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I Am Not A Phrenologist

1500 words

People seem to be confused on the definition of the term ‘phrenology’. Many people think that just the measuring of skulls can be called ‘phrenology’. This is a very confused view to hold.

Phrenology is the study of the shape and size of the skull and then drawing conclusions from one’s character from bumps on the skull (Simpson, 2005) to overall different-sized areas of the brain compared to others then drawing on one’s character and psychology from these measures. Franz Gall—the father of phrenology—believed that by measuring one’s skull and the bumps etc on it, then he could make accurate predictions about their character and mental psychology. Gall had also proposed a theory of mind and brain (Eling, Finger, and Whitaker, 2017). The usefulness of phrenology aside, the creator Gall contributed a significant understanding to our study of the brain, being that he was a neuroanatomist and physiologist.

Gall’s views on the brain can be seen here (read this letter where he espouses his views here):

1.The brain is the organ of the mind.
2. The mind is composed of multiple, distinct, innate faculties.
3. Because they are distinct, each faculty must have a separate seat or “organ” in the brain.
4. The size of an organ, other things being equal, is a measure of its power.
5. The shape of the brain is determined by the development of the various organs.
6. As the skull takes its shape from the brain, the surface of the skull can be read as an accurate index of psychological aptitudes and tendencies.

Gall’s work, though, was imperative to our understanding of the brain and he was a pioneer in the inner workings of the brain. They ‘phrenologized’ by running the tips of their fingers or their hands along the top of one’s head (Gall liked using his palms). Here is an account of one individual reminiscing on this (around 1870):

The fellow proceeded to measure my head from the forehead to the back, and from one ear to the other, and then he pressed his hands upon the protuberances carefully and called them by name. He felt my pulse, looked carefully at my complexion and defined it, and then retired to make his calculations in order to reveal my destiny. I awaited his return with some anxiety, for I really attached some importance to what his statement would be; for I had been told that he had great success in that sort of work and that his conclusion would be valuable to me. Directly he returned with a piece of paper in his hand, and his statement was short. It was to the effect that my head was of the tenth magnitude with phyloprogenitiveness morbidly developed; that the essential faculties of mentality were singularly deficient; that my contour antagonized all the established rules of phrenology, and that upon the whole I was better adapted to the quietude of rural life rather than to the habit of letters. Then the boys clapped their hands and laughed lustily, but there was nothing of laughter in it for me. In fact, I took seriously what Rutherford had said and thought the fellow meant it all. He showed me a phrenological bust, with the faculties all located and labeled, representing a perfect human head, and mine did not look like that one. I had never dreamed that the size or shape of the head had anything to do with a boy’s endowments or his ability to accomplish results, to say nothing of his quality and texture of brain matter. I went to my shack rather dejected. I took a small hand- mirror and looked carefully at my head, ran my hands over it and realized that it did not resemble, in any sense, the bust that I had observed. The more I thought of the affair the worse I felt. If my head was defective there was no remedy, and what could I do? The next day I quietly went to the library and carefully looked at the heads of pictures of Webster, Clay, Calhoun, Napoleon, Alexander Stephens and various other great men. Their pictures were all there in histories.

This—what I would call skull/brain-size fetishizing—is still evident today, with people thinking that raw size matters (Rushton and Ankney, 2007; Rushton and Ankney, 2009) for cognitive ability, though I have compiled numerous data that shows that we can have smaller brains and have IQs in the normal range, implying that large brains are not needed for high IQs (Skoyles, 1999). It is also one of Deacon’s (1990) fallacies, the “bigger-is-smarter” fallacy. Just because you observe skull sizes, brain size differences, structural brain differences, etc, does not mean you’re a phrenologist. you’re making easy and verifiable claims, not like some of the outrageous claims made by phrenologists.

What did they get right? Well, phrenologists stated that the most-used part of the brain would become bigger, which, of course, was vindicated by modern research—specifically in London cab drivers (McGuire, Frackowiak, and Frith, 1997; Woolett and McGuire, 2011).

It seems that phrenologists got a few things right but their theories were largely wrong. Though those who bash the ‘science’ of phrenology should realize that phrenology was one of the first brain ‘sciences’ and so I believe phrenology should at least get some respect since it furthered our understanding of the brain and some phrenologists were kind of right.

People see the avatar I use which is three skulls, one Mongoloid, the other Negroid and the other Caucasoid and then automatically make that leap that I’m a phrenologist based just on that picture. Even, to these people, stating that races/individuals/ethnies have different skull and brain sizes caused them to state that what I was saying is phrenology. No, it isn’t. Words have definitions. Just because you observe size differences between brains of, say either individuals or ethnies, doesn’t mean that you’re making any value judgments on the character/mental aptitude of that individual based on the size of theur skull/brain. On the other hand, noting structural differences between brains like saying “the PFC is larger here but the OFC is larger in this brain than in that brain” yet no one is saying that and if that’s what you grasp from just the statement that individuals and groups have different sized skulls, brains, and parts of the brain then I don’t know what to tell you. Stating that one brain weighs more than another, say one is 1200 g and another is 1400 g is not phrenology. Stating that one brain is 1450 cc while another is 1000 cc is not phrenology. For it to be phrenology I have to outright state that differences in the size of certain areas of the brain or brains as a whole cause differences in character/mental faculties. I am not saying that.

A team of neuroscientists just recently (recently as in last month, January, 2018) showed, in the “most exhaustive way possible“, tested the claims from phrenological ‘research’ “that measuring the contour of the head provides a reliable method for inferring mental capacities” and concluded that there was “no evidence for this claim” (Jones, Alfaro-Almagro, and Jbabdi, 2018). That settles it. The ‘science’ is dead.

It’s so simple: you notice physical differences in brain size between two corpses. That one’s PFC was bigger than OFC and with the other, his OFC was bigger than his PFC. That’s it. I guess, using this logic, neuroanatomists would be considered phrenologists today since they note size differences between individual parts of brains. Just noting these differences doesn’t make any type of judgments on potential between brains of individuals with different size/overall size/bumps etc.

It is ridiculous to accuse someone of being a ‘phrenologist’ in 2018. And while the study of skull/brain sizes back in the 17th century did pave the way for modern neuroscience and while they did get a few things right, they were largely wrong. No, you cannot see one’s character from feeling the bumps on their skull. I understand the logic and, back then, it would have made a lot of sense. But to claim that one is a phrenologist or is pushing phrenology just because they notice physical differences that are empirically verifiable does not make them a phrenologist.

In sum, studying physical differences is interesting and tells us a lot about our past and maybe even our future. Stating that one is a phrenologist because they observe and accept physical differences in the size of the brain, skull, and neuroanatomic regions is like saying that physical anthropologists and forensic scientists are phrenologists because they measure people’s skulls to ascertain certain things that may be known in their medical history. Chastizing someone because they tell you that one has a different brain size than the other by calling them outdated names in an attempt to discredit them doesn’t make sense. It seems that even some people cannot accept physical differences that are measurable again and again because it may go against some long-held belief.


You Don’t Need Genes to Delineate Race

2100 words

Most race deniers say that race isn’t real because, as Lewontin (1972) and Rosenberg (2002) state, the within-group variation is larger than the between-group variation. Though, you can circumvent this claim by not even looking at genes/allele frequencies between races, you can show that race is real by looking at morphology, phenotype and geographic ancestry. This is one of Michael Hardimon’s race categories, the minimalist concept of race. This concept does not entail anything that we cannot physically ‘see’ with our eyes (e.g., mental and psychological traits are off the table). Using these concepts laid out by Hardimon can and does prove that race is real and useful without even arguing about any potential mental and psychological differences between human races.


Morphology is one of the most simple tells for racial classification. Just by looking at average morphology between the races we can use attempt to use this data point as a premise in the argument that races exist.

East Asians are shorter with shorter limbs and have an endomorphic somatype. This is due to evolving in cold climate, as a smaller body and less surface area can be warmer much quicker than a larger body. This is a great example of Allen’s rule: that animals in colder climates will be smaller than animals in warmer climates. Using average morphology, of course, can show how the population in question evolved and where they evolved.

