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Getting Omega 3s in the public diet

by Scott Jameson

An earlier post established that Omega 3 fatty acids are an important nutrient of which hardly anybody is getting enough, and that this deficiency is making us Westerners a bit dumber and a bit crazier on the whole. Description sometimes obligates prescription, so this post is where I spitball about possible solutions, and welcome you to join me in the comments.

I’m reminded of the gubbermint mandating the lacing of our salt with sorely needed iodine, or the enrichment of white flour with nutrients lost in the removal of the bran and germ as well as the bleaching of the endosperm.

For yourself and your family, fish oil pills are fine- kelp oil if you’re one of those people. But we need solutions that work for nearly everybody, and the brilliance of the examples I listed above is that everybody eats that stuff (bread and salt) and now it’s laced with nutrients they’ve been needing. So we could produce N3s at low cost and legally mandate that certain foods contain them. Chia is a promising source: it’s cheap, it’s loaded with N3s, and it doesn’t taste fishy. Flax also works, but it’s loaded with phytoestrogens. Tons of seeds have those, I think Chia as well, but I’ve been told (incorrectly?) that flax is a particularly bad offender. Anyway, how do we load Chia or a similar seed into people’s diets?

Omega 3 eggs are one way to go. Chickens metabolize plant ALA (such as from chia or flax) into DHA and store both in their eggs. Just as we made use of the auroch and tarpan’s efforts to have a brain, we can hijack the chicken’s futile attempts to provide brain-material for her nonexistent offspring, using her eggs as a vehicle to get N3s into ourselves. It’s as simple as a mandate that a certain percentage of all chicken feed must be N3 rich seeds and/or insects.

Another obvious place to look is the plant oils that go into our food. Check out the table on the Wikipedia page for ALA: soybean and rapeseed oils have a pathetic showing for ALA content, and they’re put in absolutely everything. The State mandates that all gas will be a bit ethanol: why not all soybean and canola be 10, 20% Chia or some comparably high ALA crop?

It’s worth pointing out that you can genetically modify ALA rich vegetable oil to be on a quality closer to par with fish oil, having some of the ALA converted into the more useful EPA. Forget any concerns about GMOs you may have because the oils I’m talking about lacing with GMOs are already themselves GMOs.

We also must mandate that all infant formula be laced with N3s: EPA and DHA in particular, and tested for stuff like mercury if it comes from fish. You probably know at least one person who is autistic because they were bottlefed.

Comment your potential solutions below. I want to hear them. Double points for anyone playing the game on hard mode: free market solutions (libertarians) or animal-free solutions (vegans). If you try both, you’re a masochist and you need help.

The West’s Testosterone Decline

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The tone of this article may be slightly different than the rest. I hate when people make idiotic, rash judgments on things that they really do not understand.

People are dumb. There is nothing wrong with that, but when those dumb people discover some science, they then misinterpret the article and twist and turn it to fit a political agenda, all the while having absolutely no idea at all about the actual study nor knowing anything about the hormone testosterone! Due to this, you get some cringey articles from the alt-right because they are too ignorant to actually read something without their ideological blinders on.

The study I will be reviewing was on testosterone, which established new levels for nonobese American and European men. The problem is that the new levels are lower than the previous levels; uneducated and biased morons think that means that they (the government) are trying to feminize men and thus they—on their own—lowered testosterone levels themselves. …this is dumb. Like, really really dumb.

Over 9,000 nonobese American and European men were assayed for a harmonized normal range in males; Travison et al, (2017) used the results from a local assay which was sent to the CDC where “testosterone concentrations were measured using a higher order liquid chromatography tandem mass spectrometry method.” Then, Travison et al (2017) used the results from both tests (the local sample and CDC sample) to create a ‘harmonized reference range’ which were then used to generate the age-specific reference ranges across the whole cohort. Using this method, they discovered that the range for testosterone for nonobese males aged 19-39 was between 264-916 ng/ml.

