A lot of buzz is going around about a recent study that purports that the human-chimp split occurred in the Mediterranean—not Africa as is commonly thought (Fuss et al, 2017). This claim, however, is based off of a few teeth and jawbone with one tooth in it of a supposed hominin named Graecopithecus freybergi. A lot of wild conclusions are being jumped to about this study and these claims need to be put to rest.
On altright.com, an article was written titled Recent Discovery Shows Humans Came From Europe. The article claims that the OoA hypothesis has been “debunked by hard evidence”. Though to disprove the OoA hypothesis, a lot more will be needed than a few teeth and a jawbone. This is similar to another article on the Dailystormer, New Discovery Shows Pre-Human Hominids in Europe Before Africa, which, again, makes more wild claims.
white people are just Negroes who have lighter skin because during the Ice Age, they were wearing more clothing and thus needed lighter skin to absorb more Vitamin D. needed lighter skin to absorb more Vitamin D.
So, the reasoning behind the theory is that we are all very close together, genetically, so there isn’t really any problem with mixing us all together, and pretty much, race is a social construct.
Race is a social construct of a biological reality. OoA is based on solid evidence. Just because ‘we are close together, genetically’, as egalitarians would say, doesn’t mean we should destroy the human diversity we currently have.
Much damage to evolutionary research was done by the Jew Stephen Jay Gould3, who argued in favor of the idea of rapid evolution
This is bullshit. Stephen J. Gould and Niles Eldredge proposed Puncuated Equilibria (PE). PE occurs when a species becomes as ‘adapted’ to its environment as possible and then remains in stasis. Species speciate when the environment changes (climate), or, say an earthquake occurs and splits a population of 100 peacocks in half. Fifty of the peacocks will change due to drift, natural and sexual selection. But if the environmental conditions stay the same then species cannot change.
The proposal was that after a long time in stasis that quick speciation would occur—that would be in response to the environmental change that drives the evolution of species.
He also made much damage to the field of sociobiology, literally arguing that evolution has no role in human behavior
He argued that many functions of the ‘higher’ functions of the human brain evolved for other reasons and were coopted for other reasons, which is why he coined the term ‘exaptation’.
And the debate about spandrels—which is a phenotypic trait that is a byproduct of the evolution of another trait and not due to adaptive selection. There is a tendency to assume that all—or most—traits are due to adaptive selection. This is not true.
With this new discovery of prehumans in Europe, they are dating the European fossil as older, but we would basically end up with the same conclusions with regards to rapid evolution and thus “race not existing.” So I don’t see anything for racists to get all excited about, with the way it is currently being presented.
Punctuated Equilibria is a lot more nuanced than you’re making it out to be. It’s looking at the whole entire fossil record and noticing that for most of a species’ evolutionary history that it remains in stasis and that evolution then occurs in quick bursts.
This theory postulates that Africans, Asians, Europeans and Aboriginal Australians all evolved completely separately from different hominidae
This is not tenable. This isn’t even how it works. Neanderthals and Homo sapiens are derived from Heidelbergensis.
Erectus is in our family tree beginning 2 mya. He is an origin of AMH and us as well. However, what you’re talking about needs to be proven with genetic testing.
Africans of course are more violent (and larger) not so much because of IQ, but because of higher levels of testosterone, but no one has explained what caused this.
Claims about substantially higher levels of testosterone in blacks are not true.
Then, of course, the Asians who moved north developed higher IQs and lighter skin because of climate-related reasons.
East Asians needed bigger brains for expertise capcity; not IQ. Light skin did evolve for climatic reasons; not sexual selection as some claim.
People need to 1) learn the basics of evolutionary theory; 2) learn the basics of the OoA hypothesis; 3) stop jumping to conclusions based on little evidence and large conjecture; 4) never trust anything at face value; always do more research into something and put all ideas under intense scrutiny, even ones you strongly believe. That way, articles like the ones above don’t get writtent with complete disregard for modern-day evolutionary theory.
John Hawks, paleoanthropologist writes:
Here’s what I think: Paleoanthropology must move past the point where a mandibular fragment is accepted as sufficient evidence.
He also states that this may be a case of apes evolving “supposed hominin characters” evolved in other apes in the Miocene, citing a study by him and his colleagues showing that features that supposedly link Ardipethicus and Sahelanthropus are also found in other Miocene fossils (Wolpoff et al, 2006). Graecopithecus shares few features with Australopithecus, so Hawks says that we should begin to think about the possibility of Graecopithecus being “part of a diversity of apes that are continuous across parts of Africa and Europe.”
Finally, there is not enough evidence to back the claim that humans originated in Europe. Vertebrate paleontologist and paleobiologist Dr. Julian Benoit states that the author’s claim of the fourth molar root in Graecopithecus being similar to hominins is unfounded because “This is not a character that is conventionally used in palaeoanthropology, especially because not all hominins have similar tooth roots. This character is rather variable – and the authors go on to acknowledge this – so it’s unreliable for classification.” Further, humans aren’t the only apes with small canines and the jawbone and teeth aren’t too well preserved.
We have found thousands of hominin fossils in Africa. We know that the LCA between apes and humans existed between 6-12 mya in Africa. Graecopithecus was probably an ape species not related to humans. Even if the claim were true, it wouldn’t completely disprove the hypothesis that Man originated in Africa. Extraordinary claims require extraordinary evidence; this is not it.
People need to stop letting their biases and political beliefs get in the way of rational thought. Never take claims at face value; always look at things objectively. There needs to be a lot more evidence for the claim that Man originated in Europe; and even then, there is a mountain of evidence that anatomically modern humans arose in Africa.
In order to prove that Graecopithecus was a hominin and not another species of non-human ape, more fossils need to be found and a phylogenetic analysis needs to be done on the jawbone, comparing it with other species to see the closest relationship on the phylogeny. I assume when this is done it will show that it is related to non-human apes; not humans. Nevertheless, extraordinary claims require extraordinary evidence and people need to stop believing and agreeing with everything that ‘agrees’ with their worldviews as a fact without taking an objective look at the data. Never trust claims and always attempt to verify that what someone claims has a basis in reality. Only ask yourself what the facts are and what they show—without bias.
Would dinosaurs have reached human-like intellect had the K-T extinction (an asteroid impact near the Yucatan peninsula) not occurred? One researcher believes so, and he believes that a dinosaur called the troodon would have evolved into a bipedal, human-like being. This is, of course, the old progressive evolution shtick. This assumes that a man-like being is an inevitability, and that sentience is a forgone conclusion.
This belief largely comes from Rushton’s citation of one Dale Russel, the discoverer of the dinosaur the troodon:
Paleontologist Dale Russell (1983,1989) quantified increasing neurological complexity through 700 million years of Earth history in invertebrates and vertebrates alike. The trend was increasing encephalization among the dinosaurs that existed for 140 million years and vanished 65 million years ago. Russell (1989) proposed that if they had not gone extinct, dinosaurs would have progressed to a large-brained, bipedal descendent. For living mammals he set the mean encephalization, the ratio of brain size to body size, at 1.00, and calculated that 65 million years ago it was only about 0.30. Encephalization quotients for living molluscs vary between 0.043 and 0.31, and for living insects between 0.008 and 0.045 but in these groups the less encephalized living species resemble forms that appeared relatively early in the geologic record, and the more encephalized species resemble those that appeared later. (Rushton, 1997: 294)
This argument is simple to rebut. What is being described is complexity. The simplest possible organism are bacteria, which reside at the left wall of complexity. The left wall “induces right-skewed distributions”, whereas the right wall induces “left-skewed distributions” (Gould, 1996: 55). Knowing this, biological complexity is a forgone conclusion, which exists at the extreme end of the right tail curve. I’ve covered this in my article Complexity, Walls, 0.400 Hitting and Evolutionary “Progress”
Talking about what Troodons may have looked like (highly, highly, doubtful. The anthropometric bias was pretty strong) is a waste of time. I’ve stated this a few times and I’ll state it yet again: without our primate body plan, our brains are pretty much useless. Our body needs our brain; our brain needs our body. Troodons would have stayed quadrupedal; they wouldn’t have gone bipedal.
He claims that some dinosaurs would have eventually reached an EQ of humans—specifically the troodon. They had EQs about 6 times higher than the average dinosaur, had fingers to grasp, had small teeth, ate meat, and appeared to be social. Dale Russel claims that had the K-T extinction not occurred, the troodon would look similar to us with a brain size around 1100 cc (the size of erectus before he went extinct). This is what he believes the dinosauroid troodon would look like had they not died out 65 mya:
When interviewed about the dinosauroid he imagined, he stated:
The “dinosauroid” was a thought experiment, based on an observable, general trend toward larger relative brain size in terrestrial vertebrates through geologic time, and the energetic efficiency of an upright posture in slow-moving, bipedal animals. It seems to me that such speculation remains acceptable, particularly if directed toward non-anthropoid anatomical configurations. However, I very nearly decided not to publish the exercise because of the damaging effects it might have had on the credibility of my work in general. Most people remained polite, although there were hostile reactions from those with “ultra-quantitative” and “ultra-intuitive” world views.
Why does it look so human? Why does he assume that the ‘ideal body plan’ is what we have? It seems to be extremely biased towards a humanoid morphology, just as other reconstructions are biased towards what we think about certain areas today and how the people may have looked in our evolutionary past. Anthropocentric bias permeates deep in evolutionary thinking, this is one such example.
Thinking of this thought experiment of a possible ‘bipedal dinosauroid’ we need to be realistic in terms of thinking of its anatomy and morphology.
Let’s accept Russel’s contention as true; that troodontids or other ‘highly encephalized species’ reached a human EQ, as he notes, of 9.4, with troodontids at .34 (the highest), archaeopteryx at .32, triconodonts (early extinct mammal of the cretaceous) with a .29 EQ, and the diademodon with an EQ of .20 (Russel, 1983). Russel found that the troodontids had EQs 6 times higher than the average dinosaur, so from here, he extrapolated that the troodon would have had a brain our size. However, Stephen Jay Gould argued the opposite in Wonderful Life writing:
If mammals had arisen late and helped to drive dinosaurs to their doom, then we could legitimately propose a scenario of expected progress. But dinosaurs remained dominant and probably became extinct only as a quirky result of the most unpredictable of all events—a mass dying triggered by extraterrestrial impact. If dinosaurs had not died in this event, they would probably still dominate the large-bodied vertebrates, as they had for so long with such conspicuous success, and mammals would still be small creatures in the interstices of their world. This situation prevailed for one hundred million years, why not sixty million more? Since dinosaurs were not moving towards markedly larger brains, and since such a prospect may lay outside the capability of reptilian design (Jerison, 1973; Hopson, 1977), we must assume that consciousness would not have evolved on our planet if a cosmic catastrophe had not claimed the dinosaurs as victims. In an entirely literal sense, we owe our existence, as large reasoning mammals, to our lucky stars. (Gould, 1989: 318)
If a large brain was probably outside of reptilian design, then a dinosaur—or a descendant (troodon included)—would have never reached human-like intelligence. However, some people may say that dinosaur descendants may have evolved brains our size since birds have brains that lie outside of reptilian design (supposedly).