Regarding Europeans, they have an endomorphic somatype as well. This, again, is due to where they evolved. Morphology can tell us a lot about the evolution of a species. Though, East Asians and Europeans have similar morphologies due to evolving in similar climates. Like East Asians, Europeans have a wider pelvis in comparison to Africans, so this is yet another morphological variable we can use to show that race exists.

Finally, the largest group is ‘Africans’ who have the largest phenotypic and genetic diversity on earth. Generally, you can say that they’re tall, have long limbs and a short torso, which is due to evolving in the tropics. Furthermore, and perhaps most important, Africans have narrower pelves than East Asians and Europeans. This character is one of the most important regarding the reality of race because it’s one of the most noticeable, and we do notice in when it comes to sports competition because that certain type of morphology is conducive to athletic success. (Also read my recent article on strength and race and my article on somatype and race for more information on morphologic racial differences.)


Morphology is a part of the phenotype too, obviously, but there is a reason why it’s separated. As is true with morphology, different characters evolved due to cultural evolution (whether or not they adopted farming early) or evolution through natural selection, drift and mutation. Though, of course, favorable mutations in a certain environment will be passed on and eventually become a part of the characteristics of the population in question.

East Asians have the epicanthic fold, which probably evolved to protect the eye from the elements and UV rays on the Mongolian steppes. They also have softer features than Europeans and Africans, but this is not due to lower testosterone as is popularly stated. (Amusingly enough, there is a paper that stated that East Asians have Down Syndrome-like qualities due to their epicanthic folds to bring up one reason.) Even then, what some races find attractive or not can show how and why certain facial phenotypes evolved. To quote Gau et al (2018):

Compared with White women, East Asian women prefer a small, delicate and less robust face, lower position of double eyelid, more obtuse nasofrontal angle, rounder nose tip, smaller tip projection and slightly more protruded mandibular profile.

And they conclude:

The average faces are different from the attractive faces, while attractive faces differ according to race. In other words, the average facial and aesthetic criteria are different. We should use the attractive faces of a race to study that races aesthetic criteria.

We can use studies such as this to discern different facial phenotypes, which, again, proves that race exists.

The climate one’s ancestors evolved in dictates nose shape. In areas where it is extremely dry and also has a lot of heat, a larger mucous area is required to moisten inspired (inhaled) air, which is why a more flat and narrow nose is needed.

Zaidi et al (2017) write:

We find that width of the nares is correlated with temperature and absolute humidity, but not with relative humidity. We conclude that some aspects of nose shape may have indeed been driven by local adaptation to climate.

Though climate, of course, isn’t the only reason for differences in nose shape; sexual selection plays a part too, as seen in the above citation on facial preferences in East Asian and European women.

There are also differences in hirsutism between the races. Racial differences exist regarding upper lip hair, along with within-race differences (Javorsky et al, 2014). The self-reported races of African American, East Asian, Asian Indian, and ‘Hispanic’ predicted facial hair differences in women, but not how light their skin was. The women were from Los Angeles, USA; Rome, Italy; Akita, Japan; and London, England. Indian women had more hair than any other race, while European women had the least. Regarding within-race variation, Italian women had more hair on their upper lip than American and British women. Skin lightness was related to hair on the upper lip. (Also read my article The Evolution of Human Skin Variation for more information on racial differences in skin color.)

In 2012, an interesting study was carried out on hair greying on a sample population of a large number of the world’s ethnies titled Greying of the human hair: a worldwide survey, revisiting the ‘50’ rule of thumbThe objective of the study was to test the ’50-50-50′ rule; that at age 50, 50 percent of the population has at least 50 percent of their hair grey. Africans and Asians showed fewer grey hairs than whites who showed the most. The results imply that hair greyness varies by ethnicity/geographic origin, which is perfect for the argument laid out in this article. The global range for people over 50 with 50 percent or more of their hair grey was between 6 and 23 percent, far lower than what was originally hypothesized (Panhard, Lozano, and Loussouarn, 2012). They write on page 870:

With regard to the intensity of hair greying, the lowest values were found among African and Asian groups, especially Thai and Chinese, whereas the highest values were in subjects with the blondest hair (Polish, Scottish, Russian, Danish, CaucasianAustralian and French).

Altogether, these analyses clearly illustrate that the lowest incidences and intensities of grey hair are found in populations of the darkest hair whereas the highest intensities are found in populations with the lightest hair tones.

grey hair pca

Actual hair diversity is much more concentrated in Europeans, however (Frost, 2005). (See Peter Frost’s article Why Do Europeans Have So Many Hair and Eye Colors?) It is largely due to sexual selection, with a few climatic factors thrown in. Dark hair, on the other hand, is a dominant trait, which is found all over the world.

Zhuang et al (2010) found significant differences in facial morphology between the races, writing:

African-Americans have statistically shorter, wider, and shallower noses than Caucasians. Hispanic workers have 14 facial features that are significantly larger than Caucasians, while their nose protrusion, height, and head length are significantly shorter. The other ethnic group was composed primarily of Asian subjects and has statistically different dimensions from Caucasians for 16 anthropometric values.

Statistically significant differences in facial anthropometric dimensions (P < 0.05) were noted between males and females, all racial/ethnic groups, and the subjects who were at least 45 years old when compared to workers between 18 and 29 years of age.

Blacks had statistically significant differences in lip and face length when compared to whites (whites had shorted lips than blacks who had longer lips than whites).

Brain size and cranial morphology, too, differs by geographic ancestry which is directly related to the climate where that population evolved (Beals, Smith, and Dodd, 1984). Most every trait that humans have—on average of course—differs by geographic location and the cause of this is evolution in these locations along with being a geographically isolated breeding population.

Geographic ancestry

The final piece to this argument is using where one’s recent ancestors came from. There are five major populations from a few geographic locales: Oceania, the Americas (‘Native Americans), Europe, Africa and East Asia. These geographic locales have peoples that evolved there and underwent different selective pressures due to their environment and their bodies evolved to better suit their environment, and so racial differences in morphology and phenotype occurred so the peoples could survive better in that location. No one part of this argument is more important than any other, though geographic ancestry is the final piece of the puzzle that brings everything together. Because race is correlated with morphology and phenotype, the geographic ancestry dictates what these characteristics look like.


Thus, this is the basic argument:

P1: Differing populations have differing phenotypes, including (but not limited to) facial structure, hair type/color, lip structure, skull size, brain size etc.

P2: Differing populations have differing morphology which, along with this population’s phenotype, evolved in response to climatic demands along with sexual selection.

P3: This population must originate from a distinct geographic location.

C: If all three of the above premises are true, then race—in the minimalist sense—exists and is biologically real.

This argument is extremely simple, and along with the papers cited above in support of the three premises and the ultimate conclusion, it will be extremely hard for race deniers to counter. We can say that P1 is logically sound because geographically isolated populations differ in the above-mentioned criteria. We can say that P2 is logically sound since differing populations have differing morphology (as I have discussed numerous times which leads to racial differences in sporting competition) such as differing trunk lengths, leg lengths, arm lengths and heights which are largely due to evolution in differing climates. We can say that P3 is logically sound because the populations that would satisfy P1 and P2 do come from geographically distinct locations; that is, they have a peculiar ancestry that they only share.

This concept of minimalist race from Michael Hardimon is (his) the racialist concept of race “stripped down to its barest bones” (Hardimon, 2017: 3). The minimalist concept of race, then, does not discuss any differences between populations that cannot be directly discerned with the naked eye. (Note: You can also use the above arguments/data laid out for the populationist concept of race, which, according to Hardimon (2017: 3) is: “A nonracialist (nonessentialist, nonhierarchical) candidate scientific concept that characterizes races as groups of populations belonging to biological lines of descent, distinguished by patterns of phenotypic differences, that trace back to geographically separated and extrinsically reproductively isolated founder populations.)

Minimalist race is biologically sound, grounded in genetics (though I have argued here that you don’t need genetics to define race), and is grounded in biology. Minimalist race is defined as characteristics of the group, not of the individual. Minimalist race are biologically real. Minimalist races exist because, as shown with the data presented in this article, phenotypic and morphologic traits are unevenly distributed throughout the world which then correlates with geographic ancestry. It cannot get any more simpler than that: race exists because differences in phenotype and morphology exist which then corresponds with geographic ancestry.

hardimon flow chart

From Hardimon (2017: 177)\

No sane or logical person would deny the existence of race based on the criteria laid out in this article. We can also make another leap in logic and state that since minimalist races exist and are biologically real then geographic ancestry should be a guide when dealing with medicine and different minimalist races.

