Three times Nobel nominated anthropologist Philip Tobias, compared 7 racial and national groups in a study on brain size/weight, in which he reported that the brain size of American blacks was larger than any white group.

Bernie Douglas (April 14, 2008), Revised February 17, 2009

Brain Size and Intelligence: Biological Anthropological Perspectives

The majority of empirical studies on the matter of racial differences in brain size suggest that blacks from comparable environments will have larger brains than do whites and perhaps others. Brain sizes vary considerably within any species but this variation is not usually related to intelligence. In mammals for example, 90% of all variation in brain weight can be explained by variations in body weight (Jerison 1973). Differences in body size are used also to explain why women, on average, have smaller brains than do men (Peters, 1991; Gould, 1981) and why these differences in no way reflect that the level of male intelligence is higher than female intelligence. Studies suggest also that Neanderthals may have had, on average, larger brains than anatomically modern Homo sapien sapiens (Tattersall, 1995; Gould, 1981). Most anthropologists agree that Neanderthals, who may not have even had the capacity for forward planning, were considerably less intelligent than Homo sapien sapiens (see Tattersal, 1995, 2004; Gould, 1981; Mithen 1998).    

Among (non extinct) large mammals it is known that humans demonstrate, in relative terms, the largest brains, with the brain’s mass equaling approximately 2% of the body’s total mass. Among shrews, however, the smallest mammals who exhibit supposedly much less cognitive and behavioral flexibility than do humans, their brains can be up to 10% (!) of their body mass. That is, shrews possess brains that are 5 times heavier than human brains, in relative terms (Van Dongen, 1998). Thus, the relationship between relative brain size and intelligence is speculative. Some have speculated that perhaps absolute or relative size of the cerebral cortex, might better predict intelligence. However, human cortical volume is considerably exceeded by that of the elephant’s and large cetaceans, both in absolute and relative terms, (Jerison, 1973; Haug, 1987). Moreover, the prefrontal cortex in humans is not disproportionally large when compared with other primates (Jerison, 1997; Semendeferi, 2002).

Paleoanthropological evidence now suggests that the large brain size in humans may be the result of the gastrointestinal tract structure and its musculoskeletal supports (Henneberg, 1998), and that this may be related to richer, meat-based diets and extra-oral food processing. This along with other evidence suggests that the gross anatomy of the hominid brain is not related to its functional capabilities (ibid). Moreover, fossil evidence suggests that relative brain/body size ratios increased several times during human evolution, starting around 2 million years ago and reached its current state probably before the lineage leading to modern humans split from that leading to Neanderthals, 500,000 years ago (McHenry 1994). Perhaps more interesting, however, is that there has been at least one “reduction” (read: not increase!) of relative human brain size starting 35, 000 years ago (Ruff et al, 1997; Woods et al, 2006).

Race and Brain Size:

Three time Nobel nominated anthropologist Philip Tobias (1970) compared 7 racial and national groups in a study on brain size/weight in which it was reported that the brain size of American blacks was larger than any white group (including American, English and French whites) except those from the Swedish sub sample who had the largest brains of any sample in the study. It was also estimated that American blacks had some 200 million more neurons than American whites, and brains that were reported to be 54g heavier (See Tobias 1970; Weizmann et al. 1990). While Harvard archeologist Gould (1981, 1996) discovered upon recalculating Morton’s highly suspicious brain size data that the blacks in his sample were on average slightly larger in brain volume than whites. Morton included in his sample of blacks more females than he included in the white sample. For example, in his analysis of Hottentotts (black tribe from South Africa) all measured crania were of females; the Englishmen were all mature men. Morton had also eliminated especially large brains from the African group and especially small brains from the European group (Gould, 1981, 1996). After correcting these biases and errors, it was shown that the black sample actually had larger brains than did the white sample (ibid).

Interestingly, during the time periods in which the samples for the above mentioned studies were gathered, anthropomorphic research has shown that blacks were on average physically smaller (in stature) than whites, lived in inferior environments and received poorer nutrition (e.g. Alan 2006, 2007; ). Indicating that in spite of these environmental disadvantages, relatively lower anthropomorphic measurements and poorer nutritional intake, blacks still demonstrated larger brain volume. Tobias (1970) discusses factors which influence brain weight; in this discussion nutrition is included as being a major contributor. Tobias (1970) also discusses the sampling problems one may encounter with fresh brains. He argued that lack of standardization in sampling procedures often means that studies of brain weight of different races by different investigators may not be comparable, and therefore most comparisons are not reliable. These were concerns kept in close consideration by Tobias while conducting his own investigation into “racial” differences in brain size.

Friedrich Tiedemann (a famous 17th century craniometrist) noted that many anthropologists in his time simply chose the smallest-brained African ‘skull’ they could find and then published a single drawing as "proof" of what every (Caucasian) observer already "knew" in any case! Tiedemann produced the largest compilation of cranial data ever assembled, with all items based entirely on his own measurements of skulls representing all races. From his extensive tables, Tiedemann concluded that no differences in brain sizes can distinguish human races (See Gould, 1999). In some instances the favor went in the direction of blacks.

Cranial Size, Morphology and Continental Groups:

Most craniometric evidence shows that there is virtually no correlation between the intensity of different selective force gradients and cranial size (inappropriately referred to by some as “brain size”) or morphology in modern human populations. That is, different continental groups will differ very little in relative cranial size so that neutral expectations can be observed with respect to most craniometric variables (Harvati and Weaver, 2006; Keita, 2004; Roseman and Weaver, 2004; Roseman, 2004; Gould, 1981, 1996; Brace, 2001).