However, one of the most famous fossils ever found, archaeopteryx, was within reptilian design, having feathers and along with wings which would have been used for gliding (whether or not they flew is debated). Birds descend from therapods. Anchiornis, and other older species are thought to be the first birds. Most of birds’ traits, such as bipedal posture, hinged ankles, hollow bones and S-shaped neck in birds are derived features from their ancestors.
If we didn’t exist, then if any organism were to come close to our intelligence, I would bet that some corvids would, seeing as they have a higher packing density and interconnections compared to the “layered mammalian brain” (Olkowicz et al, 2016). Nick Lane, biochemist and author of the book The Vital Question: Evolution and the Origins of Complex Life believes a type of intelligent ocotopi may have evolved, writing:
Wind back the clock to Cambrian times, half a billion years ago, when mammals first exploded into the fossil record, and let it play forwards again. Would that parallel be similar to our own? Perhaps the hills would be crawling with giant terrestrial octopuses. (Lane, 2015: 21)
We exist because we are primates. Our brains are scaled-up primate brains (Herculano-Houzel, 2009). Our primate morphology—along with our diet, sociality, and culture—is also why we came to take over the world. Our body plan—which, as far as we know, only evolved once—is why we have the ability to manipulate our environment and use our superior intelligence—which is due to the number of neurons in our cerebral cortex, the highest in the animal kingdom, 16 billion in all (Herculano-Houzel, 2009). Why postulate that a dinosaur could have looked even anywhere close to us?
This is also ignoring the fact that decimation and diversification also ‘decide the fates’ so to speak, of the species on earth. Survival during an extinction event is strongly predicated by chance (and size). The smaller an organism is, the more likely it will survive an extinction event. Who’s to say that the troodon doesn’t go extinct due to an act of contingency, say, 50 mya if the K-T extinction never occurred?
In conclusion, the supposed ‘trend’ in brain size evolution is just random fluctuations—inevitabilities since life began at the left wall of complexity. Gould wrote about a drunkard’s walk in his book Full House (Gould, 1996) in which he illustrates an example of a drunkard walking away from a bar with the bar wall being the left wall of complexity and the gutter being the right wall. The gutter will always be reached; and if he hits the wall, he will lean against the wall “until a subsequent stagger propels him in the other direction. In other words, only one direction of movement remains open for continuous advance—toward the gutter” (Gould, 1996: 150).
I bring up this old example to illustrate but one salient point: In a system of linear motion structurally constrained by a wall at one end, random movement, with no preferred directionality whatever, will inevitably propel the average position away from a starting point at the wall. The drunkard falls into the gutter every time, but his motion includes no trend whatever toward this form of perdition. Similarly, some average or extreme measure of life might move in a particular direction even if no evolutionary advantage, and no inherent trend, favor that pathway (Gould, 1996: 151).
We humans are lucky we are here. Contingencies of ‘just history’ are why we are here, and if we were not here—if the K-T extinction never occurred—and the troodon or another dinosaur species survived to the present day, they would not have reached our ‘level’ of intelligence. To believe so is to believe in teleological evolution—which certainly is not true. Anthropometric bias runs deep in evolutionary biology and paleontology. People assume that since we are—according to some—the ‘pinnacle’ of evolution, that us, or something like us, would eventually have evolved.
Any ‘trends’ can be explained as life moving away from the left wall of complexity, with the left wall—the mode of life, the modal bacter-–being unchanged. We are at the extreme tail of the distribution of complexity while bacteria are at the left wall. Complex life was inevitable since bacteria, the most simple life, began at the left wall. And so, these ‘trends’ in brain size are just that, increasing complexity, not any type of ‘progressive evolution’. Evolution just happens, natural selection occurs based on the local environment, not any inherent or intrinsic ‘progress’.
Gould, S. J. (1989). Wonderful life: the burgess Shale and the nature of history. New York: Norton.
Gould, S. J. (1996). Full house: The Spread of Excellence from Plato to Darwin. New York: Harmony Books.
Herculano-Houzel, S. (2009). The human brain in numbers: a linearly scaled-up primate brain. Frontiers in Human Neuroscience,3. doi:10.3389/neuro.09.031.2009
Lane, N. (2015). The vital question: energy, evolution, and the origins of complex life. New York: W.W. Norton & Company.
Olkowicz, S., Kocourek, M., Lučan, R. K., Porteš, M., Fitch, W. T., Herculano-Houzel, S., & Němec, P. (2016). Birds have primate-like numbers of neurons in the forebrain. Proceedings of the National Academy of Sciences,113(26), 7255-7260. doi:10.1073/pnas.1517131113
Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).
Russell, D. A. (1983). Exponential evolution: Implications for intelligent extraterrestrial life. Advances in Space Research,3(9), 95-103. doi:10.1016/0273-1177(83)90045-5
What is the relationship between traumatic brain injury (TBI) and IQ? Does IQ decrease? Stay the same? Increase? A few studies have looked at the relationship between TBI and IQ, and the results may be quite surprising to some. Tonight I will look through a few studies and see what the relationship is between TBI and IQ—does IQ decrease substantially or is there only a small decrease? Does it decrease for all subtests or only some?
TBI and IQ
In a sample of 72 people with TBI who had significant brain injuries had an average IQ of 90 (study 1; Bigler, 1995). Bigler also says that whatever correlation exists between brain size and IQ “does not persist post injury” (pg 387). This finding has large implications: can there be a minimal hit to IQ depending on age/severity of injury/brain size/education level?
As will be seen when I review another study on IQ and brain injury, every individual in the cohort in Bigler (1995) was tested after 42 days of brain injury. This does matter, as I will get into below.
Table 1 in study 1 shows that whatever positive relationship between IQ and brain size that is there before injury does not persist after injury (Bigler, 1995: 387). Study 1 showed that, even with mild-to-severe brain damage, there was little change in measured IQ—largely because the correlation between brain size and IQ is .51 at the high end (which I will use—the true correlation is between .24 [Pietschnig et al, 2015] to .4 [Rushton and Ankney, 2009]), this means that if the correlation were to be that high, brain size would only explain 25 percent of the variation in IQ (Skoyles, 1999). That leaves a lot of room for other reasons for differences in brain size and IQ in individuals and groups.
In study 2 (Bigler, 1995: 389-391), he looked into whether or not there were differences in IQ between high and low brain volume people (95 men). Results summed in table 3 (pg 390). Those with low brain volume (1185), aged 28, had an IQ of 82.61 while those with high brain volume (1584), aged 34 had an IQ of 92 (both cohorts had similar education). Bigler showed in study 1 IQ was maintained post injury, so we can say that this was their IQ preinjury.
In table 2, Bigler (1995) compares IQs and brain volumes of mild-to-moderate and moderate-to-severe individuals with TBI. Brain volume in the moderate-to-severe group was 1289.2 whereas for the mild-to-moderate TBI-suffering individuals had a mean brain volume of 1332.9. Amazingly, both groups had IQ scores in the normal range (90.0 for moderate-to-severe TBI and 90.7 for individuals suffering from mild-to-moderate TBI. In study 3, Bigler (1995) shows that trauma-induced atrophic changes in the brain aren’t related to IQ postinjury, nor to the amount of focal lesion volume.
Nevertheless, Bigler (1995) shows that those with bigger brains had less of a cognitive hit after TBI than those with smaller brains. PumpkinPerson pointed me to a study that shows that TBI stretches far back into our evolutionary history, with TBI seen in australopithecine fossils along with erectus fossils found throughout the world. This implies that TBI was a driver for brain size (Shivley et al, 2012); if the brain is bigger, then if/when TBI is acquired, the cognitive hit will be lessened (Stern, 2002). This is a great theory for explaining why we have large brains despite the negatives that come with them—if we were to acquire TBI in our evolutionary past, then the hit to our cognition would not be too great, and so we could still pass our genes to the next generation.
The fact that changes in IQ are minimal when brain damage is acquired shows that brain size isn’t as important as some brain-size-fetishists would like you to believe. Though, preinjury (PI) IQ was not tested, I have one study where it was.
Wood and Rutterford (2006) showed results similar to Bigler (1995)—minimal change to IQ occurs after TBI. The whole cohort pre-injury (PI) had a 99.79 IQ. T1 (early measure) IQ for the cohort was 90.96 while T2 (late measure) IQ for the cohort was 92.37. For people with greater than 11th-grade education (n=30), IQ decreased from 106.57 PI to 95.19 in T1 to 100.17 in T2. For people with less than an 11th-grade education (n=44), IQ PI was 95.16 and decreased to 86.99 in T1 and increased to 87.96 in T2. Male (n=51) and female (n=23) were similar, with male PI IQ being 99.04 to women’s 101.44 with a 90.13 IQ in T1 for men with a 90.72 IQ in T1 for women. In T2 for men it was 92.94 and for women, it was 92.83. So this cohort shows the same trends as Bigler (1995).
The most marked difference in subtests post-injury was in vocabulary (see table 3) with similarities staying the same, and digit symbol, and block design increasing between T1 and T2. Neither group differed between T1 and T2. The only significant association in performance change over time was years of education. Less educated people were at greater risk for cognitive decline (see table 2).
The difference for PI IQ after T2 for less educated people was 7.2 whereas for more educated people it was 6.4. Though more educated people gained back more IQ points between T1 and T2 (4.98 points) compared to less educated people (.97 IQ points). And: “The participants in our study represent a subgroup of patients with severe head injury reported in a larger study assessing long‐term psychosocial outcome.”
Bigler (1995) didn’t have PI IQ, but Wood and Rutterford (2006) did, and from T1 to T2 (Bigler 1995 tested what would be equivalent to T1 in the Wood and Rutterford 2006 study), IQ hardly increased for those with lower education (.97 points) but substantially increased for those with higher education (4.98 points) with there being a similar difference between PI IQ and T2 IQ for both groups.