Now, people who don’t understand why this study was done (to see the range of testosterone in men to see the actual range) would say ‘aha! They are trying to lower testosterone and feminize men!”, like the retards Chateau Heartiste and ‘Zeiger‘ from the Daily Stormer. I won’t cover the article from Heartiste (because there’s nothing of substance there to talk about, just some inane drivel), so I’ll cover ‘Zeiger’s’ main points.

Zeiger writes:

The feds have started a process to lower the official “standard” levels of testosterone in men, presumably in an effort to solve the grave “toxic masculinity” problem we’ve got going on here in America.

No. No one has ‘started a process to lower’ the levels of testosterone in America. You do not understand science, so why the hell are you talking about it?

The problem here is that it’s basically a hoax study.

….is this guy a retard? How is this a ‘hoax study’?

The blood samples were obtained not from healthy, athletic males, but from males who were already the subjects of other medical studies. In other words, they were largely composed of ordinary people who ate crappy standard diets, lived sedentary lifestyles, drank water loaded with chemicals, and who are exposed to a whole bunch of estrogen-mimicking chemicals.

….you mean the average man in America? You think they should control for weight, when the average man in America is obese/overweight? Why control for all of those variables when you’re attempting to see what the range is in a large cohort to get a better idea of what the actual range is in men so that they could better diagnose low testosterone and any other maladies involved with it? This study was done to establish the range for the average American and European male, not one who is athletic, low body fat, etc. You’d need to actually understand why the study was undertaken to get that, though.

Now, this new, much lower range of what is considered “normal” testosterone levels is becoming the standard pushed by the CDC (Center for Disease Control) and applied by the various private testing organizations.

You don’t even understand why this ‘new, much lower range’ is considered ‘normal’ and why it’s ‘becoming the standard pushed by the CDC’ and ‘applied by the various private testing corporations’. Because that is the new range for nonobese American and European males aged 19-39!

The old reference range comes from the Framingham Heart Study in which men aged 19-40 were assayed (Bhalin et al, 2011; assays were done in the morning after an overnight fast so I have no problem with this). ‘Zeiger’ writes:

The old standard was based on actual healthy males. Now they’ve dropped the standard to “non-obese.” As a rule, the fatter someone is, the lower their testosterone. This means that the broadening of the criteria for “healthy” to include men who are pretty fat, but short of “obese” will certainly lead to a lower average testosterone level.

Did you know that in the old reference sample (Bhalin et al, 2011), the average BMI of the whole cohort aged 19-39 was 25.2 (average age 32.7)? For men with an average age of 33.3, they had a BMI of 27.4 and men aged 40 had BMI 28 (see table 1; Bhalin et al, 2011). I don’t take BMI as a predictor of health (indeed men with a 27 BMI had a lower risk of mortality than men in other BMI categories), but it is a predictor of testosterone levels. ‘Lean males’ are not between BMI 25 and 28; unless they were testing some IFBB pros, which I know they did not. So they values were similar. He wouldn’t know that though because he’s clueless to the literature.

For one, it makes it a lot harder to get testosterone hormones prescribed to you by a doctor, since your T levels need to be absolutely rock bottom in order to be considered “deficient.”

No, retard. If you’re feeling lethargic, have low energy, low sex drive, etc, then you will be assayed and compared against the new harmonized values. If you’re teetering on the low-end of the normal range variation, then you will get some TRT (testosterone replacement therapy). You’ve never worked with people with low testosterone, so shut the fuck up.

In addition, if this process continues, you could start seeing men with healthy testosterone begin to be seen as “pathological” because their levels are “too high” compared with the new standard. So power-lifters who watch their diets could start being prescribed drugs to lower their T levels.

This is dumb. If I get prescribed drugs to lower my testosterone levels, I’ll be sure to let my readers know (I compete and watch my diet) and my levels are above average for my age.

