are erroneous and have no place in evolutionary biology (Gould, 1996). Rushton (1997: 293) attempted to apply r/K selection theory to human populations to try to revive the concept of the scala naturae, as can be clear by reading the very end of Race, Evolution, and Behavior.
This, of course, goes back to Rushton’s erroneous application of r/K selection theory to human races. He (and others) wrongly assert that Mongoloids are more K-selected than Africans who are more r-selected while Caucasians are in the middle—it also being asserted that K organisms, supposedly Mongoloids, “are the most K evolved” (Lynn, 2012). However, if r/K selection theory were applicable to humans, Mongoloids would be r and Africans would be K. Rushton further attempts to provide evidence for this ‘evolutionary progress’ by citing Dale Russel (1983; 1989) and his thought experiment troodon that he imagines would have eventually have gained human-like bipedalism and a large brain. Nevertheless, Rushton himself doesn’t say that it was only one dinosaur that would have supposedly had human-like intelligence and mobility, Reptile brains, however, lie outside of mammalian design (Hopson, 1977: 443; Gould, 1989: 318), and so, Russel’s theory is falsified.
This use of r/K selection theory as an attempt at bringing back the scala naturae may seem like an intuitive concept; some races/animals may seem more ‘advanced’ or ‘complex’ than others. However, since Rushton’s application of r/K selection theory is not correctly applied (nor does it apply to humans) and any of the claims that Rushton—or anyone else—makes while invoking the theory can be disregarded since he misused r and K selection.
In an attempt to “[restore] the concept of “progress” to its proper place in evolutionary biology,” Rushton (2004) proposed that g—the general factor of intelligence—sits atop a matrix of correlated traits that he proposes to show why evolution is synonymous with ‘progress’, including how and why K evolved organisms are so-called ‘more highly K evolved’—which is a sly attempt to revive the concept of scala naturae. Rushton’s (2004) paper is largely copy and pasted from his 1997 afterword in Race, Evolution, and Behavior—especially the part about ‘progress in evolution’ (which has been addressed in depth).
As can be seen, Ruston attempted to revive the scala naturae by giving it a new name, along with the misuse of ecological theory to make it seem like evolution is synonymous with progress and that K organisms are ‘more evolved’, makes no sense in the context of how ecological theory is (or was) applied to organisms. Rushton’s theory is correct, if and only if he applied r and K correctly to human races. Rushton did not apply r/K selection theory correctly to human races, so Rushton’s claims and any that follow from them are, on their face, immediately wrong. The claims by Rushton et al showing evolution to be ‘progressive’ have been shown to be demonstrably false since evolution is local change, not ‘progress’ (Gould, 1989; 1996).
Conclusion
Rushton’s r/K selection theory has enamored many since he proposed it in 1985. He was relentlessly attacked in the media for his proposals about black penis size, testosterone, brain size, sexual frequency, etc. However, the explanation for said racial differences in behavior—his r/K selection theory—has been summarily rebutted for misapplying ecological theory and not understanding evolution (Anderson, 1991; Graves, 2002). Even ignoring his racial comparisons, his application of the theory would still be unacceptable as he didn’t recognize agents of selection nor alpha selection.
Rushton is wrong because
(i) he misapplied r/K selection in application to human races (Africans would be K, Mongoloids would be r; rule-following and intelligence can be selected for in either environment/with any of the agents of r- or K-selection),
(ii) he arbitrarily designated Africans as r and Mongoloids as K due to current demographic trends (the true application of r and K is described above, which Rushton showed no understanding of),
(iii) the races do not differ in levels of testosterone nor penis size,
(iv) testosterone does not cause prostate cancer nor does it cause crime, so even if there was a large difference between blacks and whites, it would not explain higher rates of PCa in blacks, nor would it explain higher rates of crime,
(v) the scala naturae is a long-dead concept no longer in use by evolutionary biologists, along with its cousin ‘evolutionary progress’, while r/K selection is the attempt at reviving both,
(vi) human races are not local populations; since human races are not local populations then his application of r/K selection to humans is erroneous.
Rushton was informed numerous times he wrongly applied ecological theory to human populations. Yes, E.O. Wilson did say that if Rushton had noticed variation in any other animal that ‘no one would have batted an eye’, however, that does not say a word about Rushton’s incorrect application of r/K selection to human races. No race of humans is more ‘highly evolved’ than another.
Anyone who uses Rushton’s theory as an explanation for observed data is using incorrect/misapplied theory meaning that, therefore, by proxy, their theory is wrong. Rushton’s r/K theory is wrong, and people need to stop invoking it as an explanation for racial differences in behavior, politics, religion, and any other variable they can think of. If Rushton’s application of the theory is wrong, then it logically follows that anything based off of his theory is wrong as well.