It is clear that race exists in the minimal sense; you do not need genes to show that race is real, nor that race has any utility in a medical context. This is important for race deniers to understand: genes are irrelevant when talking about the reality of race; you only need to just use your eyes and you’ll see that certain morphologies and phenotypes are distributed across geographic locations. It is also very easy to get someone to admit that races exist in this minimalist-biological sense. No one denies the existence of Africans, Europeans, ‘Native’ Indians, East Asians and Pacific Islanders. These populations differ in morphology and other physical characters which are unevenly distributed by geographic ancestry, so, therefore: minimialist races exist and are a biological reality.

Microcephaly and Normal IQ

1400 words

In my last article on brain size and IQ, I showed how people with half of their brains removed and people with microcephaly can have IQs in the normal/above average range. There is a pretty large amount of data out there on microcephalics and normal intelligence—even a family showing normal intelligence in two generations despite having dominantly inherited microcephaly.

Microcephaly is a condition in which an individual has a head circumference of 2 SD below the mean. Though most would think that would doom all microcephalics to low IQs, 15 percent of microcephalics have IQs in the normal range. This is normally associated with mental retardation, but this is a medical myth (Skoyles and Sagan, 2002: 239), though there are numerous cases of microcephalics having normal IQs (Dorman, 1991). Numerous studies show that it’s possible for normal people to have small brains. Giedd et al (1996) showed a wide variation in head circumference. Of the 104 individuals who had their heads scanned, volume for the cerebellum ranged from 735 cc in a 10 year old boy to 1470 cc in a 14 year old boy (Skoyles, 1999: 4, para 12). Though Giedd et al (1996) did not report total brain volumes in their subjects, brain volume can be inferred. Skoyles (1999; 4, para 12) writes:

The cerebral cortex makes up only 86.4% of brain volume when measured by MRI (Filipek, Richelme, Kennedy & Caviness, 1994), so the total brain volume of the 10-year-old would be larger at 850.7 cc. Brains at 10 years are about 4.4% smaller than adult size (Dekaban & Sadowsky, 1978), suggesting that that brain would grow to an adult size of 888 cc. Even using the lower figure of 80% cerebrum to brain ratio derived from anatomical studies suggests a figure of only 960 cc.

The variation of 888 cc to 960 cc depending on which value for the cerebrum to brain ratio you use still shows that people can have brains 450-300 cc lower than average and still be ‘normal’.

Researchers began noticing many cases of both individuals and families exhibiting features of microcephaly—but they had normal intelligence (Simila, 1970;Seemanova et al, 1985; Rossi et al, 1987Teebi et al, 1987; Sherrif and Hegab, 1988Desch et al, 1990Opitz and Holt, 1990Evans, 1991; Heney et al, 1991Green et al, 1995Rizzo and Pavone, 1995; Teebi and Kurash, 1996; Innis et al, 1997Kawame, Pagon, and Hudgens, 1997Abdel-Salam et al, 1999Digweed, Reis, and Sperling, 1999Woods, Bond, and Enard, 2005; Ghaoufari-Fard et al, 2015). This is a pretty huge blow to the brain size/IQ correlation, for if people with such small heads can have normal IQs, why do we have such large brains that leave us with such large problems (Skoyles and Sagan, 2002: 240-244)?

If we can have smaller heads—which would make childbirth easier and allow us to continue to have smaller pelves which would be conducive to endurance running since we are the running ape, why would brains have gotten so much larger from that of erectus (where modern people can have normal IQs with erectus-sized brains) if it is perfectly possible to have a brain on around the size of early erectus? In any event, these anomalies need an explanation, and Skoyles (1999) hypothesizes that people with smaller heads but normal IQs may have a lower capacity for expertise. This is something that I will look into in the future, as it may explain these anomalies, along with the true reason why our brains began increasing around 3 mya.

Sells (1977)—using the criteria of 2 SD below mean head size—showed that 1.9 percent of the children he tested (n=1009) had IQs indistinguishable from their normocephalic peers. Watemberg et al (2002) studied 1,393 patients. They found that almost half of their patients with microcephaly  (15.4% of their patients studies had microcephaly) had IQs within the normal limits, while among those with sub-normal intelligence, 30 percent had borderline IQs or were mildly mentally retarded (it’s worth noting that l-glutamate can raise IQ scores by 5-20 points in the mild to moderate mental deficiency; Vogel, Braverman and Draguns, 1966 review numerous lines of evidence that glutamate raises IQ in mentally deficient individuals). Sassaman and Zartler (1982) showed that 31.9 percent of microcephalics had normal intelligence, 6.9 percent of them had average intelligence.

Head circumference does not directly correlate with IQ in microcephalic patients (Baxter et al, 2009). Dorman (1991: 268) writes: “Decreased head size may or may not be associated with lowered intelligence, indicating that small head size by itself does not affect intelligence. The presence of subgroups of microcephalic persons who typically have normal intelligence is sufficient to rule out a causal relationship between head size and intellect. … It can be added that reduction in brain size without such structural pathology, as mayvoccur in some genetic conditions or evenvas a result of normal variation, does not
affect intelligence. 

Tenconi et al (1981) write: “We were able to examine five other members of this family (1-3; 11-1; 11-4; 11-5; 11-8) and found no abnormalities: they were of normal intelligence, head circumference, and ophthalmic evaluation. Members of the grandmother’s family who refused to be examined appeared to be of normal intelligence and head appearance and did not have any serious eye problems.

Stoler-Poria et al (2010) write: “There was a K-ABC cognitive score < 85 (signifying developmental delay) in two (10%) children from the study group and in one (5%) child from the control group: one of the children in the study group (the one with HC below − 3 SD) scored significantly below the normal range (IQ = 70), while the other scored in the borderline range (IQ = 83); the child from the control group also scored in the borderline range (IQ = 84).” Whereas Thelander and Pryor (1968) showed that individuals with head circumferences 2-2.6 SDs below the mean had average IQs, though the smaller their HC, the lower their IQ. Ashwal et al (2009: 891) write: “The students with microcephaly had a similar mean IQ to the normocephalic group (99.5 vs 105) but had lower mean academic achievement scores (49 vs 70).” So it seems that microcephalics can have normal IQs, but have lower academic achievement scores.

Primary microcephalics have higher IQs than secondary microcephalics (Cowie, 1987). Primary microcephaly is microcephaly that one is born with whereas secondary microcephaly is acquired.

There is one case study of a girl with microcephaly where Tan et al (2014) write: “Most recent measures of general intelligence (performed at 6½ years of age) reveal a below average full scale IQ of 75 with greatest impairment in processing speed. On the Wechsler Preschool and Primary Scale of Intelligence III Revised (for children 2 years 6 m – 7 years 3 m), she obtained a Verbal IQ of 83, Nonverbal IQ of 75, and Processing speed 71. On the Wechsler Individual Achievement Testing (WIAT) she showed significant struggles in secondary language on tasks of early reading (SS 60), word reading (SS 70), reading comprehension (SS 69) and struggles in math on the task of numerical operations (SS 61) (WPPSI – R and WIAT mean = 100 and SD = 15). Parents report subjectively that differences in development relative to her sisters are becoming more apparent with time.

It is not a foregone conclusion that if an individual has microcephaly that they will have a low IQ and be mentally retarded, as reviewed above, there are numerous cases of individuals with microcephaly and normal IQs, with this even being seen in families—that is, multiple families with normal IQs yet have microcephaly. Numerous people with Nijmegen breakage syndrome (a type of microcephaly) can have normal IQs. Rossi et al (1987) reported that for 6 Italian families (n=21 microcephalics) with autsomally inherited microcephaly, for those administered psychometric tests (n=12), all had normal IQs but one, with an IQ range of 99 to 112 for a mean of 99.3.