All of this is based on an obviously flawed methodology.

No, it isn’t. You don’t understand the methodology because you don’t understand science and you don’t understand testosterone.

It’s a transparent push to feminize men and normalize being a low-T faggot.

Nice appeal to emotion at the end there. You don’t understand science so you don’t understand the methodology so this lets you use the new study to support your biases. I strongly recommend that you do some heavy reading into this because you don’t know shit about this matter.

Ten years ago, Travison et al (2007) observed that there was a substantial “and as yet unrecognized, age-independent population-level decrease in T in American men, potentially attributable to birth cohort differences or to health or environmental effects not captured in observed data.” Testosterone levels have declined in America, independent of chronological aging. (See Nyante et al, 2007 for contrary view, they state that there is no decrease in testosterone, also see table 4 which shows that blacks had higher levels than whites, with whites having 5.28 ng/ml and blacks having 5.9 ng/ml for an 11 percent difference. Using previous NHANES data, Nyante et al, 2007 showed that the levels in whites were 5.38 while in blacks it was 5.28 for a .05 percent difference. Nevertheless, this is more evidence for the honor culture hypothesis (Mazur, 2016) which shows why low-income blacks have higher levels of testosterone than better-educated blacks of the same age range.)

Further, a substantial proportion of the intercohort variation was due to assay differences, i.e., saliva, blood, etc (Travison et al, 2017). Further, Travison et al (2017) tested men with BMIs less than 30, the same as Bhalin et al (2011) which was the old reference. But people need to read the actual studies cited to get the truth, and not just speak from emotion (ironic…) about something that they literally have no clue about. Also, read the LabCorp statement on this matter.

Yes, we do have a testosterone decline in the West, and no, it is not due to any nefarious plot to lower testosterone levels or feminize men; if people knew how to read scientific papers then I wouldn’t have to write this article in the tone that I did, but alas you can’t have everything you want in life.

I did write in the past that the testosterone decline in the West is the cause of our fertility problems (this article compliments the linked article), and to higher fertility rates in the West, testosterone levels must also be raised. People who have no idea about how and why studies are carried out shouldn’t talk about them. People who do not understand what they are talking about should not talk about them. Recall that I blasted Heartiste’s Big Food Shilling a few months back, and I also did the same last month rebutting the article that ‘Man ‘originated’ in Europe‘. These people clearly have no understanding of science and quickly latch on to anything that will affirm their worldviews without having the actual knowledge to assess what they are talking about.

I hope that Heartiste and Zeiger actually educate themselves on the matters they write about, because this is just embarrassing and shows no understanding of science or of the hormone testosterone. There is a lot of bullshit floating around out there, mostly from uneducated morons who don’t know a thing about what they are writing about, it just conforms to their worldview and they will thusly write about it all the while being ignorant to the reality of the matter. I wish ideologues would stop writing about things that are not educated in. Alas, I don’t think that will happen anytime soon because people have an agenda to push, science be damned (which is ironic because these same people get on the Left for doing the same. . .).

This is a serious problem, as I have noted before, so to change this, change diet to whole foods, get more exercise, stop drinking from plastic water bottles; you need to shape your own environment in order to have higher testosterone levels; I have extensively documented that testosterone increases or decreases based on a ton of environmental factors. That we are experiencing a large decline in testosterone here in the West shows that we are not as active, we are eating shitty food, and men are not being as dominant as they were in the past.

So yes, in two days time the testosterone reference range for men in America and Europe will be between 264 to 916 ng/ml, and no it is not due to them, this is the actual level in nonobese men. People need to stop the fear mongering bullshit and people need to stop talking about shit that they literally have no understanding of.

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 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 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 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 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 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 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 ReligionI 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):

tree-of-life-i-think

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?

f1-large

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.

blf4lad

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

1300 words

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.

agentsofselection

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

terra_map

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 habitatThis 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, 2006Rostand, 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 assertionLynn, (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.