Brain-derived neurotrophic protective factor (BDNF) also promotes survival and synaptic plasticity in the human brain (Barbey et al, 2014). They genotyped 156 Vietnam War soldiers with frontal lobe lesion and “focal penetrating head injuries” for the BDNF polymorphism. Though they did find differences in the groups with and without the BDNF polymorphism, writing that there were “substantial average differences between these groups in general intelligence (≈ half a standard deviation or 8 IQ points), verbal comprehension (6 IQ points), perceptual organization (6 IQ points), working memory (8 IQ points), and processing speed (8 IQ points) after TBI” (Barbey et al, 2014). This supports the hypothesis that BDNF is protective against TBI; and since BDNF was important in our evolutionary history which is secreted by the brain while endurance running (Raichlen and Polk, 2012), this could have also been another protective factor against hits to cognition that were acquired, say, during hunts or fights.
Nevertheless, one study found in a sample of 181 children Crowe et al (2012) found that children with mild-to-moderate TBI had IQ scores in the average range, whereas children with severe TBI had IQ scores in the low average range (80 to 90; table 3).
Infants with mild TBI had IQ scores of 99.9 (n=20) whereas infants with moderate TBI has IQs of 98.0 (n=23) and infants with severe TBI had IQs of 90.7 (n=7); preschoolers with mild TBI had IQ scores of 103.8 (n=11), whereas preschoolers with moderate TBI had IQ scores of 100.1 (n=19) and preschoolers with severe TBI had IQ scores of 85.8 (n=13); middle schoolers with mild TBI had IQ scores of 93.9 (n=10), whereas middle schoolers with moderate TBI had IQ scores of 93.5 (n=21), and middle schoolers with severe TBI had IQ scores of 86.1 (n=14); finally, children with mild TBI in late childhood had a mean FSIQ of 107.3 (n=17), while children with moderate TBI had IQs of 99.5 in late childhood (n=15), and children with severe TBI in late childhood had FSIQs of 94.7 (Crowe et al, 2012; table 3). This shows that age of acquisition and severity influence IQ scores (along with their subtests), and that brain maturity matters for maintaining average intelligence post-TBI. Königs et al (2016) also show the same trend; the outlook is better for children with mild TBI, while children faired far worse with severe TBI compared to mild when compared to adults (also seen in Crowe et al, 2012).
People who got into motor vehicle accidents suffered a loss of 14 IQ points (n=33) after being tested 20 months postinjury (Parker and Rosenblum, 1996). The WAIS-IV Technical and Interpretive Manual also shows a similar loss of 16 points (pg 111-112), however, the 22 subjects were tested within 6 to 18 months within acquiring their TBI, with no indication of whether or not a follow-up was done. IQ will recover postinjury, but education, brain size, age, and severity all are factors that contribute to how many IQ points will be gained. However, adults who suffer mild, moderate, and severe TBIs have IQs in the normal range. TBI severity also had a stronger effect on children aged 2 to 7 years of age at injury, with white matter volume and results on the Glasgow Coma Scale (which is used to assess consciousness after a TBI) were related to the severity of the injury (Levin, 2012).
TBI can occur with a minimal hit to IQ (Bigler, 1995; Wood and Rutterford, 2006; Crowe et al, 2012). IQs can still be in the average range at a wide range of ages/severities, however the older one is when they suffer a TBI, the more likely it is that they will incur little to no loss in IQ (depending on the severity, and even then they are still in the average range). It is interesting to note that TBI may have been a selective factor in our brain evolution over the past 3 million years from australopithecines to erectus to Neanderthals to us. However, the fact that people with severe TBI can have IQ scores in the normal range shows that the brain size/IQ correlation isn’t all it’s cracked up to be.
Barbey AK, Colom R, Paul E, Forbes C, Krueger F, Goldman D, et al. (2014) Preservation of General Intelligence following Traumatic Brain Injury: Contributions of the Met66 Brain-Derived Neurotrophic Factor. PLoS ONE 9(2): e88733. https://doi.org/10.1371/journal.pone.0088733
Bigler, E. D. (1995). Brain morphology and intelligence. Developmental Neuropsychology,11(4), 377-403. doi:10.1080/87565649509540628
Crowe, L. M., Catroppa, C., Babl, F. E., Rosenfeld, J. V., & Anderson, V. (2012). Timing of Traumatic Brain Injury in Childhood and Intellectual Outcome. Journal of Pediatric Psychology,37(7), 745-754. doi:10.1093/jpepsy/jss070
Green, R. E., Melo, B., Christensen, B., Ngo, L., Monette, G., & Bradbury, C. (2008). Measuring premorbid IQ in traumatic brain injury: An examination of the validity of the Wechsler Test of Adult Reading (WTAR). Journal of Clinical and Experimental Neuropsychology,30(2), 163-172. doi:10.1080/13803390701300524
Königs, M., Engenhorst, P. J., & Oosterlaan, J. (2016). Intelligence after traumatic brain injury: meta-analysis of outcomes and prognosis. European Journal of Neurology,23(1), 21-29. doi:10.1111/ene.12719
Levin, H. S. (2012). Long-term Intellectual Outcome of Traumatic Brain Injury in Children: Limits to Neuroplasticity of the Young Brain? Pediatrics, 129(2), e494–e495. http://doi.org/10.1542/peds.2011-3403
Parker, R. S., & Rosenblum, A. (1996). IQ loss and emotional dysfunctions after mild head injury incurred in a motor vehicle accident. Journal of Clinical Psychology,52(1), 32-43. doi:10.1002/(sici)1097-4679(199601)52:1<32::aid-jclp5>3.3.co;2-1
Pietschnig, J., Penke, L., Wicherts, J. M., Zeiler, M., & Voracek, M. (n.d.). Meta-Analysis of Associations Between Human Brain Volume And Intelligence Differences: How Strong Are They and What Do They Mean? SSRN Electronic Journal. doi:10.2139/ssrn.2512128
Raichlen, D. A., & Polk, J. D. (2012). Linking brains and brawn: exercise and the evolution of human neurobiology. Proceedings of the Royal Society B: Biological Sciences,280(1750), 20122250-20122250. doi:10.1098/rspb.2012.2250
Rushton, J. P., & Ankney, C. D. (2009). Whole Brain Size and General Mental Ability: A Review. The International Journal of Neuroscience, 119(5), 692–732. http://doi.org/10.1080/00207450802325843
Shively, S., Scher, A. I., Perl, D. P., & Diaz-Arrastia, R. (2012). Dementia Resulting From Traumatic Brain Injury: What Is the Pathology? Archives of Neurology, 69(10), 1245–1251. http://doi.org/10.1001/archneurol.2011.3747
Skoyles R. J. (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise
Stern, Y. (2002). What is cognitive reserve? Theory and research application of the reserve concept. Journal of the International Neuropsychological Society,8(03), 448-460. doi:10.1017/s1355617702813248
Wood, R. L., & Rutterford, N. A. (2006). Long‐term effect of head trauma on intellectual abilities: a 16‐year outcome study. Journal of Neurology, Neurosurgery, and Psychiatry, 77(10), 1180–1184. http://doi.org/10.1136/jnnp.2006.091553
Note: This article is high speculation based on the finding that occurred last week of the modification of mastodon bones in Ice Age California. If it is an actual archaeological site, along with being the age it’s purported to be, there are, in my opinion, only two possibilities for who could be responsible: erectus or the Denisova. Though I will cover evidence that Erectus did make it to America between 40-130,000ya, and rule out that Neanderthals are the hominid responsible.
It was discovered last week that there was human activity at an archeological site in San Diego, California, dated to about 130,000 years ago. Researchers discovered pieces of bone and teeth from a mastodon—that looked to have been modified by early humans. This discovery—if it shows that there was a hominid in the Americas 130,000ya—would have us rethink hominin migrations in the ancient past.
The bones and teeth show signs of having been modified by humans with “manual dexterity and experiential knowledge.” The same pattern was discovered in Nebraska and Kansas, where it was ruled out that carnivorous animals were responsible (Holen et al, 2017).
Now, we only have a few pieces of broken bone and some teeth from a mastodon. It is possible that ‘Natives’ dug up the mastodon skull and modified it, but I like to think outside of the box sometimes. When I first read the ScienceDaily article on the matter, the first hominin that popped into my head that could be responsible for this is erectus. But what is the evidence that he could have made it to the Americas that long ago?
Erectus in America
Evidence for erectus in America is scant. We have discovered no erectus skeletons in the Americas, and we only have a few pieces of bone to go off of to guess which hominid did this (and I doubt it was Homo sapiens or Neanderthals, I will explain my reasoning below).
I’ve been documenting on my blog for the past six months that, contrary to popular belief, erectus was not a ‘dumb ape’ and that, in fact, erectus had a lot of modern behaviors. If it turns out to be true that erectus made it to America, that wouldn’t really surprise me.
Erectus had a wider territory than the other hominid candidates (Neanderthals, Homo sapiens) and the other candidate—the Denisova—were situated more to the middle of the Asian continent. So this, really, leaves us only with erectus as the only possible candidate for the mysterious hominin in Caliofornia—and there is evidence that (albeit, extremely flimsy), erectus may have possibly made it to America, from a paper published back in 1986. Dreier (1986) writes that there is evidence of Man in America before 30kya, and if this is true, then it must be erectus since the estimated dates are between 50-70 kya—right around the time that AMH began migrating out of Africa. Dreier (1986) goes through a few different discoveries that could have been erectus in America, yet they were only modern skeletons. However, absence of evidence is not evidence of absence. (Though I will return to this specific point near the end of the article.)
How could erectus have possibly made it to America?
This is one of the most interesting things about this whole scenario. There is evidence that erectus made rafts. If erectus did make it to Flores (Stringer, 2004; Hardaker, 2007: 263-268; Lieberman, 2013)—eventually evolving into floresiensis (or from habilis or a shared common ancestor with habilis)—then he must have had the ability to make rafts. Since we have found erectus skulls at Java, and since certain bodily proportions of floresiensis are ‘scaled-down’ from erectus, along with tools that erectus used, it’s not out of the realm of possibility that erectus had the ability to navigate the seas.
One way that hominins can get to America is through the Bering strait. However, Dreier (1986) assumes that erectus was not cold-adapted, and insists that erectus could have only gone into higher latitudes for only a few months out of the year when it was warmer. As you can see from the above map of erectus’ territory, he lived along the coast of China and into some of the islands around SE Asia. While we don’t have any skeletal evidence, we can infer that it was late Asian erectus who, could have possibly, made it to the Americas. So since it was late in erectus’ evolution, we would expect him to have a large brain size in order to 1) survive in Africa and 2) since brain size predicts the success of a species in novel environments (Sol et al, 2008), erectus would have had a larger brain in these locations. So it seems that erectus did have the same adaptability that we do—especially if he actually did make it to the Americas.