In conclusion, microcephalics can have normal IQs and live normal lives, despite having heads, on average, that are 2 SDs below the mean. These anomalies (and there are many, many more) need explaining. This is great evidence that a larger brain does not always mean a higher IQ, as well as yet more evidence that it was possible for Homo erectus to have an IQ in our range today, which means that we may not need brains our current size for our intellect and achievements. To conclude, I will provide a quote from Dorman (1991):

The normal intelligence found by SELLS in school children with small head size also militates against any straightforward relationship between diminished head size and lowered intelligence.

With the correlation between brain size and IQ being .4 (Gignac and Bates, 2017), this does not rule out the ‘outliers’ reviewed in this article. These cases deserve an explanation, for if large brains lead to high IQs, why do these people with heads significantly smaller have IQs in the normal range? (See Skoyles, 1999: 8, para 31 for an explanation for the brain size/IQ correlation.)

My Response to Jared Taylor’s Article “Breakthroughs in Intelligence”

1300 words

Here is my reply to Jared Taylor’s new article over at AmRen Breakthroughs in Intelligence:

“The human mind is not a blank slate; intelligence is biological”

The mind is not a ‘blank slate’, though there is no ‘biological’ basis for intelligence (at least in the way that hereditarians believe). They’re just correlations. (Whatever ‘intelligence’ is.)

“there is no known environmental intervention—including breast feeding”

There is a causal effect of breast feeding on IQ:

While reported associations of breastfeeding with child BP and BMI are likely to reflect residual confounding, breastfeeding may have causal effects on IQ. Comparing associations between populations with differing confounding structures can be used to improve causal inference in observational studies.

Brion, M. A., Lawlor, D. A., Matijasevich, A., Horta, B., Anselmi, L., Araújo, C. L., . . . Smith, G. D. (2011). What are the causal effects of breastfeeding on IQ, obesity and blood pressure? Evidence from comparing high-income with middle-income cohorts. International Journal of Epidemiology, 40(3), 670-680. doi:10.1093/ije/dyr020

Breastfeeding is related to improved performance in intelligence tests. A positive effect of breastfeeding on cognition was also observed in a randomised trial. This suggests that the association is causal.

Horta, B. L., Mola, C. L., & Victora, C. G. (2015). Breastfeeding and intelligence: a systematic review and meta-analysis. Acta Paediatrica, 104, 14-19. doi:10.1111/apa.13139

before long we should be able to change genes and the brain itself in order to raise intelligence.

Which genes? 84 percent of genes are expressed in the brain. Good luck ‘finding’ them…

These results corroborate with the results from previous studies, which have shown 84% of genes to be expressed in the adult human brain 

Negi, S. K., & Guda, C. (2017). Global gene expression profiling of healthy human brain and its application in studying neurological disorders. Scientific Reports, 7(1). doi:10.1038/s41598-017-00952-9

“Normal people can have extraordinary abilities. Prof. Haier writes about a non-savant who used memory techniques to memorize 67,890 digits of π! He also notes that chess grandmasters have an average IQ of 100; they seem to have a highly specialized ability that is different from normal intelligence. Prof. Haier asks whether we will eventually understand the brain well enough to endow anyone with special abilities of that kind.”

Evidence that intelligence is not related to expertise.

“It is only after a weight of evidence has been established that we should have any degree of confidence in a finding, and Prof. Haier issues another warning: “If the weight of evidence changes for any of the topics covered, I will change my mind, and so should you.” It is refreshing when scientists do science rather than sociology.”

Even with the “weight of evidence”, most people will not change their views on this matter.

“Once it became possible to take static and then real-time pictures of what is going on in the brain, a number of findings emerged. One is that intelligence appears to be related to both brain efficiency and structure”

Patterns of activation in response to various fluid reasoning tasks are diverse, and brain regions activated in response to ostensibly similar types of reasoning (inductive, deductive) appear to be closely associated with task content and context. The evidence is not consistent with the view that there is a unitary reasoning neural substrate. (p. 145)

Nisbett R. E., Aronson J., Blair C., Dickens W., Flynn J., Halpern D. F., Turkheimer E. Intelligence: New findings and theoretical developments. American Psychologist. 2012;67:130–159. doi: 10.1037/a0026699.

“Early findings suggested that smart people’s brains require less glucose—the main fuel for brain activity—than those of dullards.”

Cause and correlation aren’t untangled; they could be answering questions in a familiar format, for instance, and this could be why their brains show less glucose consumption.

“It now appears that grey matter is where “thinking” takes place, and white matter provides connections between different areas of grey matter. Some brains seem to be organized with shorter white-matter connections, which appear to allow more efficient communication, and there seem to be sex differences in the ways the part of the brain are connected. One of the effects of aging is deterioration of the white-matter connections, which reduces intelligence.”

Read this commentary (pg. 162): Norgate, S., & Richardson, K. (2007). On images from correlations. Behavioral and Brain Sciences, 30(02), 162. doi:10.1017/s0140525x07001379

“Brain damage never makes people smarter”

This is wrong:

You would think that cutting out one-half of people’s brains would kill them, or at least leave them vegetables needing care for the rest of their lives. But it does not. Consider this striking story. A boy starts having seizures at 10 years of age when his right cerebral hemisphere atrophies. By the time he is 12, the left side of his body is paralyzed. When he is 19, surgeons decide to operate and remove the right side of his brain, as it is causing gits in his intact left one. You might think this would lower his IQ or leave him severely retarded, but no. His IQ shoots up 14 points, to 142! The mystery is not so great when you realize that the operation has gotten rid of the source of his fits, which had previously hampered his intelligence. When doctors saw him 15 years later, they described him as “having obtained a university diploma . . . [and now holding] a responsible administrative position with a local authority.”

Skoyles, J. R., & Sagan, D. (2002). Up from dragons: the evolution of human intelligence. New York: McGraw-Hill (pg. 282)

“Prof. Haier wants a concerted effort: “What if a country ignored space exploration and announced its major scientific goal was to achieve the capability to increase every citizen’s g-factor [general intelligence] by a standard deviation?””

Don’t make me laugh. You need to prove that ‘g’ exists first. Glad to see some commentary on epigenetics that isn’t bashing it (it is a real phenomenon, though the scope of it in regards to health, disease and evolution remains to be discovered).

As most readers may know, I’m skeptical here and a huge contrarian. I do not believe that g is physiological and if it were then they better start defining it/talking about it differently because I’ve shown that if it were physiological then it would not mimick any known physiological process in the body. I eagerly await some good neuroscience studies on IQ that are robust, with large ns, their conclusions show the arrow of causality, and they’re not just making large sweeping claims that they found X “just because they want to” and are emotionally invested in their work. That’s my opinion about a lot of intelligence research; like everyone, they are invested in their own theories and will do whatever it takes to save face no matter the results. The recent Amy Cuddy fiasco is the perfect example of someone not giving up when it’s clear they’re incorrect.

I wish that Mr. Taylor would actually read some of the literature out there on TBI and IQ along with how people with chunks of their brains missing can have IQs in the normal range, showing evidence that most a lot of our brain mass is redundant. How can someone survive with a brain that weighs 1.5 pounds (680 gms) and not need care for the rest of his life? That, in my opinion, shows how incredible of an organ the human brain is and how plastic it is—especially in young age. People with IQs in the normal range need to be studied by neuroscientists because anomalies need explaining.

If large brains are needed for high IQs, then how do these people function in day-to-day life? Shouldn’t they be ‘as dumb as an erectus’, since they have erectus-sized brains living in the modern world? Well, the human body and brain are two amazing aspects of evolution, so even sudden brain damage and brain removal (up to half the brain) does not show deleterious effects in a lot of people. This is a clue, a clue that most of our brain mass after erectus is useless for our ‘intelligence’ and that our brains must have expanded for another reason—family structure, sociality, expertise, etc. I will cover this at length in the future.

Small Brain, Normal IQ

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Emil Kirkegaard left a short commentary on John Skoyles’ 1999 paper Human Evolution Expanded Brains to Increase Expertise Capacity, not IQin which Emil writes in his article Evolution and imperfect mediators:

If we condense the argument, it becomes a little clearer:

John Skoyles (1999) [Condensed argument from Emil; paragraph 2] Brain expansion causes problems. Thus, whatever selected for increased brain size must have offered compensating benefits. People can have below average size brains yet exhibit normal intelligence. Thus, the compensating benefit offered by large brains is unlikely to be intelligence. Why should evolution have increased brain size with its associated problems for something smaller sized brains could have without expansion?