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.
Why Testosterone Does Not Cause Crime
1900 words
Edit: (The correlation between aggression and testosterone isn’t .14 as Book et al (2001) state; the true correlation is .08 (Archer, Graham-Kevan and Davies, 2005) So it’s even lower than I thought. This is one of the many reasons why testosterone does not cause crime. It’s just feminist bullshit and fear mongering from people who do not understand the hormone and what it does in the body. The misconceptions come from Rushton’s r/K selection bullshit which has been summarily refuted.)
Recently, I’ve written at length on racial differences in testosterone and how the correlation between testosterone and physical aggression is .14. Pitifully low to account for the cause of crime and any overall differences in racial crime (that will be touched on at length in the future). Tonight I will show, yet again, why testosterone does not cause crime by looking at what times most crimes are committed by both adults and children under the age of 18. This will definitively put the ‘testosterone causes crime’ myth to bed for good.
Before I get into the time of day that most crimes are committed, I must talk about the production of testosterone in the body. There are no ‘genes for’ testosterone (although men who had three certain alleles had a 6.5 fold higher risk of having low testosterone; Ohlsson et al, 2011, I am unaware of there being a variation by race; over 10,000 Caucasian men were studied). There is, however, an indirect control of testosterone synthesis by DNA. DNA regulates the production of testosterone by coding for enzymes that convert cholesterol to testosterone (testosterone is a cholesterol-based hormone).
There are five simple steps to the production of testosterone: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone). That’s how testosterone is produced in the body. It is indirectly controlled by DNA.
Above is a graph from the Office of Juvenile Justice and Delinquency Prevention which shows the time of day that most crimes are committed. Notice how crime goes up as the time of day goes on and since kids are at school, they’re more likely to fight. This then peaks at 3 pm when kids are getting out of school.
Now look at rates of crime for adults. At its peak of 10 pm, it’s vastly lower than that of people under the age of 18, which is important to keep in mind. You can see how at 8 am that rates of crime are low for adults and high for kids, right when they would be entering school so there would be a lot of other kids around and the chance for violence goes up. Keep the times of 8 am (kids when they enter school), 12 pm (when most kids go on lunch) and 3 pm (when most kids get out of school) along with the hours of 12 pm to 8 pm for adults (when 74 percent of crimes are committed by adults).
- In general, the number of violent crimes committed by adults increases hourly from 6 a.m. through the afternoon and evening hours, peaks at 10 p.m., and then drops to a low point at 6 a.m. In contrast, violent crimes by juveniles peak in the afternoon between 3 p.m. and 4 p.m., the hour at the end of the school day.
- Nearly one-third (29%) of all violent crime committed by juvenile offenders occurs between 3 p.m. and 7 p.m. In comparison, 26% of all violent committed by adult offenders occurs between 8 p.m. and 12 p.m.
So since testosterone varies by day and levels are highest at 8 am and lowest at 8 pm (Brambilla et al, 2009; however testing men aged 45 years of age and older is fine before 2 pm due to a blunted circadian rhythm; Long, Nguyen, and Stevermer, 2015), then how could testosterone account for why men commit most of their crimes at night and why the crime that children commit spikes when they go to school, go to lunch and get out of school? The answer is that it doesn’t because testosterone does not cause crime. What testosterone does cause, however, are feelings of confidence and dominance, which does not—surprisingly—lead to increased aggression and assault on others (Booth et al, 2006).
What testosterone does cause, however, is social dominance and success, not physical aggression and maladjustment (Shcaal et al, 1996). The effects of environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Furthermore, aggressive behavior is first noticed in infancy and reaches its peak before school age (Tremblay et al, 2004; Cote et al, 2006). Though testosterone does seem to have an effect on aggression in preschool boys, however genetic and environmental causality has not been established (Sanchez-Martin et al, 2000).
Nevertheless, the meta-analyses I cited last week show that testosterone has an extremely low correlation of .14, so other factors must be at play. However, Sanchez-Martin et al (2000:778-779) also note that “Tremblay et al (1998) suggested that associations between testosterone titer and physical aggression are likely to be observed in contexts where such attack leads to social dominance. This may be true of the preschool boys in the present study. The data generated in the present study generally support Scerbo and Kolko (1994), who studied older children (7 to 14 years of age). They found a significant relationship between testosterone levels and aggression (as assessed by clinical staff).”
It’s interesting to note that in the case of Scerbo and Kolko (1994) that after controlling for age and size, testosterone correlated with aggression when rated by staff but not parents or teachers. ‘Staff’ refers to clinic staff at a facility where the children were assessed for hyperactivity disorders. Of course, the staff would rate higher levels of aggression compared to parents of teachers—people who are around the children every day—since they would want a higher chance for diagnosis for certain drugs to ‘cure’ the hyperactivity, but I digress. Testosterone does not induce aggression in children, but it does induce social dominance and confidence which does not lead to aggression (Rowe et al, 2004; Booth et al, 2006).