Dreier (1986) posits that erectus could have traveled along the Aluetian island chain in Alaska, eating marine life (shells, mollusks, clams, etc), and so he would not have had to “deviate from the 53 north latitude vitamin D barrier drastically since almost the entire Aleutian Island chain falls between the 50 and 55 north latitude lines, and access via this route may have been possible during glaciation when sea levels in the area dropped as much as 100 meters” (Dreier, 1986: 31). Erectus could have gotten vitamin D from shells, mollusks and other marine life, as they are extremely high in vitamin D (Nair and Maseeh, 2012). I will contend that erectus rafted to America, but the Aluetian island route is also plausible.
Dreier (1986) ends up concluding that our best bet for finding erectus skeletons in America is along with Pacific coast, and there may be some submerged underwater. However, with the new discovery last week, I await more work into the site for some more answers (and of course questions).
However, contra Dreier’s (1986) claim that we should stop looking for sites with human activity earlier than 30,000 years, this new finding is promising.
Why not Neanderthals?
Neanderthals were seafarers, just like erectus, and later, us. However, there is evidence for Neanderthals sailing the seas 100kya, however, earlier dates of seafaring activity “as far back as 200 ka BP can not be excluded.” (Ferentinos et al, 2012). Further—and perhaps most importantly—the range of the Neanderthals was nowhere near the Pacific Ocean—whereas erectus was. So since there is little evidence of seafaring 200kya (which cannot be excluded), then we’re still left with the only possibility being erectus go to the Americas either by walking the Aleutian islands or rafting across the Pacific.
Could erectus have killed animals as large as a mastodon?
Erectus was killing elephants (Elephas antiquus) around 400kya in the Levant (Ben-Dor et al, 2011). Then, when the elephants went extinct, erectus had to hunt smaller, quicker game and thus evolved a smaller body to deal with the new environmental pressure—chasing a new food source. So erectus did have the ability to kill an animal that big, another positive sign that this is erectus we are dealing with in California 130,000 years ago.
An erectus skeleton in America?
An osteologist discovered a brow bone in the Americas, and in an unpublished report in 1990, he says the brow’s thickness and structure is comparable to African erectus, with a reanalysis showing it was closer to Asian erectus—just what we would expect since Asian erectus may have been a seafarer (Hardaker, 2007). However, the author of the book reiterates the Texas A&M osteologists’ findings writing: “these comparisons do not imply that preHomo sapiens were in the Americas” (Steen-McIntyre, 2008).
Humanlike cognition in erectus?
Humanlike thinking evolved 1.8 mya, right around the time erectus came into the picture (Putt et al, 2017). Volunteers created Auchulean tools while wearing a wearing a cap that measured brain activity. Visual attention and motor control were needed to create the “simpler Oldowan tools”, whereas for the “more complex Auchelian tools” a “larger portion of the brain was engaged in the creation of the more complex Acheulian tools, including regions of the brain associated with the integration of visual, auditory and sensorimotor information; the guidance of visual working memory; and higher-order action planning.” This discovery pushes back the advent of humanlike congition, since the earliest tools of this nature are found around 1.8 mya. There is a possibility that some erectus may have had IQs near ours, as studies of microcephalics show that a large amount have higher than average IQs (Skoyles, 1999).
Evidence is mounting that erectus was more than the ‘dumb ape’ that some people say he is. If erectus did make it to America—and the possibility is there—then human migratory patterns need to be rewritten. I hope there is more evidence pointing to what hominid was in the area at that time—and if there is evidence of humanlike activity there, it most likely is erectus. It is extremely possible that erectus could have gotten to America, as there is evidence that he was at least in northern China. So he could have sailed to the Americas or walked along the Aluetian islands.
The evidence for erectus in America is compelling, and I hope more is discovered about what went on at this site and who was there. Even if it wasn’t erectus, there is still some compelling evidence that he did make it to America.
Ben-Dor, M., Gopher, A., Hershkovitz, I., & Barkai, R. (2011). Man the Fat Hunter: The Demise of Homo erectus and the Emergence of a New Hominin Lineage in the Middle Pleistocene (ca. 400 kyr) Levant. PLoS ONE,6(12). doi:10.1371/journal.pone.0028689
Dreier, Frederick G., (1986). Homo Erectus in America: Possibilities and problems. Lambda Alpha Journal of Man, v.17, no.1-2, 1985-1986. Citing: Gifford, E.W., (1926). California Anthropometry. University of California Publications in Archaeology and Ethnology.22:217-390
Ferentinos, G., Gkioni, M., Geraga, M., & Papatheodorou, G. (2012). Early seafaring activity in the southern Ionian Islands, Mediterranean Sea. Journal of Archaeological Science,39(7), 2167-2176. doi:10.1016/j.jas.2012.01.032
Hardaker, C. (2007). The first American: the suppressed story of the people who discovered the New World. Franklin Lakes, NJ: New Page Books, a division of The Career Press.
Holen, S. R., Deméré, T. A., Fisher, D. C., Fullagar, R., Paces, J. B., Jefferson, G. T., . . . Holen, K. A. (2017). A 130,000-year-old archaeological site in southern California, USA. Nature,544(7651), 479-483. doi:10.1038/nature22065
Lieberman, D. (2013). The Story of the human body – evolution, health and disease. Penguin.
Putt, S. S., Wijeakumar, S., Franciscus, G. R., Spencer. P. J. The functional brain networks that underlie Early Stone Age tool manufacture. Nature Human Behaviour, 2017
Skoyles R. J. (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise
Sol, D., Bacher, S., Reader, S., & Lefebvre, L. (2008). Brain Size Predicts the Success of Mammal Species Introduced into Novel Environments. The American Naturalist,172(S1). doi:10.1086/588304
Steen-McIntyre, V. (2008) A Review of the Valsequillo, Mexico Early-Man Archaeological Sites (1962-2004) with Emphasis on the Geological Investigations of Harold E. Malde. Presentation at 2008 Geological Society of America Joint Annual Meeting Oct. 5-9, Houston, Texas
Stringer, C. (2004, October 27). A stranger from Flores. Retrieved May 09, 2017, from http://www.nature.com/news/2004/041027/full/news041025-3.html
It’s well-known that blacks have narrower hips than whites (Rushton, 1997; Handa et al, 2008). These pelvic differences then account for part of the variation in elite sporting events such as sprinting and jumping (Entine, 2000). These pelvic differences are the result of climatic variation and sexual selection.
The evolution of the pelvis is due to bipedalism. We are bipeds because of our S-shaped spine, which helps us to cope with differing loads. The human pelvis had to evolve in two ways—to make birthing babies easier and to become more efficient for bipedal walking. Termed the ‘obstetric dilemma’, it has implications for osteoarthritis in both men and women (Hogervorst, Heinse, and de Vos, 2009). Having a more efficient bipedal gait meant the body could allocate energy to other parts of the body—mainly our growing brains/neuronal count. Over time, the brain grew while the pelvis had to shrink for more efficient bipedalism. The pelvis also got narrower in our evolution, being wider in Australopithicenes, while becoming more narrow when erectus appeared—which is the first instance of a humanlike pelvis in the fossil record—which increased how far we could travel as well as reduce our energy expenditure (Lieberman, et al, 2006). Further discussion can be found in my article Man the Athlete.
So we began evolving a narrower pelvis in comparison to our ancestors because it was more efficient for heat dissipation. Smaller trunks are more efficient for heat dissipation (Lieberman, 2015), whereas wider trunks are more efficient for thermoregulation in colder climes (Weaver and Hublin, 2008; Weaver, 2009; Gruss and Schmidt, 2015). Now, simply applying this logic to Eurasians and Africans (I am grouping East Asians and Europeans together since they were a single breeding population up until about 23,000-6,500ya), we can see one reason why that population has wider pelves than Africans.
When anatomically modern humans (AMH) left Africa between 50-100kya, human skeletal morphology was just like modern-day Africans’ today. When Man migrated into northerly climes, however, a wider pelvis was needed to retain heat in colder climes (Gruss and Schmidt, 2015). So, along with a wider pelvis evolving due to climatic demands on the body, as we migrated north the human brain expanded due to the climate of the area, along with expanding the pelvis to better thermoregulate (which a bigger brain also does in northerly climes). I did argue two months back (and added to Skoyles’ (1999) theory) that brain size increased for expertise capacity and not IQ since Arctic people needed more tools, as well as tools that were more complex, in comparison to peoples who evolved in a hotter climate. So selection then occurred for larger brains and pelvis due to the demand for thermoregulation and bigger brains—which then led to earlier births and more helpless babes, which higher levels of intelligence were then needed to care for them (Piantadosi and Kidd, 2016). The helplessness of infants predicts the intelligence of adults in the primate genera (Piantadosi and Kidd, 2016), so I will assume that this holds within primate species as well (I am not able to locate a citation that this doesn’t hold within the primate genera; if I am in error, please provide a citation). Since African children are born earlier and more mature than Eurasian children who are born slightly later and more helpless/less developed, this is one reason why Eurasians have higher levels of intelligence than Africans (which is independent of any direct effects of climate I may add!).
So since Eurasians needed a larger brains to make more tools in the Arctic/colder climes, their brains needed to expand in size for increased expertise capacity, which would then have further selected for wider pelves in Eurasian women. Climatic variation caused the wider hips/bigger brains in Eurasians, which then allowed the evolution of larger brains in comparison to those who remained in Africa.
Finally, the obstetric dilemma has been recently called into question; there is evidence that a wider pelvis does not increase locomotor costs in humans (Warrener et al, 2015), a treadmill tracked their gait, as well as the motion of their pelvis. This study is used as evidence that the obstetric dilemma is wrong—they argue that there is no trade-off between narrower hips in men and wider hips in women. However, as the authors point out, all subjects in the study walked/ran at the same speed. Let’s say that the speed was heightened; do you think the women/men with wider pelves would have had the same locomotor costs as the men/women with narrower pelves? The answer is, obviously, no.
The pelvis of all of the races of Man has evolved the way they are due to environmental/climatic demands. A wider pelvis is better for thermoregulation in colder climates, while a narrower pelvis/body is more efficient for heat loss (Gruss and Schmidt, 2015).
Thus, we can look at the evolution of brain size/pelvic size in a few ways: 1) The amount of tools/complexity of the tools in the area that led to a need for an increase in brain size for more ‘chunks’ (Gobet and Simon, 1998), which then—along with colder climates—selected for larger brains and a wider body/pelvis which made birthing babes with large heads/brains easier along with helping to conserve heat due to the wider body (Gruss and Schmidt, 2015); 2) Since people in higher altitudes needed a high amount of expertise to survive, further selection for bigger brains, wider pelves occurred because of this; 3) Africans have smaller pelves in comparison to Eurasians because they evolved in hotter climes and didn’t have the amount of tools that peoples in more northerly climes did—which also increased brain size; 4) putting this all together, we can say that because Africans live in hotter climates, they need narrow pelves in order to lose body heat; Eurasians, after they migrated into more northerly climes, needed a wider body/pelvis in order to retain heat. When Man migrated north, he needed the ability to become an expert in, say, tool-making and thus needed a bigger brain for more informational chunks (Simon and Gobet, 1998; Skoyles, 1999). Due to this, Eurasians have wider pelves since they needed larger brains for a higher expertise capacity (Skoyles, 1999).