I merely edited out the unnecessary parts. Now try substituting some other trait, say fighting ability and some mediator of it.

Muscle size increases causes problems. Thus, whatever selected for increased muscle size must have offered compensating benefits. People can have below average size muscles yet exhibit normal fighting ability. Thus, the compensating benefit offered by large muscles is unlikely to be fighting ability. Why should evolution have increased muscle size with its associated problems for something smaller sized muscles could have without increase?

See the issue? This argument works for any imperfect physical underpinning of a trait, which is to say, basically all of them. Longer legs didn’t evolve for running well for some people with short legs run well. Bigger/stronger hears didn’t evolve for better cardio, because some people smaller/weaker hearts have good cardio. Longer arms didn’t evolve for fighting because some short armed people fight well. Darker skin didn’t evolve as a protection against sun exposure for some relative light skinned people don’t get skin cancer or sunburns. Larger eyes didn’t evolve for seeing better for some people with smaller eyes see well. Bigger ears… Bigger noses… Stronger hands… …

I don’t agree. Our brains sap about 20 percent of our daily energy needs while being 2 percent of our overall body mass whereas, in other primates, their brains cost about 9 percent of their daily energy needs (Fonseca-Azevedo and Herculano-Houzel, 2012).

In regards to Emil’s counterarguments, I’ll address them one by one:

Long legs: People with longer legs were better runners and could escape from predators and chase prey. People with shorter legs were killed.

Bigger/stronger hearts: Those with a larger heart (sans cardiomegaly) could run for longer distance (remember, we are distance runners; Carrier, 1984; Skoyles and Sagan, 2002Bramble and Lieberman, 2004; Mattson, 2012) and so long legs and bigger/stronger hearts tie in with each other.

Long arms: This, again, goes back to our morphology in Africa. Long limbs are more conducive to heat dissipation (Lieberman, 2015). So those who had the right body plan for distance running could survive better during our evolutionary history.

Dark skin: A light-skinned person who spends enough time without protection in a tropical climate will develop skin cancer. (It is hypothesized that skin cancer is what caused the evolution of dark skin; Greaves, 2014, though this was contested by Jablonksi and Chaplin, 2014.)

Large eyes: Bigger eyes don’t mean better eyesight in comparison to smaller ones.

All in all, the brain size argument is 100 percent different from these arguments: large brains come with large problems. Further, there is evidence (which will be reviewed below) that people can live long, normal lives with half of their brain missing

The brain-size/IQ puzzle

The oft-repeated wisdom is that our brains evolved to such a large size so we could become more intelligent. And looking at when our brains began to increase (starting with erectus, which had to do with the advent of cooking/fire use), we can see that that’s when our modern body plan appeared. We can ascertain this by looking at Nariokotome boy, an erectus that lived about 1.6 mya.

Further, in regards to brain size, there was a man named Daniel Lyon. What was so extraordinary about this man is that, at the time of his death, had a brain that weighed 1.5 pounds (see Wilder, 1911)! Skoyles and Sagan (2002: 239) write:

Upon examination, anatomists could find no difference between it [Lyon’s brain] and other human brains apart from its size with one exception: The part of his brain attached to the brainstem, the cerebellum, was near normal size. Thus, the total size of Lyon’s cerebral hemisphere was smaller than would be suggested by a total brain weight of 1.5 lb. We do not know how bright he was—being a watchman is not particularly intellectually demanding—but he clearly was not retarded. A pound and a half brain may not be enough to manage a career as an attorney, a professor of theology, or a composer, but it was sufficient to let Lyon survive for 20 years in New York City.

Skoyles and Sagan (2002) review numerous lines of evidence of individuals with small brains/people with severe TBI living full lives, even having IQs in the average/above average range. They write (pg 238):

You would think that cutting out one-half of people’s brains would kill them, or at least leave them vegetables needing care for the rest of their lives. But it does not. Consider this striking story. A boy starts having seizures at 10 years of age when his right cerebral hemisphere atrophies. By the time he is 12, the left side of his body is paralyzed. When he is 19, surgeons decide to operate and remove the right side of his brain, as it is causing gits in his intact left one. You might think this would lower his IQ or leave him severely retarded, but no. His IQ shoots up 14 points, to 142! The mystery is not so great when you realize that the operation has gotten rid of the source of his fits, which had previously hampered his intelligence. When doctors saw him 15 years later, they described him as “having obtained a university doploma . . . [and now holding] a responsible administrative position with a local authority.” (18)

They also write about the story of an Argentinian boy who had a right hemispherectomy when he was 3-years-old who was notable for “the richness of his vocabulary and syntax” and also “attends English classes at school, in which he attains a high level of success (20; quote from Skoyles and Sagan, 2002: 238).

It is also a “medical myth that microcephaly (having a head smaller than two standard deviations (SD) below average circumference) is invariably linked to retardation.” (Skoyles and Sagan, 2002: 239).

There are some important things to be noted in regards to the study of Nariokotome boy’s skeleton and skull size. Skoyles and Sagan (2002: 240) write (emphasis mine):

So how well equipped was Homo erectus? To throw some figures at you (calculations shown in the notes), easily well enough. Of Nariokotome boy’s 673 cc of cortex, 164 cc would have been prefrontal cortex, roughly the same as half-brained people. Nariokotome boy did not need the mental competence required by cotemporary hunter-gatherers. … Compared to that of our distant ancestors, Upper Paleolithic technology is high tech. And the organizational skills used in hunts greatly improved 400,000 years ago to 20,000 years ago. These skills, in terms of our species, are recent, occurring by some estimates in less than the last 1 percent of our 2.5 million year existence as people. Before then, hunting skills would have required less brain power, as they were less mentally demanding. If you do not make detailed forward plans, then you do not need as much mental planning abilities as those who do. This suggests that the brains of Homo erectus did not arise for reasons of survival. For what they did, they could have gotten away with much smaller, Daniel Lyon-sized brains.

Lastly, I will touch on the fact that since we are running apes, that we need a narrow pelvis. As I stated above, our modern body plan came to be around 1.6 mya with the advent of erectus, which could be inferred from footprints (Steudel-Numbers, 2006Bennett et al, 2009). Now the picture is beginning to become clearer: if people with brains the size of erectus could have intelligence in the modern range, and if our modern body plans evolved 1.6 mya (which is when our brains began to really increase in size due to metabolic constraints being unlocked due to erectus’ cooking ability), then you can see that it’d be perfectly possible for modern Homo sapiens to have brains the size of erectus while still having an IQ in the normal range.

Lastly, Skoyles and Sagan (2002: 245) write (emphasis mine):

Kanzi seems to do remarkably well with a chimp-sized brain. And while we tend to link retardation with small brains, we have seen that people can live completely normal lives while missing pieces of their brains. Brain size may enhance intelligence, but it seems we can get away without 3 pounders. Kanzi shows there is much potential in even 13 oz.

So Skoyles and Sagan do concede that brain size may enhance intelligence, however, as they have argued (and as Skoyles does in his 1999 paper), it is perfectly possible to live a normal life with half a brain, as well as have an average/above average IQ (as reviewed in Skoyles, 1999). So if people with erectus-sized brains can have IQs in the normal range and live normal lives, then brains must have increased for another reason, which Skoyles has argued is expertise capacity.

Large brains are, clearly, not needed for high IQs.

(Also search for this paper: Reiss, A. L., Abrams, M. T., Singer, H. S., Ross, J. L. & Denckla, M. B. (1996). Brain development, gender and IQ in children: A volumetric imaging study. Brain, 119, 1763-1774. where they show that there is a plateau, and a decrease in IQ in the largest brains; see table 2. I also reviewed some studies on TBI and IQ and how even those with severe TBI can have IQs in the normal range (Bigler, 1995; Wood and Rutterford, 2006; Crowe et al, 2012). Yet more evidence that people with half of their brains missing can lead normal lives and have IQs in the modern range.)