There was also little difference in testosterone between socially dominant prisoners and aggressive prisoners (Ehrenkraz, Bliss, and Sheard, 1974). Furthermore, the testosterone increase leading to pubertal development in boys is not associated with increased aggression (Tremblay et al, 1998; Booth et al, 2006: 171). Indeed, increased body size is a marker for physical aggression in children, and I doubt these children have high muscle mass so, I assume, they have high levels of body fat and thusly lower levels of testosterone than they would have if they were leaner. Yet another strike against the ‘testosterone causes crime/physical aggression’ hypothesis.
Indeed, this has some implications for the honor culture hypothesis of why low-income blacks have higher levels of testosterone than similarly aged blacks with some college (Mazur, 2016). The patterns for crime as shown by the OOJDP shows that crime rises as the day progresses from the morning until its peak at 3 pm for children and then sharply declines while for adults it peaks at 10 pm.
Testosterone does increase when a challenge is issued; when one man feels his reputation is threatened, the propensity for violence is increased, but this was most notably seen in Southern men (Cohen et al, 1996). So the same would be said for this ‘culture of honor’ found in low-income black neighborhoods, the so-called ‘code of the street’ as stated by Anderson (1994: 88): “Moreover, if a person is assaulted, it is important, not only in the eyes of his opponent but in the eyes of his “running buddies,” for him to avenge himself. Otherwise, he risks being “tried” (challenged) or “moved on” by any number of others. To maintain his honor, he must show he is not someone to be “messed with” or “dissed.””
This culture of honor is found all over the world, including Brazil where homicide can be explained by the need to maintain honor and can be understood by taking into account cultural factors; biological, psychological and socioeconomic factors do not explain murder in Northeast Brazil as well as honor and culture (de Souza et al, 2015). People in honor cultures also have a higher chance of self-harm (Osterman and Brown, 2011) as well as a higher chance of committing violence in school (Brown, Osterman, and Barnes, 2009).
Testosterone does not cause crime; it does not cause aggression. Increases in testosterone before, during and after events are a physiologic process to prime the body for competition. As cited above, dominant behavior does not necessarily lead to violence in most cases, which may be surprising for some. Indeed, honor and culture may explain a nice amount of the homicide and violence rate in the South. Since testosterone is highest at 8 am and lowest at 8 pm and the rates of crime committed by adults and children are vastly different than the diurnal variance in the day, then testosterone does not cause crime and its increase is not associated with crime, but social dominance and confidence which does not lead to crime.
Hopefully—if anyone still believes testosterone to be the boogeyman its made out to be—I’ve put those misconceptions to rest. Racial differences in testosterone cannot be the cause of racial differences in crime—because there is either no statistical difference in testosterone between the races or the difference is non-existent. Testosterone is clearly a beneficial hormone—as I have extensively documented. Misunderstandings of the hormone are abound—especially in the HBD sphere—only due to literally a few paragraphs in a book (Rushton, 1997) and one study that showed blacks have higher testosterone than whites which was the cause of their higher rates of prostate cancer (Ross et al, 1986). The study is hard to find so I had to buy access to it. I will cover this in the future, but I discovered that they assayed the subjects when it was convenient for them—between the hours of 10 am and 3 pm—which is unacceptable. You cannot gauge racial differences in testosterone from a small study (n=50) and a non-representative sample (college students). For these reasons, the study should be thrown in the trash—especially when formulating evolutionary hypotheses.
Testosterone is one of the most important hormones for vital functioning. By knowing how it is processed in the body and that there are no ‘genes for’ testosterone (‘low testosterone genes’ notwithstanding) along with how testosterone has a low relationship with physical aggression one should not be scared of having high levels, on the contrary, one should be scared of having low levels. I have once again proven my case that testosterone is not related to violence in showing the diurnal variation in testosterone levels in adults, as well as the time of day that crimes are committed by both adults and children. High testosterone means high confidence and high dominance—and those two traits have a lot to do with masculinity—which do not lead to violence.
I know why testosterone does not cause crime—because I have an understanding of the hormone, how its produced in the body and what its effects on the body are. The most important thing to note here, is that even if blacks had 15 percent higher testosterone than whites, it still wouldn’t explain higher rates of crime or disease such as prostate cancer. So those who try so hard to prove that blacks have higher levels of the hormone do so in vain, because even if they did it wouldn’t mean anything for any theories they may have. The myth of testosterone causing aggression and crime need to be put to bed for good.
NotPoliticallyCorrect 