When Man migrated north, he needed the ability to become an expert in, say, tool-making and thus needed a bigger brain for more informational chunks (Simon and Gobet, 1998; Skoyles, 1999). Due to this, Eurasians have wider pelves than Africans; so they can birth larger-brained children. The width of the female pelvis, too, was shaped by sexual selection (Lassek and Gaulin, 2009). Therefore, the evolution of the modern pelvis in human populations comes down to climatic variation, which, in turn, affects how large of a brain the babe is able to have. Climate constrains brain size in either ‘direction’, big or small. We don’t even need to look at the variation within modern Homo sapiens to see the pattern in pelvic size we do today; because the pelvic differences noted among Man definitely were in effect millions of years ago, with hominids in colder climates having wider pelves while hominids in warmer climates had narrower pelves.
Along with everything above, the evolution of the human pelvis has a few implications for the human races today. Some recent studies have shown that there is no obstetric dilemma at all, with birth complications being caused by babies with higher weights than in our ancestral past, due to environmental mismatches causing higher-weight babies (Warrener et al, 2015; Betti, 2017), which was also beneficial for the evolution of our large brains (Cunnane and Crawford, 2003) with the largest amount of cortical neurons in the animal kingdom. However, marked differences in locomotion would be seen in people who had wide pelves compared to narrow pelves; which is what we see in elite running competitions: the elite runners have narrower pelves. So wider pelves don’t impede normal bipedal walking, but it does impede being able to efficiently run, as evidenced in participants of elite sprinting and marathon competitions. Looking at champion athletes and studying their locomotion (along with other traits as I’ve covered here) you can see that those with narrower pelves win more competitions than those with wider pelves (and happen to have different muscle fiber competition, fat distribution/percent, and morphology).
Racial differences in the pelvis explain the reasons behind why a certain race dominates in certain elite competitions; it largely comes down to skeletal morphology. These skeletal differences have evolutionary underpinnings, with the same pelvic differences seen in hominins that evolved in colder/warmer climates in the past. These pelvic differences (along with body fat percentage/distribution, musculoskeletal morphology, muscle fiber type, lean mass percentage, lower Vo2 max, poorer running economy, a larger Q-angle [4.6 degrees greater than men], etc) are why women are less efficient runners. People with wider hips are more likely to have be endomorphic while people with narrower hips are more likely to be ecto and meso. Not surprisingly, people from northerly climes consistently win WSM competitions whereas East and West Africans dominate bodybuilding and sprinting/marathons due to having a narrower pelvis and other advantageous morphological traits that lead to success in the sport. Nevertheless, pelvic differences between the races largely come down to differences in climate, which was also seen in ancient hominins. These pelvic differences further lead to racial differences in elite sporting competition.
Betti, L. (2017). Human Variation in Pelvic Shape and the Effects of Climate and Past Population History. The Anatomical Record,300(4), 687-697. doi:10.1002/ar.23542
Cunnane, S. C., & Crawford, M. A. (2003). Survival of the fattest: fat babies were the key to evolution of the large human brain. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology,136(1), 17-26. doi:10.1016/s1095-6433(03)00048-5
Dr. John R. Skoyles (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise
Entine, J. (2000). Taboo: why Black athletes dominate sports and why we are afraid to talk about it. New York: PublicAffairs.
Gobet, F., & Simon, H. A. (1998). Expert Chess Memory: Revisiting the Chunking Hypothesis. Memory,6(3), 225-255. doi:10.1080/741942359
Gruss, L. T., & Schmitt, D. (2015). The evolution of the human pelvis: changing adaptations to bipedalism, obstetrics and thermoregulation. Philosophical Transactions of the Royal Society B: Biological Sciences,370(1663), 20140063-20140063. doi:10.1098/rstb.2014.0063
Hogervorst, T., Heinse W.B., & de Vos J., (2009) Evolution of the hip and pelvis. Acta Orthopaedica, 80:sup336, 1-39, DOI: 10.1080/17453690610046620
Lieberman, D. E., Raichlen, D. A., Pontzer, H., Bramble, D. M., & Cutright-Smith, E. (2006). The human gluteus maximus and its role in running. Journal of Experimental Biology,209(11), 2143-2155. doi:10.1242/jeb.02255
Lieberman, D. E. (2015). Human Locomotion and Heat Loss: An Evolutionary Perspective. Comprehensive Physiology, 99-117. doi:10.1002/cphy.c140011
Piantadosi, S. T., & Kidd, C. (2016). Extraordinary intelligence and the care of infants. Proceedings of the National Academy of Sciences,113(25), 6874-6879. doi:10.1073/pnas.1506752113
Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).
Handa, V. L., Lockhart, M. E., Fielding, J. R., Bradley, C. S., Brubakery, L., Cundiffy, G. W., … Richter, H. E. (2008). Racial Differences in Pelvic Anatomy by Magnetic Resonance Imaging. Obstetrics and Gynecology, 111(4), 914–920.
Warrener, A. G., Lewton, K. L., Pontzer, H., & Lieberman, D. E. (2015). A Wider Pelvis Does Not Increase Locomotor Cost in Humans, with Implications for the Evolution of Childbirth. PLoS ONE, 10(3), e0118903.
Weaver, T. D., & Hublin, J. (2009). Neandertal birth canal shape and the evolution of human childbirth. Proceedings of the National Academy of Sciences,106(20), 8151-8156. doi:10.1073/pnas.0812554106
Weaver, T. D. (2009). The meaning of Neandertal skeletal morphology. Proceedings of the National Academy of Sciences,106(38), 16028-16033. doi:10.1073/pnas.0903864106
The study of political bias is very important. Once the source of what motivates political bias—which no doubt would translate to other facets of life—is found, individual action can be taken to minimize any future bias. Two recent studies found that contrary to other studies showing that conservatives are more biased than liberals, both groups were equally as biased.
Everyone is biased—even physicians (Cain and Detsky, 2008). When beliefs we hold to be true are questioned, we do anything we can to shield ourselves from conflicting information. Numerous studies have looked into biases in politics, with some studies showing that conservatives are more likely to be biased towards their views more than liberals. However, recent research has shown that this is not true.
Frimer, Skitka, and Motyl, (2017) showed there were similar motives to shield one’s self from contradictory information. Hearing opposite viewpoints—especially for staunch conservatives and liberals—clearly leads to them doing anything possible to, in their heads, defend their dearly held beliefs. In four studies (1: people would forgo the chance to win money if they didn’t have to hear the opposite sides’ opinions on the same-sex marriage debate; 2: thinking back to the 2012 election; 3: upcoming elections in the US and Canada; “a range of other Culture War Issues” (Frimer, Skitka, and Motyle, 2017); and 4: both groups reported similar diversions towards hearing the opposite group’s beliefs), both groups reported that hearing the other side’s beliefs would induce cognitive dissonance (Frimer, Skitka, and Motyle, 2017). They meta-analyzed all of their studies and still found that both groups would “rather remain in their ideological bubbles”.
Ditto et al (2017) also had similar findings. They meta-analyzed 41 studies with over 12,000 participants, testing two hypotheses: 1) conservatives would be more biased than liberals and 2) there would be equal amounts of bias. They discovered that the correlation for partisan bias was “robust”, with a correlation of .254. They showed that “liberals (r = .248) and conservatives (r = .247) showed nearly identical levels of bias across studies” (Ditto et al, 2017).
These two studies show what we know is true: it’s extremely hard/damn near impossible to change one’s view. Someone can be dead wrong, yet attempt to gather up whatever kind of data they possibly can to shield themselves from the truth.
This all comes down to one thing: the backfire effect. When we are presented with contradictory information, we immediately reject it. Everyone is affected by this bias. One study showed that corrections frequently failed to correct political misconceptions, with these attempted corrections actually doing the opposite, people increased their misconception of the group in question (Nyhan and Riefler, 2010). The thing is, people lack the knowledge about political matters which then affects their opinions. These studies show why it’s next to impossible to change one’s view in regards to anything, especially political matters.
New York University’s Professor of Ethical Leadership and social psychologist with a specialty in morality Jonathan Haidt also talks about partisan bias in his outstanding book on religion and politics The Righteous Mind: Why Good People are Divided by Politics and Religion (Haidt, 2013). This book is outstanding and I highly recommend it. I’ve written about some of his thoughts in his book, his theory on the evolution of morality is very well argued. Moral reasoning is just a post-hoc search for reasons to justify the judgments that people have already made. When asked why people are so averse to questions they find morally wrong, they cannot give good reasons to why they find the scenarios morally wrong (Haidt, 2001). More specifically, people couldn’t say why it was morally wrong to have sex with a sibling even though they were told that they used birth control and both enjoyed the act, suffering no emotional damage. This is direct evidence for Haidt’s ‘wag-the-dog’ illusion.
Haidt (2001: 13) writes:
If moral reasoning is generally a post-hoc construction intended to justify automatic moral intuitions, then our moral life is plagued by two illusions. The first illusion can be called the “wag-the-dog” illusion: we believe that our own moral judgment (the dog) is driven by our own moral reasoning (the tail). The second illusion can be called the “wag-the-otherdog’s-tail” illusion: in a moral argument, we expect the successful rebuttal of an opponent’s arguments to change the opponent’s mind. Such a belief is like thinking that forcing a dog’s tail to wag by moving it with your hand should make the dog happy.
Except the opponent’s mind is never changed. People always search for things to affirm their worldviews.
In his book, Haidt cites a study done on 14 liberals and conservatives who were stuck into an fMRI machine to scan their brains when shown 18 slides to see how their brain changed when viewing them (Weston et al, 2006). The first of which slide one set was George W. Bush praiding Ken Lay, the CEO of Enron. After, they were shown a slide in which the former President avoided mentioning Lay’s name. “At this point, Republicans were squirming” (Haidt, 2013: 101). Then they were finally shown a slide that said that Bush “felt betrayed” by the CEO’s actions and was shocked to find out that he was corrupt. There was a set of similar slides showing similar contradictory statements from John Kerry. The researchers had engineered situations that made the individual uncomfortable when shown their candidate contradicted themselves, while at the same time not showing any signs of being uncomfortable when it was shown their ideological opposite was caught being a hypocrite (Haidt, 2013: 101).