Evidence for Natural Selection in Humans: East Asians Have Higher Frequency of CASC5 Brain Size Regulating Gene

1500 words

Brain size is one physical difference that the races differ on. East Asians have bigger brains than Europeans who have bigger brains than Africans (Beals et al, 1984; Rushton, 1997). What caused these average differences and the ultimate causes for them have been subject to huge debate. Is it drift? Natural/sexual selection? Mutation? Gene flow? Epigenetic? One reason why brains would need to be large in colder climates is due to heat retention, while in tropical climates heads need to be smaller to dissipate heat. One of the biggest criticisms of HBD is that there is no/little evidence of recent natural selection between human races. Well, that has changed.

CASC5 “performs two crucial functions during mitosis, being required for correct attachment of chromosome centromeres to the microtubule apparatus, and also essential for spindle-assembly checkpoint (SAC) signaling” (Shi et al, 2016). The gene has been found to be important in recent human evolution along with neurogenesis.

Shi et al (2016) genotyped 278 Han Chinese (174 females and 104 males with a mean age of 36) who were free of maladies or genetic defects. They had the coding sequences of CASC5 for humans, chimpanzees, gorillas, baboons, gibbons, orangutans, tarsiers, Denisovans, and Neanderthals. They downloaded genotypes from the Human Genome Project for their analysis.

They compared CASC5 among three human species: humans, Neanderthals, and Denisovans. Using chimpanzees as an outgroup, they discovered 45 human-specific mutations, 48 Neanderthal-specific mutations, and 41 Neanderthal-specific mutations. Further, when one exon region was aligned among modern humans, non-human primates and other mammalian species, 12 amino acid sites showed divergence between modern humans, Neanderthals, and Denisovans with 8 occurring in modern humans. Of the 8 sites in humans, 6 are preserved which implies that they were important in our evolutionary history.

Shi et al (2016) write:

At the population level, among the 8 modern human amino acid changes, two (H159R and G1086S) are fixed in current human populations, and the other six are polymorphic Fig. 1). Surprisingly, 5 of the 6 amino acid polymorphic sites showed deep between-population divergence in allele frequencies. East Asians possess much higher frequencies of the derived alleles at four sites (T43R-rs7177192, A113T-rs12911738, S486A-rs2412541 and G936R-rs8040502) as compared to either Europeans or Africans (Fig. 1), while E1285K-rs17747633 is relatively enriched in Europeans (46%), and rare in East Asians (10%) and Africans (3%). No between-population divergence was observed for T598 M-rs11858113 (Fig. 1).


So East Asians have a much higher frequency of this derived trait. This is direct evidence for natural selection in recent human evolution in regards to the physical structure of the brain.

Since most of the amino acid polymorphic sites showed between-population divergence, they decided to analyze the three classical races using 1000 genomes. The variation between the races could be due to either genetic drift or natural selection. When they analyzed certain gene regions, they observed a signal of positive selection for East Asians but not Europeans or Africans. They further tested this selection signal using “the standardized integrated haplotype score (iHS) which is used for detecting recent positive selection with incomplete sweep (i.e. the selected allele is not yet fixed)” (Shi et al, 2016). Using this method, they discovered a few SNPs with large iHS values in Europeans (7 SNPs at 4.2 percent) and none in Africans.

They also conducted a genome-wide scan of Fst, iHS, and “XPCLR (searching for highly differentiated genomimc regions as targets of selective sweeps)” (Shi et al, 2016). Several SNPs had high Fst, iHS and XPCLR scores, which indicate that these alleles have been under positive selection in East Asians. Among the fixed amino acid sites in human populations, East Asians showed 5, Europeans showed 1, and Africans showed 0 which, the authors write, “[imply] that these amino acid changes may have functional effects” (Shi et al, 2016). Furthermore, using the HDGP, they obtained the frequency of the 6 amino acid sites in 53 populations. This analysis showed that 4 of the 6 amino acid sites are “regionally enriched in East Asia .. in line with the suggested signal of population-specific selection in this area” (Shi et al, 2016).

Then, since CASC5 is a brain size regulating gene, they looked for phenotypic effects. They recruited 167 Han Chinese (89 men, 178 women) who were free of maladies. They genotyped 11 SNPs and all of the frequencies followed Harvey-Weinberg Equilibrium (which states that allele and genotype frequencies will remain constant in a population from generation to generation in the absence of evolutionary pressures; Andrews, 2010). In the female sample, 5 regions were related to gray matter volume and four were on the amino acid polymorphic sites. Interestingly, the four alleles which showed such a stark difference between East Asians and Europeans and Africans showed more significant associations in Han Chinese females than males. Those carrying the derived alleles had larger brain volumes in comparison with those who had the ancestral alleles, implying recent natural selection in East Asia for brain size.

Shi et al (2015) also attempted two replications on this allele writing:

We further conducted a replication analysis of the five significant CAC5 SNPs in two other independent Han Chinese samples (Li et al. 2015; Xu et al. 2015). The results showed that three SNPs (rs 7177192, rs11858113 and rs8040502) remained significant in Replication-1 for total brain volume and gray matter volume (Xu et al. 2015), but no association was detected in Replication-2 (Li et al. 2015) (Table S4).

It is very plausible that the genes that have regulated brain growth in our species further aid differences in brain morphology within and between races. This effect is seen mostly in Han Chinese girls. Shi et al (2016) write in the Discussion:

If this finding is accurate and can be further verified, it suggests that that [sic] after modern humans migrated out of Africa less than 100,000 years ago, the brain size may still be subject to selection.

I do believe it is accurate. Of course, the brain size could still be subject to selection; there is no magic field shielding the brain against selection pressure. Evolution does not stop at the neck.

So Shi et al (2016) showed that there were brain genes under recent selection in East Asians. What could the cause be? There are a few:

  1. Climate: In colder climates you need a smaller body size and big brain to survive the cold to better thermoregulate. A smaller body means there is less surface area to cover, while a larger head retains heat. It, obviously, would have been advantageous for these populations to have large brains and thus get selected for them—whether by natural or sexual selection. This could also have to do with the fact that one needs bigger eyes in colder environments, which would cause an increase in the size of the brain for the larger eyes, as well as being sharper visio-spatially.
  2. Intelligence: East Asians in this study showed that they had high levels of gray matter in the skull. Further, large brains are favored by an intermediately challenging environment (Gonzalez-Forero, Faulwasser, and Lehmann, 2017).
  3. Expertise: I used Skoyle’s (1999) theory on expertise and human evolution and applied it to racial differences in brain size and relating it to the number of tools they had to use which differed based on climate. Now, of course, if one group uses more tools then, by effect, they would need more expertise with which to learn how to make those tools so large brains would be selected for expertise—especially in novel areas.
  4. Vision: Large brains mean large eyes, and people from cold climates have large eyes and large brains (Pearce and Dunbar, 2011). Decreasing light levels select for larger eye size and visual cortex size in order to “increase sensitivity and maintain acuity“. Large eyeballs mean enlarged visual cortices. Therefore, in low light, large brains and eyes get selected for so one can see better in a low light environment.

Of course, all four of the examples below could (and probably do) work in tandem. However, before jumping to conclusions I want to see more data on this and how the whole of the system interacts with these alleles and these amino acid polymorphic sites.

In sum, there is now evidence for natural selection on East Asians (and not Africans or Europeans) that favored large brains, particularly gray matter, in East Asians with considerable sexual dimorphism favoring women. Four of the genes tested (MCPH1, ASPM, CDK5RAP2, and WDR62) are regulated by estradiol and contribute to sexual dimorphism in human and non-human primates (Shi et al, 2016). Though it still needs to be tested if this holds true for CASC5.

This is some of the first evidence that I have come across for natural selection on genes that are implicated in brain evolution/structural development between and within populations. It does show the old “Rushton’s Rule of Three“, that is, Mongoloids on top, Caucasians in the middle, and Negroids on bottom, though Caucasians were significantly closer to Africans than Mongoloids in the frequency of these derived alleles. I can see a HBDer going “They must be related to IQ”, I doubt it. They don’t ‘have’ to be related to IQ. It just infers a survival advantage in low light, cold environments and therefore it gets selected for until it reaches a high frequency in that population due to its adaptive value—whether spreading by natural or sexual selection.