This study shows that emotional and intuitive processes are the causes for such extreme biases, with one only employing reasoning when it supports their own conclusions. Weston et al (2006) saw that when the individuals looked at the final slides, they had a sense of ‘escape’ and ‘release’. They cite further studies showing that this sense of escape and release is associated with the release of dopamine in the nucleus accumbens and dorsal striatum in other animals (Weston et al, 2006). So the subjects experienced this small hit of dopamine when they saw the final slide that showed everything was “OK”. If this is true, then this explains why we engage in these ‘addictive behaviors’—believing things with such conviction, even when shown contradictory information.
Like rats that cannot stop pressing a button, partisans may be simply unable to stop believing weird things. The partisan brain has been reinforced so many times for performing mental contortions that free it from unwanted beliefs. Even partisanship may be literally addictive. (Haidt, 2013: 103)
Haidt has also been covering the recent University protests that have been occurring around the country. About fifty years ago, a judge predicted the political turmoil we see in Universities today, writing:
No one can be expected to accept an inferior status willingly. The black students, unable to compete on even terms in the study of law, inevitably will seek other means to achieve recognition and self-expression. This is likely to take two forms. First, agitation to change the environment from one in which they are unable to compete to one in which they can. Demands will be made for elimination of competition, reduction in standards of performance, adoption of courses of study which do not require intensive legal analysis, and recognition for academic credit of sociological activities which have only an indirect relationship to legal training. Second, it seems probable that this group will seek personal satisfaction and public recognition by aggressive conduct, which, although ostensibly directed at external injustices and problems, will in fact be primarily motivated by the psychological needs of the members of the group to overcome feelings of inferiority caused by lack of success in their studies. Since the common denominator of the group of students with lower qualifications is one of race this aggressive expression will undoubtedly take the form of racial demands–the employment of faculty on the basis of race, a marking system based on race, the establishment of a black curriculum and a black law journal, an increase in black financial aid, and a rule against expulsion of black students who fail to satisfy minimum academic standards.
This seems to have come true today, seeing as political diversity has decreased in psychology, for instance, in the past fifty years (Duarte et al, 2015). In America, they found that 58-66 percent of social science professors identified as liberals, whereas only 5-8 percent identified as conservatives. Self-identified Democrats also outnumbered Conservatives by almost 8 to 1. Other researchers found that 52 to 77 percent of humanities professors were liberal with only 4-8 percent identifying as Conservative, for a ratio of about 5 to 1, favoring liberals. Finally, 84 percent of psychologists identified as liberal, with only 8 percent identifying as conservative for a 10.5 to 1 ratio (Duarte et al, 2015). However, this skew has only existed for about fifty years. When our institutions show this heavy skew in political beliefs, self-affirming, self-fulfilling prophecies will affect the quality of what is taught to students which will have a negative effect on the type of education received.
Finally, when talking about political biases, one cannot go without mentioning Stephen Jay Gould. Although I’ve come to love his work on evolutionary theory, he was horribly wrong on human differences and let his motivations, biases and political views cloud his judgement and drive him to be grossly dishonest in his posthumous attacks of a man long dead who could no longer defend himself in one Samuel Morton, which first appeared in 1978. This culminated in his widely acclaimed (and, as fas as I can tell, still given to college students to read) book Mismeasure of Man (Gould, 1981). In the book, he attacked Morton for being biased in his measurements of his skull collection. However, in 2011, an anthropology team lead by Jason Lewis remeasured Morton’s skulls and found that Morton was not biased and his measurements were correct (Lewis et al, 2011). Gould was the one who ended up showing the huge bias that he accused Morton of and, ironically for Gould, he was the case study in avoiding bias in scholarship and science, not Morton.
However, as is usually the case, long debates such as this are not so easily settled. Philosopher Michael Weisberg (Weisberg, 2014) argued that Gould’s arguments against Morton were sound and that “Although Gould made some errors and overstated his case in a number of places, he provided prima facie evidence, as yet unrefuted, that Morton did indeed mismeasure his skulls in ways that conformed to 19th century racial biases.” Further, Kaplan, Pigliucci and Banta (2015) argue that Gould’s problem with Morton’s measurements came down to how the measurements should have been done (lead shot or seed). They contend that many of Lewis et al’s (2011) claims against Gould were “misleading” and “had no relevance to Gould’s published analysis.” They also argue that both Gould’s and Morton’s methods (inclusion/exclusion of skulls, how to compute averages, etc) were “inappropriate”. Nevertheless, the point is, this debate seems to be far from over and I await the next chapter. Whatever the case may be, Gould vs. Morton is a perfect case of politics and bias in science.
Everyone is biased. Researchers, physicians, normal everyday people, etc. But where we become most biased is when politics comes into play. To become better, well-rounded people with a myriad of knowledge, we need to listen to other’s viewpoints without immediately rejecting them. But, first, we must recognize the cognitive bias and attempt to correct it. Political differences begin in the brain and then are shaped by experience. These political differences then lead to feelings of disgust when hearing of the views of the ‘opposite team’. Both sides of the political spectrum are equally as biased, contrary to each groups’ perception of this particular issue. There are differences in the brain between Conservatives and Liberals, and when they see their ‘enemy’ engage in contradictory behavior they get joy, whereas when they see their guy engage in the same contradictory behavior they show disgust.
The long debate on Morton’s skulls that’s been raging for over forty years is the perfect look into how politics, motivation, and bias comes into effect in science, no matter which camp ultimately ends up being right (I’m in the Morton camp, obviously). Studying the causes and effects of why we have such strong biases can lead to a better understanding of the causes of these underlying defense mechanisms—the causes of the backfire effect and similar cognitive biases. Everyone and anyone—from the scientist to the layman—should always let what the facts say guide their points of view and not their emotions.
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
by Scott Jameson
RaceRealist and I have been ruminating on a lot of stuff lately. Here’s a fun one: what economic system works best relative to what we know about human health? In my mind there are two approaches: the libertarian approach, and quasi-fascism.
In the libertarian approach, there’s no regulation of sugar placed in our food. That’s already the case. But here’s an improvement: you don’t have to pay for anyone’s gastric bypass after they overeat that sugar.
In the fascist approach, there is regulation of sugar, because a fascist state does not allow people to poison each other for profit. You still have to pay for others’ medical expenses, but those expenses will be lower.
Here’s an advantage to the libertarian approach. In that society, the people who stuff their faces and refuse to get off the couch- who are dumber and lazier on average, probably- will have a higher mortality rate on average. Eugenics need not cost a dime.
But you run into a snag, sand in the gears of your hands-off system, when Big Food kicks out a whole bunch of crappy dietary advice, at which point a minority of reasonably intelligent people will be led astray, perhaps to the grave. How could a libertarian society stop that from taking place? Would it even bother? Could the system broadly work in spite of this snag?
A libertarian society doesn’t pay for idiots to have children. That’s good, but half of your population (women) are unlikely to ever support it. Women don’t do libertarianism; observe Rand Paul’s demographic Achilles Heel on page 25. When women asked men what to do about so-and-so’s eighth unpaid for child, we’d have to look them in the eyes and give a deadpan “let’s hope private charity can handle it.” There was a time, before FDR, when women would’ve accepted that answer. They were still in the kitchen back then, and I don’t know how to put them back there.
A fascist society has more hands-on eugenics, possibly genome editing or embryo selection. Also good. Expensive, but obviously worth it.
We welcome your input on these issues.
As an aside, White men are well-known as the most conservative, small government, nationalist group out there in our current political atmosphere. I always hear people spewing the schmaltziest nonsense about the values of the Founding Fathers. They were, relative to our political compass, nationalist libertarians. Accordingly, modern nationalists and libertarians do best with the exact same demographics that used to vote on candidates back then: property-owning White men. The sole reason that Ron and Rand Paul couldn’t get elected is that they are too similar to the Founding Fathers. Any other candidate who blathers on about the Founding values is simply a liar, and their obvious lies show a disrespect of your intelligence.
If you’re a libertarian, but not an ethno-nationalistic and patriarchal thinker, then you simply haven’t gotten the memo: women and minorities do not want to create the same world that you do, nor will they ever. Evolution gave us women who want social safety nets and other races which are better off if they parasitize off of your tax dollars. All of the most libertarian societies that ever existed (early US, ancient Athens, Roman Republic) were entirely run by White men, and adding women to the electorate gave us the welfare state. Aristophanes was right.
We’re also ruminating on the difference between IQ and expertise. I know of no mentally complicated task of which one can be a master without being intelligent. Take the IQs of chess grandmasters and you will find no morons.
Contrast that with purely physical activities. I bet you there are some really stupid people out there who are great at dancing for example. A prodigiously capable cerebellum may not predict an equally capable frontal lobe.
Discounting tasks which exclusively require things like simple physical coordination, muscle memory, etc, I ought to think that IQ is the biggest component of expertise.
Back in October, I wrote that floresiensis is either descended from Erectus or habilis, since those were the only two hominins in the region. Yesterday a study was published titled The affinities of Homo floresiensis based on phylogenetic analyses of cranial, dental, and postcranial characters (Argue et al, 2017), in which Argue et al argue that floresiensis was not descended from a shipwrecked Erectus, as is a popular view. Another theory is that floresiensis is descended from habilis. The third theory is that floresiensis is Homo sapiens with a pathology, but that has been disproven (Falk et al, 2009). It was commonly thought that the LB1 floresiensis specimen was a pathological human inflicted with Laron syndrome which is a type of growth hormone deficiency (Laron and Klinger, 1994).
Argue et al found that floresiensis and erectus had completely different bone structures, particularly in the pelvis and jaw. They now believe that the theory that floresiensis is a derived form of an erectus that swam or rafted to Flores has been defintively refuted. They found that floresiensis was a sister species to habilis. So either a common ancestor of floresiensis or habilis swam to Flores from Africa, or floresiensis evolved in Africa and swam to Flores. They used new phylogenetic techniques to ascertain that floresiensis is stil a part of our lineage, but shows no phylogenetic relationship to erectus on the tree.
According to Baab (2016), biogeography shows that Indonesian erectus is the best fit with what is currently known. She says if floresiensis was derived from erectus that it “implies some degree of body size reduction and more marked brain size reduction.”
Kubo, Kono, and Kaifu (2013) conclude that the evolution of floresiensis from early Javanese erectus is possible when comparing the brain cases of both specimens. However, if floresiensis descended from habilis, then the brain size reduction wouldn’t be as marked (and is still due to island dwarfism, just not on as large of a scale as it would be if floresiensis were descended from erectus). The LB1 specimen also shows the closest neural affinities to early Asian erectus (Baab, Mcnulty, and Harvati, 2013; but see Vannuci, Barron, and Holloway, 2013 for the microcephalic view). Weston and Lister, (2009) showed that there was a 30 percent reduction in brain size in Magalasy hippos, which lends credence to the insular dwarfism hypothesis for floresiensis. Craniofacial morphology also shows that floresiensis evolved from Asian erectus (Kaifu et al, 2011).
The teeth of unknown hominin found at Mata Menge are intermediate between floresiensis and erectus, being 600,000 years older than where floresiensis was found (van den Bergh et al, 2016). This lends credence to the hypothesis that floresiensis is derived from erectus. Furthermore, insular dwarfism is seen in primate species isolated on islands, with changes in body size seen in child populations even on large islands not far from the mainland (Bromham and Cardillo, 2007, Welch, 2009). Genetically isolated on islands, primates can become bigger if the parent population was smaller, or smaller if the parent population was bigger. This is due to differing energy demands relative to the parent population, along with differing predators/prey.
The island rule even holds in the deep sea. As is the case with islands, the deep sea is also associated with decreased food availability. Looking at several species of gastropods, McClain, Boyer, and Rosenberg (2006) found that the island rule held in small-bodied shallow species. They were found to have larger bodied deep-sea representatives, with the same being true for large bodied deep-sea gastropods. Further, island dwarfism in elephants on the islands Sicily, Malta, Cyprus; mammoths on the California channel islands; and red deer on the island Jersey involved body mass changes of 5- to 100-fold over 2,300 to 120,000 generations (Evans et al, 2012).
So the overall hypothesis that island dwarfism is still intact, albeit if floresiensis is derived from habilis, the reduction in brain/body size would be smaller than if floresiensis evolved from early Asian erectus.
Further evidence for brain/body size reduction due to less food availability is noted by Daniel Lieberman in his book The Story of the Human Body: Evolution, Health, and Disease (Lieberman, 2013). While talking about the evolution of floresiensis on page 123 he writes:
The same energetic constraints and processes also affect hunter-gatherers . 62
And in the 62nd footnote on page 391 he writes:
Several human “pygmy” populations (people whose height does not exceed 150 centimeters, or 4.9 feet) have evolved in energy limited places like rain forests or islands. Perhaps the small size of the Dmansi hominins from Georgia also reflected selection to save energy among the first colonists of Eurasia.
Either way, if floresiensis evolved from erectus or habilis, considerable reductions in brain size have to be explained, since the smallest erectus brain ever found is 600 cubic centimeters while the smallest habilis brain ever found is 510 cubic centimeters (Lieberman, 2013: 124), with floresiensis having a brain 417 cubic centimeters (Falk et al, 2007).
What is most important about the insular dwarfism hypothesis in regards to the evolution of floresiensis is the effect of energy reduction/food availability and quality in regards to populations isolated on islands from parent populations. Floresiensis was able to survive on about 1200 kcal by shrinking, needing to consume about 1400 kcal during lactation compared to 1800 kcal for an erectus female who needed about 2500 kcal during lactation (Lieberman, 2013: 125). The cognitive price for the reduction in the brain size of floresiensis is not known, but since brains are so energy expensive (Aiello and Wheeler, 1995; Herculano-Houzel and Kaas, 2011; Fonseca-Azevedo and Herculano-Houzel, 2012), the reduction seen in floresiensis is no surprise.
Energy is one of the most important drivers for the evolution of a species, the evolution of floresiensis is one major example of this. Whether floresiensis evolved from habilis or erectus, reduced energy on the island caused the brain and body size of floresiensis to get smaller to cope with fewer things to eat. Keep in mind that habilis was a meat-eater as well, and with lower-quality energy on the island, the brain would have to reduce in size as it’s one of the most expensive organs in the body. As I’ve been saying for a long time now, the quality of energy is most important to the evolution of a species—especially Man. Cooking was imperative to our evolution, and with a lower-quality diet, we, too, would evolve smaller brains and bodies to compensate for reduced energy consumption since our brains take 25 percent of our daily energy requirements to power despite being 2 percent of our overall body weight.
The evolution of floresiensis shows how important energy is in the evolution of species. Its biggest implication—no matter if floresiensis evolved from habilis or erectus—is how important diet quality is to evolution, as I’ve noted here, here, here, here, here, and here. Without our high-quality diet, we, too, would suffer the same body/brain size reductions that floresiensis did.
Aiello, L. C., & Wheeler, P. (1995). The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human and Primate Evolution. Current Anthropology,36(2), 199-221. doi:10.1086/204350
Argue, D., Groves, C. P., Lee, M. S., & Jungers, W. L. (2017). The affinities of Homo floresiensis based on phylogenetic analyses of cranial, dental, and postcranial characters. Journal of Human Evolution. doi:10.1016/j.jhevol.2017.02.006
Baab, K. L., Mcnulty, K. P., & Harvati, K. (2013). Homo floresiensis Contextualized: A Geometric Morphometric Comparative Analysis of Fossil and Pathological Human Samples. PLoS ONE,8(7). doi:10.1371/journal.pone.0069119
Baab, K.L. (2016). The place of Homo floresiensis in human evolution. Journal of Anthropological Sciences, 94, 5-18.
Bergh, G. D., Kaifu, Y., Kurniawan, I., Kono, R. T., Brumm, A., Setiyabudi, E., . . . Morwood, M. J. (2016). Homo floresiensis-like fossils from the early Middle Pleistocene of Flores. Nature,534(7606), 245-248. doi:10.1038/nature17999
Bromham, L., & Cardillo, M. (2007). Primates follow the ‘island rule’: implications for interpreting Homo floresiensis. Biology Letters,3(4), 398-400. doi:10.1098/rsbl.2007.0113
Evans AR, Jones D, Boyer AG, Brown JH, Costa DP, et al. (2012) The maximum rate of mammal evolution. Proc Natl Acad Sci USA 109: 4187–4190.
Falk, D., Hildebolt, C., Smith, K., Morwood, M. J., Sutikna, T., Jatmiko, … Prior, F. (2007). Brain shape in human microcephalics and Homo floresiensis. Proceedings of the National Academy of Sciences of the United States of America, 104(7), 2513–2518. http://doi.org/10.1073/pnas.0609185104
Falk, D., Hildebolt, C., Smith, K., Jungers, W., Larson, S., Morwood, M., . . . Prior, F. (2009). The type specimen (LB1) of Homo floresiensis did not have Laron Syndrome. American Journal of Physical Anthropology,140(1), 52-63. doi:10.1002/ajpa.21035
Fonseca-Azevedo, K., & Herculano-Houzel, S. (2012). Metabolic constraint imposes tradeoff between body size and number of brain neurons in human evolution. Proceedings of the National Academy of Sciences,109(45), 18571-18576. doi:10.1073/pnas.1206390109
Herculano-Houzel, S., & Kaas, J. H. (2011). Gorilla and Orangutan Brains Conform to the Primate Cellular Scaling Rules: Implications for Human Evolution. Brain, Behavior and Evolution, 77(1), 33–44. http://doi.org/10.1159/000322729
Kaifu, Y., Baba, H., Sutikna, T., Morwood, M. J., Kubo, D., Saptomo, E. W., . . . Djubiantono, T. (2011). Craniofacial morphology of Homo floresiensis: Description, taxonomic affinities, and evolutionary implication. Journal of Human Evolution,61(6), 644-682. doi:10.1016/j.jhevol.2011.08.008
Kubo, D., Kono, R. T., & Kaifu, Y. (2013). Brain size of Homo floresiensis and its evolutionary implications. Proceedings of the Royal Society B: Biological Sciences,280(1760), 20130338-20130338. doi:10.1098/rspb.2013.0338
Laron, Z., & Klinger, B. (1994). Laron Syndrome: Clinical Features, Molecular Pathology and Treatment. Hormone Research,42(4-5), 198-202. doi:10.1159/00018419
Lieberman, D. (2013). The Story of the human body – evolution, health and disease. Penguin.
Mcclain, C. R., Boyer, A. G., & Rosenberg, G. (2006). The island rule and the evolution of body size in the deep sea. Journal of Biogeography,33(9), 1578-1584. doi:10.1111/j.1365-2699.2006.01545.x
Vannucci, R. C., Barron, T. F., & Holloway, R. L. (2011). Craniometric ratios of microcephaly and LB1, Homo floresiensis, using MRI and endocasts. Proceedings of the National Academy of Sciences of the United States of America, 108(34), 14043–14048. http://doi.org/10.1073/pnas.1105585108
Welch, J. J. (2009). Testing the island rule: primates as a case study. Proceedings of the Royal Society B: Biological Sciences,276(1657), 675-682. doi:10.1098/rspb.2008.1180
Weston, E. M., & Lister, A. M. (2009). Insular dwarfism in hippos and a model for brain size reduction in Homo floresiensis. Nature, 459(7243), 85–88. http://doi.org/10.1038/nature07922
Misinformation about testosterone and strength in regards to race is rampant in the HBD-o-sphere. One of the most oft-repeated phrases is that “Blacks have higher levels of testosterone than whites”, even after controlling for numerous confounds. However, the people who believe this literally only cite one singular study with 50 blacks and 50 whites. Looking at more robust data with higher ns shows a completely different story. Tonight I will, again, go through the race/testosterone conundrum (again).
Type I fibers fire first when heavy lifting. Whites have more type I fibers. Powerlifters and Olympic lifters have a greater amount type IIa fibers, with fewer type IIx fibers (like whites). This explains why blacks are hardly represented in powerlifting and strongman competitions.
Somatype, too, also plays a role. Whites are more endo than blacks who are more meso. Endomorphic individuals are stronger, on average, than mesomorphic and ectomorphic individuals.
Blacks have narrower hips and pelves. This morphological trait further explains why blacks dominate sports. Some people may attempt to pick out one variable that I speak about (fiber type, morphology, somatype, fat mass, etc) and attempt to disprove it, thinking that disproving that variable will discredit my whole argument. However, fiber typing is set by the second trimester, with no change in fiber type from age 6 to adulthood (Bell et al, 1980).
It is commonly believed that blacks have higher levels of testosterone than whites. However, this claim is literally based off of one study (Ross et al, 1986) when other studies have shown low to no difference in T levels (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Richard et al 2014). People who still push the “blacks-have-higher-T-card” in the face of this evidence are, clearly, ideologues who want to cushion their beliefs when presented with contradictory evidence (Nyhan and Reifler, 2010).
‘Honor Culture’ and testosterone
In all of my articles on this subject, I have stated—extensively—that testosterone is mediated by the environment. That is, certain social situations can increase testosterone. This is a viewpoint that I’ve emphatically stated. I came across a paper while back that talks about a sociological perspective (I have huge problems with social ‘science’, [more on that soon] but this study was very well done) in regards to the testosterone difference between blacks and whites.