There is No ‘Marching Up the Evolutionary Tree’

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The notion that there is any ‘progress’ to evolution is something that I have rebutted countless times on this blog. My most recent entry being Marching Up the ‘Evolutionary Tree’? which was a response to Pumpkin Person’s article Marching up the evolutionary tree. Of course, people never ever change their views in a discussion (I have seen it, albeit it is rare) due, mainly to, in my opinion, ideology. People have so much time invested in their little pet theories that they cannot possibly fathom at the thought of being wrong or being led astray by shoddy hypotheses/theories that confirm their pre-existing beliefs. I will quote a few comments from Pumpkin Person’s blog where he just spews his ‘correlations with brain size and ‘splits’ on the ‘evolutionary tree” that ‘proves that evolution is progressive’, then I will touch on two papers (I will cover both in great depth in the future) that directly rebut his idiotic notion that so-called brain size increases across our evolutionary history (and even before we became humans) are due to ‘progress in evolution’

One of my co-bloggers Phil wrote:

I think you mistyped that, but i see your point. Problem, however, most of your used phylogenies were unbalanced.

To which PP replied:

Based on the definition you provided, but not based on any meaningful definition. To me, an unbalanced tree is . . .

This is literally meaningless. Keep showing that you’ve never taken a biology class in your life, it really shows.

All it is is ignorance to basic biological thinking, along with an ideology to prove his ridiculous Rushtonian notion that ‘brain size increases prove that evolution is progressive’.

PP writes:

You have yet to present ANY scientific logic, and my argument about taxonomic specificity is clearly beyond you.

Scientific logic?! Scientific logic?! Please. Berkely has a whole page on misconceptions on evolution that directly rebut his idiotic, uneducated views on evolution. It doesn’t help that his evolution education most likely comes from psychologists. Nevertheless, PP’s ‘argument’ is straight garbage. Taxonomic specificity’ is meaningless when you don’t have an understanding of basic biological concepts and evolution. (I will have much more to say on his ‘taxonomic specificity’ below.)

PP writes:

Was every tree perfect? No, but most were pretty close, and keep in mind that any flawed trees would have the effect of REDUCING the correlation between brain size/encephalization and branching, because random error is a source of statistical noise which obscures any underlying relationship. So the fact that I repeatedly found such robust correlation in spite of alleged problems with my trees, makes my conclusions stronger, not weaker.

The fact that you ‘repeatedly’ found ‘correlations’ in spite of the ‘problems’ with your trees makes your ‘conclusions’ weaker. Comparing organisms over evolutionary time and you notice a ‘trend’ in brain size. Must mean that evolution is progressive and brain size is its calling card!!

PP writes:

I’m right and all the skeptics you cite are wrong.

Said like a true idealogue.

Here is where PP’s biggest blunder comes in:

It’s not how many splits they have that I’ve been measuring, it’s how many splits occur on the tree before they branch off. Here’s a source from 2017:

Eukaryotes represent a domain of life, but within this domain there are multiple kingdoms. The most common classification creates four kingdoms in this domain: Protista, Fungi, Plantae, and Animalia.

So you needed ‘a source from 2017’ to tell you something that is literally taught on the first day of biology 101? Keep showing how uneducated you are here.

PP writes:

Nothing fallacious about a correlation between number of splits and brain size/encephalization.

Post hoc, ergo propter hoc:

Post hoc, ergo propter hoc is a Latin phrase for “after this, therefore, because of this.” The term refers to a logical fallacy that because two events occurred in succession, the former event caused the latter event.[1][2]

Magical thinking is a form of post hoc, ergo propter hoc fallacy, in which superstitions are formed based on seeing patterns in a series of coincidences. For example, “these are my lucky trousers. Sometimes good things happen to me when I wear them.”

P1: X happened before Y.
P2: (unstatedY was caused by something (that happened before Y).
C1: Therefore, X caused Y.

Here is PP’s (fallacious) logic:

P1: splits (X) happened before Y (brain size increase)
P2: (unstated) brain size increase was caused by something (that happened before brain size increaes [splits on the tree])
C1: therefore, splits caused brain size increase

Now, I know that PP will argue that ‘splits on the evolutionary tree’ denote speciation which, in turn, denotes environmental change. This is meaningless. You’re still stating that Y was caused by something (that happened before Y) and therefore inferring that X caused Y. That is the fallacy (which a lot of HBD theories rest on).

PP writes:

You don’t get it. Even statistically insignificant correlations become significant when you get them FIVE TIMES IN A ROW. If you want to believe it was all a coincidence, then fine.

Phylogenies are created from shared derived factors. Berkely is the go-to authority here on this matter. (No that’s not appeal to authority.)  Biologists collect information about a given animal and then infer the evolutionary relationship. Furthermore, PP’s logic is, again, fallacious. Berkely also has tips for tree reading, which they write:

Trees depict evolutionary relationships, not evolutionary progress. It’s easy to think that taxa that appear near one side of a phylogenetic tree are more advanced than other organisms on the tree, but this is simply not the case. First, the idea of evolutionary “advancement” is not a particularly scientific idea. There is no unbiased, universal scale for “advancement.” Second, taxa with extreme versions of traits (which might be perceived as more “advanced”) may occur on any terminal branch. The position of a terminal taxon is not an indication of how adaptive, specialized, or extreme its traits are.

He may emphatically argue (as I know he will) that he’s not doing this. But, as can be seen from his article, X is ‘less advanced’ than Y, therefore splits, brain size, correlation=progress. This is dumb.

For anyone who wants to know how (and how not to) read phylogenies, read Gregory (2008). These idotic notions that PP espouses are what Freshman in college believe due to ‘intuitiveness’ about evolution. It’s so rampant that biologists have writen numerous papers on the matter. But some guy with a blog and no science background (and an ideology to hammer) must know more than people who do this for a living (educate people on phylogenies).

On Phil’s response to see the Deacon paper that I will discuss below, PP writes:

That’s not a rebuttal.

Yes it is, as I will show shortly.

The first paper I will discuss is Deacon’s (1990) paper Fallacies of Progression in Theories of Brain-Size Evolution. This is a meaty paper with a ton of great ideas about phylogenies, along with numerous fallacies that people go to when reading trees (my favorite being the Numerology fallacy, which PP uses, see below).

Deacon argues that since people fail to analyze allometry, this anatomists have mistaken artifacts for evolutionary trends. He also argues that many structural’brain size increases’ from ‘primitive to advanced forms’ (take note here, because this is what PP did and this is what discredits his idiotic ideology) are the result of allometric processes.


Source: Evolution of consciousness: Phylogeny, ontogeny, and emergence from general anesthesia Mashour and Alkire (2013)

This paper (and picture) show it all. This notion of scala naturae (which Rushton (2004) attempted to revive with r/K selection theory has been rebutted by me) was first proposed by Aristotle. We now know how the brain structure evolved, so the old ‘simple scala naturae‘ is, obviously, out of date in the study of brain evolution.

This paper is pretty long and I don’t have time to discuss all of it so I will just provide one quote that disproves PP’s ‘study’:

Whenever a method is discovered for simplifying the representation of a complex or apparently nonsystematic numerical relationship, the method of simplification itself provides new insight into the phenomenon under study. But reduction of a complex relationship to a simple statistic makes it far easier to find spurious relationships with other simple statistics. Numerology fallacies are apparent correlations that turn out to be artifacts of numerical oversimplification. Numerology fallacies in science, like their mystical counterparts, are likely to be committed when meaning is ascribed to some statistic merely by virtue of its numeric similarity to some other statistic, without supportive evidence from the empirical system that is being described.

Deacon also writes in another 1990 article titled Commentary on Ilya I. Glezer, Myron So Jacobs, and Peter J Morgane (1988) Implications of the “initial brain’9 concept for brain evolution in Cetacea:

The study of brain evolution is one of the last refuges for theories of progressive evolution in biology, but in this field its influence is still pervasive. To a great extent the apparent “progress” of mammalian brain evolution vanishes when the effects of brain size and functional specialization are taken into account.