Some people when they read this, however, may go immediately to the part of the paper that says what they want it to say without fully assessing the paper. In this section, I will explain the paper and how it confirms my assertions/arguments.
Mazur (2016) begins the paper talking about ‘honor culture‘, which is a culture where people avoid intentionally offending others while also maintaining a status for not backing down from a confrontation. This theory was proposed by Richard Nisbett in 1993 to explain why the South had higher rates of violence—particularly the Scotch-Irish.
However parsimonious the theory may sound, despite its outstanding explanatory power, it doesn’t hold while analyzing white male homicides in the South. It also doesn’t hold analyzing within-county homicide rates either, since apparently poverty better explains higher homicide rates.
But let’s assume it’s true for blacks. Let’s assume the contention to be true that there is an ‘honor culture’ that people take part in.
Young black men with no education had higher levels of testosterone than educated whites and blacks. Looking at this at face value—literally going right to the section of the paper that says that poor blacks had higher testosterone, nearly 100 ng/ml higher than the mean testosterone of whites. As Mazur (2016) notes, this contradicts his earlier 2009 study in which he found no difference in testosterone between the races.
Note the low testosterone for both races at age 20-29—ranging from about 515 to 425—why such low testosterone levels for young men? Anyway, the cause for the higher levels is due to the type of honor culture that blacks participate in, according to Mazur (which is consistent with the data showing that testosterone rises during conflict/aggressive situations).
Mazur cites Elijah Anderson, saying that most youths have a “code of the streets” they take part in, which have to do with interpersonal communication such as “gait and verbal expressions” to deter aggressive behavior.
Testosterone is not a causal variable in regards to violent behavior. But it does rise during conflicts with others, watching a favorite sports team, asserting dominance, and even how you carry yourself (especially your posture). Since low-class blacks participate in these types of behaviors, then they would have higher levels of testosterone due to needing to “keep their status.”
When testosterone rises in these situations, it increases the response threat in mens’ brains, most notably showing increased activity in the amygdala. Further, dominant behavior and posture also increase testosterone levels. Putting this all together, since blacks with only a high school education have higher testosterone levels and are more likely to participate in honor culture compared to whites and blacks with higher educational achievement, then they would have higher testosterone levels than whites and blacks with a high school education who do not participate in honor culture.
Further, as contrary to what I have written in the past (and have since rescinded), there is no indication of higher testosterone levels in black women with low education. It seems this ‘honor culture’ effect on testosterone only holds for black men with only a high school education.
Mazur’s (2016) most significant finding was that black men aged 20-29 with only a high school education had 91 ng/ml higher testosterone than whites. Among older and/or educated men, testosterone did not vary. This indicates that since they have attained higher levels of educational success, there is no need to participate in ‘honor culture’.
This is yet further evidence for my assertion that environmental variables such as posture, dominance, and aggressive behavior raise testosterone levels.
The honor culture hypothesis is found to hold in Brazil in a comparative study of 160 inmates and non-inmates (De Souza et al, 2016). As Mazur (2016) notes, the honor culture hypothesis could explain the high murder rate for black Americans—the need to ‘keep their status’. It’s important to note that this increase in testosterone was not noticed in teenage or female blacks (because they don’t participate in honor culture).
There is a perfectly good environmental—not genetic—reason for this increase in testosterone in young blacks with only a high school education. Now that we know this, back to race and strength.
Mazur (2009) found that black men in the age range of 20-69, they averaged .39 ng/ml higher testosterone than whites, which is partly explained by lower marriage rates and low adiposity. White men are more likely to be obese than black men, since black men with more African ancestry are less likely to be obese. When controlling for BMI, blacks are found to have 2.5-4.9 percent more testosterone than whites (Gapstur et al, 2002, Rohrmann et al, 2007, Richard et al, 2014). There is little evidence for the assertion that blacks have higher levels of testosterone without environmental triggers.
Blacks between the age of 12 and 15 average lower levels of testosterone than whites. However, after the age of 15, “testosterone levels increase rapidly” with blacks having higher peak levels than whites (seen in table 2 below). After adjusting for the usual confounds (BMI, smoking, age, physical activity, and waist circumference), blacks still had higher levels of testosterone—which is attributed to higher levels of lean mass.
As seen above in table 2 from Hu et al (2014), the difference in total testosterone between blacks and whites aged 20-39 was 6.29 ng/ml and 5.04 ng/ml respectively, with free testosterone for whites being 11.50 and 13.56 for blacks and finally bioavailable testosterone for whites and blacks aged 20-39 was 281.23 and 327.18 ng/ml respectively. These small differences in testosterone cannot account for racial disparities in violence nor prostate cancer—since there is no relationship between prostate cancer and testosterone (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).
In regards to Africans, the best studies I can find comparing some African countries with the West study salivary testosterone. However, there is a direct correlation between salivary testosterone and free serum testosterone (Wang et al, 1981; Johnson, Joplin, and Burrin, 1987). Of the studies I could find, Kenyan pastoralists called the Ariaal have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Campbell, Gray, and Ellison, 2006) while men in Zimbabwe had levels “much lower” compared to Western populations (Lukas, Campbell, and Ellison, 2004). Lastly, among men aged 15 to 30, salivary testosterone levels in an American sample was 335 pmol//l compared to 286 pmol/l in men from the Congo (Elisson et al, 2002). Even certain African populations don’t have higher testosterone levels than Western peoples.
The meme that blacks have higher rates of testosterone in comparison to whites needs to be put to rest. This is only seen in blacks who participate in ‘honor culture’, which is an environmental variable. This is in contrast to people who believe that it is genetic in nature—environmental variables can and do drive hormones. Mazur (2016) is proof of that. Mazur (2016) also shows that the honor culture hypothesis doesn’t hold for teens or black males—so they don’t have elevated levels of testosterone. Certain studies of African populations, however, do not show higher levels of testosterone than Western populations.
Looking at the complete literature—rather than a select few studies— we can see that testosterone levels between white and black Americans are not as high as is commonly stated (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Hu et al, 2014; Richard et al, 2014). Further, even if blacks did have higher levels of testosterone than whites—across the board (sans honor culture), it still wouldn’t explain higher rates of black violence when compared to whites, nor would it explain higher prostate cancer rates (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).
Only blacks with low educational achievement have higher levels of testosterone—which, even then is not enough to explain higher rates of violence or prostate cancer acquisition. Other factors explain the higher murder rate (i.e., honor culture, which increases testosterone, the environmental trigger matters first and foremost) and violent crime that blacks commit. But attempting to explain it with 30-year-old studies (Ross et al, 1986) and studies that show that environmental factors increase testosterone (Mazur, 2016) don’t lend credence to that hypothesis.
Bell, R. D., Macdougall, J. D., Billeter, R., & Howald, H. (1980). Muscle fiber types and morphometric analysis of skeletal muscle in six-year-old children. Medicine & Science in Sports & Exercise,12(1). doi:10.1249/00005768-198021000-00007
Campbell, B., O’rourke, M. T., & Lipson, S. F. (2003). Salivary testosterone and body composition among Ariaal males. American Journal of Human Biology,15(5), 697-708. doi:10.1002/ajhb.10203
Campbell, B. C., Gray, P. B., & Ellison, P. T. (2006). Age-related patterns of body composition and salivary testosterone among Ariaal men of Northern Kenya. Aging Clinical and Experimental Research,18(6), 470-476. doi:10.1007/bf03324846
De Souza, Souza, B. C., Bilsky, W., & Roazzi, A. (2016). The culture of honor as the best explanation for the high rates of criminal homicide in Pernambuco: A comparative study with 160 convicts and non-convicts. Anuario de Psicología Jurídica,26(1), 114-121. doi:10.1016/j.apj.2015.03.001
Ellison, P. T., Bribiescas, R. G., Bentley, G. R., Campbell, B. C., Lipson, S. F., Panter-Brick, C., & Hill, K. (2002). Population variation in age-related decline in male salivary testosterone. Human Reproduction,17(12), 3251-3253. doi:10.1093/humrep/17.12.3251
Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race—the CARDIA male hormone study. Cancer Epidemiol Biomarkers Prev 2002; 11: 1041–7, , , , , .
Hu, H., Odedina, F. T., Reams, R. R., Lissaker, C. T., & Xu, X. (2014). Racial Differences in Age-Related Variations of Testosterone Levels Among US Males: Potential Implications for Prostate Cancer and Personalized Medication. Journal of Racial and Ethnic Health Disparities,2(1), 69-76. doi:10.1007/s40615-014-0049-8
Johnson, S. G., Joplin, G. F., & Burrin, J. M. (1987). Direct assay for testosterone in saliva: Relationship with a direct serum free testosterone assay. Clinica Chimica Acta,163(3), 309-318. doi:10.1016/0009-8981(87)90249-x
Lopez, D. S., Peskoe, S. B., Joshu, C. E., Dobs, A., Feinleib, M., Kanarek, N., . . . Platz, E. A. (2013). Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males. Cancer Causes & Control,24(4), 817-826. doi:10.1007/s10552-013-0154-8
Lukas, W. D., Campbell, B. C., & Ellison, P. T. (2004). Testosterone, aging, and body composition in men from Harare, Zimbabwe. American Journal of Human Biology,16(6), 704-712. doi:10.1002/ajhb.20083
Mazur, A. (2009). The age-testosterone relationship in black, white, and Mexican-American men, and reasons for ethnic differences. The Aging Male,12(2-3), 66-76. doi:10.1080/13685530903071802
Mazur, A. (2016). Testosterone Is High among Young Black Men with Little Education. Frontiers in Sociology,1. doi:10.3389/fsoc.2016.00001
Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633
Nyhan, B., & Reifler, J. (2010). When Corrections Fail: The Persistence of Political Misperceptions. Political Behavior,32(2), 303-330. doi:10.1007/s11109-010-9112-2
Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x
Richards, R. J., Svec, F., Bao, W., Srinivasan, S. R., & Berenson, G. S. (1992). Steroid hormones during puberty: racial (black-white) differences in androstenedione and estradiol–the Bogalusa Heart Study. The Journal of Clinical Endocrinology & Metabolism,75(2), 624-631. doi:10.1210/jcem.75.2.1639961
Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028
Ross R, Bernstein L, Judd H, Hanisch R, Pike M, Henderson B. Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst. 1986 Jan;76(1):45–48
Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572
Wang, C., Plymate, S., Nieschlag, E., & Paulsen, C. A. (1981). Salivary Testosterone in Men: Further Evidence of a Direct Correlation with Free Serum Testosterone. The Journal of Clinical Endocrinology & Metabolism,53(5), 1021-1024. doi:10.1210/jcem-53-5-1021