(It’s worth noting that in the author’s response to Deacon, he did not have any qualms about ‘progressive brain-size’.)

In regards to PP’s final ‘correlation’ on human races and brain-size, this is a perfect quote from McShea (1994: 1761):

If such a trend [increase in brain size leading to ‘intelligence’] in primates exists and it is driven, that is, if the trend is a direct result of concerted forces acting on most lineages across the intelligence spectrum, then the inference is justified. But if it is passive, that is, forces act only on lineages at the low-intelligence end, then most lineages will have no increasing tendency. In that case, most primate species—especially those out on the right tail of the distribution like ours—would be just as likely to lose intelligence as to gain it in subsequent evolution (if they change at all).

The ‘trend’ is passive. Homo floresiensis is the best example. We are just as likely to lose our ‘intellect’ and our ‘big brains’ as we are to ‘get more intelligent’ and ‘smaller brains’. The fact of the matter is this: environment dictates brain size/whatever other traits an organism has. Imagine a future environment that is a barren wasteland. Kilocalories are scarce; do you think that humans would keep their big brains—which are two percent of their body weight accounting for a whopping 25 percent of total daily energy needs—without enough high-quality energy? When brain size supposedly began to increase in our taxa is when erectus learned to control fire and cook meat (Hlublik et al, 2017).

All in all, there is no ‘progress’ to evolution and, as Deacon argues, so-called brain-size increases across evolutionary time disappear after adjustments for body size and functional specialties are taken into account. However, for the idealogue who looks for everything they can to push their ideology/worldview, things like this are never enough. “No, that wasn’t a rebuttal! YOU’RE WRONG!!” Those are not scientific arguments. If one believes in ‘evolutionary progress’ and that brain-size increases are the proof in the pudding that evolution is ‘progressive’ (re has a ‘direction’), then they must rebut Deacon’s arguments on allometry and his fallacies in his 1990 paper. Stop equating evolution with ‘progress’. Though, I can’t fault laymen for believing that. I can, however, fault someone who supposedly enjoys the study of evolution. You’re wrong. The people you cite (who are out of their field of expertise) are wrong.

Evolution is an amazing process. To equate it with ‘progress’ does not allow one to appreciate the beauty of the process. Evolution does carry baggage with it, and if I weren’t so used to the term I would use Descent by Modification (DbM, which is what Darwin used). Nevertheless, progressionists will hide out in whatever safehold they can to attempt to push their idealogy that is not based on science.

(Also read Rethinking Mammalian Brain Evolution by Terrence Deacon. I go more in depth on these three articles in the future.)


Dinosaurs, Brains, and ‘Progressive Evolution’

1800 words

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 brainFrontiers 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

Traumatic Brain Injury and IQ

1900 words

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.

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.

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>;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.

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.

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.

Our Vampiric Brains

1100 words

Much has been written in the scientific literature on our brain size increase, which has doubled in the timespan of about 3 million years. It is assumed that our brains became bigger so we could become smarter. However, recent data shows that the amount of blood our brains use dramatically increased over the course of human evolution—the amount of blood our brains use increased some 600 percent over the course of human evolution, substantially more than our brain size increase (350 percent).

Seymour, Bosiocic, and Snelling (2016) showed that while there was a 3.5-fold increase in brain size while there was a 6-fold increase in total cerebral blood flow rate. This is due to increased interneuron connectivity, synaptic activity and cognitive function which all depend on the cerebral metabolic rate. This is yet another reason why cooking was so important during our brain evolution. If the brain has a higher metabolic rate, only a high-quality diet will allow it to function. This can only occur if and only if there is a high-quality diet in the first place.

The metabolic intensity of cerebral tissue in our lineage could only be satisfied by a high-quality cooked diet. Clearly, the evolution of the human brain most always goes back to nutrition and the quality of the human diet. Without erectus’ control of fire around 1.5 mya, our brains wouldn’t have been able to grow this big, nor would we have the cerebral blood flow we eventually had. The below picture is figure 1 from the paper. The left slide is Australopithecus Afarensis, the middle is a Neanderthal, and the right is archaic Homo Sapiens.


They measured the lumen radius of the internal carotid arteries and were able to deduce that there were large changes in cerebral blood flow in hominin evolution due to the increasing size of the ICAs. Arterial size, blood flow rate and metabolic rate are tightly related. So if there are bigger ICAs, then that hominin had more blood flow to feed a bigger brain. This is clear evidence that as our brain size increased that we needed more blood to feed our growing brain.

Kilroy et al (2013) hypothesize that due to widespread anatomical differences in the anterior cingulate cortex (ACC), PFC and insula and subcortical cortices, those regions must be a “central node of the brain’s network underlying individual differences in intellectual development throughout childhood and adolescence.” Cerebral blood flow in the subgenual/ACC correlates the highest with IQ. They also showed that it’s possible to delineate “where CBF is modulated by IQ.” More blood flow in these regions means a higher IQ. Since the ICAs grew larger over the course of hominin brain evolution to increase intelligence, it’s no surprise that more blood flow to certain parts of the brain is related to higher intelligence in children and adolescents.

Even CBF at rest is correlated with higher intelligence and creativity (Takeuchi et al, 2011). They showed that gray and white matter in the brain is correlated with CBF at rest and significantly and positively with psychometric intelligence. Further, the Raven’s Advanced Progressive Matrices (RAPM) and scores on the creativity test that were administered to the cohort correlated positively with white matter and cerebral blood flow. They also noticed that there was an association between negative mood and increased cerebral blood flow. Grey and white matter CBF at rest were both correlated with the RAPM and the creativity test administered. This is yet more evidence that blood flow to certain parts of the brain dictates intelligence (and most likely individual differences in intelligence as well).

The more vampiric a brain is (especially in certain regions), the higher one’s intelligence will be, on average. By looking back at the fossil skulls of our hominin ancestors and the radius of the ICA, we can infer that as hominin evolution ‘progressed’ through time, the ICA radius increased which meant increased blood flow to the brain. This is directly related to brain metabolism and could only be afforded with a high-quality diet which started with the advent of tool-making and the use of fire to cook by erectus. Cerebral blood flood in the anterior cingulate cortex is significantly and positively correlated with IQ. CBF at rest is also correlated with IQ and certain regions of the brain. This shows that a brain with a higher metabolic rate will be, on average, more intelligent than a brain that has a lower one. The current data on intelligence and CBF points to increased blood flow in certain parts of the brain is related to higher levels of intelligence. This does make sense, as our blood flow to the brain increased by 600 percent over the course of human evolution. So, in a way, we can say that along with our brain size increasing for expertise capacity (which was most definitely needed over the course of hominin evolution) (Skoyles, 2009) along with more cerebral blood flow due to larger arteries and a higher metabolic rate.

This does make sense, as our blood flow to the brain increased by 600 percent over the course of human evolution. So, in a way, we can say that along with our brain size increasing for expertise capacity (which was most definitely needed over the course of hominin evolution) (Skoyles, 2009) along with the need for more blood to the brain to increase intelligence (as blood will also shuttle oxygen to the brain). This is yet another reason why our not-so-special brains are remarkable compared to the rest of the animal kingdom—the one variable that gives us our cognitive superiority over other animals is the ability to cook and use fire. A lot of our physiologic, anatomic and brain evolution can be explained simply as: no cooking, fire, and meat, no big brains (and as a consequence, everything you see around you today would not be here), and the only thing that can drive such a metabolically demanding brain is cooking and eating high-quality foods. The outstanding number of neurons crowded into our cerebral cortex along with much blood our vampiric brain guzzles explains our cognitive superiority over other animals.


Kilroy, E., Yan, L., Wang, D. J., Dapretto, M., Mendez, M. F., Liu, C. Y., & Kim, Y. C. (2011). Relationships between Cerebral Blood Flow and IQ in Typically Developing Children and Adolescents. Journal of Cognitive Science,12(2), 151-170. doi:10.17791/jcs.2011.12.2.151

Seymour, R. S., Bosiocic, V., & Snelling, E. P. (2016). Fossil skulls reveal that blood flow rate to the brain increased faster than brain volume during human evolution. Royal Society Open Science,3(8), 160305. doi:10.1098/rsos.160305


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