Research shows that positive selective force correlations relating to craniometric variables can be observed, and only vaguely, in samples from extreme cold “arctic” environments such as Inuit types and Siberians (Roseman, 2004; Harvati and Weaver, 2006). Harvati and Weaver (2006) found using a global climate data set constructed by interpolating observations from thousands of climate stations around the world, a weak association between cranial centroid sizes and climatic variables which approached but did not reach significance. This effect completely disappeared when an Inugsuk (a people from Greenland similar to Eskimos) sample was removed from the analysis (ibid). Roseman (2004) also observed similar findings with a Siberian sample – That is, when the Serbian sample was removed from the analysis there was no indication that environmental temperature or latitude played any role in cranial size.    

Keita (2004) found using principal components analysis on male crania from the northeast quadrant of Africa and selected European and other African series no consistent differences in cranial size. There were, however, some distinguishing differences in relationship to cranial shape between European and African samples, particularly with respect to nasal aperture and changes in the maxilla (part of the upper jaw from which the teeth grow). The primary goal of the study was to assess the anatomical basis of patterns of craniofacial variation along an African–European continuum with special focus on North Africa. Particular interest was paid to whether a sharp boundary separates any of these groups from each other (see Keita, 2004). In terms of overall cranial size, tropical African groups were found in many instances to have larger crania than European groups. For example, on close inspection of the 2 dimensional PC scatter plots designating cranial size/shape, the Teita (Kenya) sample appeared to have the largest crania of any group in the analysis, followed by Norse (Norway) and then Zulu. African crania were also found to be broader (wider) than European crania on average. Surprisingly, one European sample, Berg (Hungarian), correlated more closely with African samples in this respect than with other European samples. Tremendous overlap between all groups was observed for most variables (see Keita, 2004).

Other physical anthropological research has also shown the crania of Sub-Saharan Africans to be wider or broader, on average, than European and North African samples - exhibiting greater relative cranial breadth.  Bruner and Manzi (2004) showed that Sub-Saharan specimens show a generalized vertical facial flattening, with consequent widening of the entire structure. This pattern involves interorbital and orbital enlargement, widening and flattening of the nasal bones and aperture, maxillary development and upper rotation, and a general widening and lowering of the face. The face shortens vertically and this flattening leads to a relative lateral enlargement of the whole morphology and maxillary frontward rotation (see Bruner and Manzi, 2004). The pattern toward the other extreme shows the opposite processes, with a general vertical stretching related to a lateral narrowing; as seen in European and North African samples (ibid).

Despite some trends observed among African crania, Roseman and Weaver (2007) found that the amount of phenotypic variation in human cranial morphology decreases at the population level the further one travels from Sub-Saharan Africa. That is, African populations tend to exhibit more cranial variation than do other world populations (Roseman and Weaver, 2007; Hanihara et al, 2003; Keita, 2004). Relethford (1994) and Relethford and Harpending (1994) also found that the amount of morphological variation among major geographic groups is relatively low, and is compatible with those based on the genetic data, where Africa shows the most variation. Extensive research in human genetics on presumably neutral loci has also shown that the overwhelming majority of human diversity is found among individuals within local populations. In sum, studies of craniometric diversity are similar to genetic apportionments, implying that interregionally differing selection pressures have played a limited role in producing contemporary human cranial diversity (Roseman and Weaver, 2004; also see Brace, 2001).

Brain Size from the perspective of Evolutionary Genetics:

Molecular genetics have discovered several genes that when mutated may result in a substantial reduction in brain volume or a condition known as: ‘Autosomal recessive primary microcephaly’. One such gene, the gene microcephalin (MCPH1) regulates brain size during development and has experienced positive selection in the lineage leading to Homo sapiens (Zhang, 2003; Evans et al, 2005). Within modern humans a group of closely related haplotypes, known as ‘haplogroup D’ arose from a single copy at this locus (Evans, 2006). Globally, D alleles are young and first appeared about 37,000 years ago, with high frequency haplotypes being rare in Asia and particularly Africa. The highest frequencies of this haplotype are seen in Europe/Eurasia. However, there is contradictory research that has also shown these genes to be very common among Papua New Guinea Highlanders (Yu et al, 2007). A second microcephalin gene, ‘ASPM’ (abnormal spindle like Microcephaly associated), went an episode of positive selection that ended some time ago between 6–7 million and 100,000 B.P. (Zhang, 2003). Newer D variants have shown positive selection arising about 5,800 years ago (Evans et al, 2005); although other research calls this date into serious question as well as whether these genes have really seen positive selection (Voight 2006; Yu et al, 2007).  

Evolutionary geneticists interested in Microcephaly believe that D alleles may have first arisen in an archaic homo species (particularly, “Neanderthals”) about 1.1 million years ago before being introduced to Homo sapien sapiens breeding populations in Europe about 37, 000 years ago. This may have possibly resulted because of interspecies breeding (Evans et al, 2006). One team of researchers believes that microcephalin shows by far the most compelling evidence of admixture among the human loci examined thus far (Evans et al, 2006). There is, indeed, much paleoanthropological evidence that is congruent with theories suggesting that Europeans may share close biological relationships with Neanderthals (Brace, 1979, 2005; Trinkaus, 2007; Wolpoff, 2004; Gutiérrez et al, 2002). For example, numerous craniofacial, dental, and postcranial traits in European early modern humans are unlikely to have come from middle Paleolithic modern humans; while many of these traits have been shown through the use of anthropological methods to be distinctly Neanderthal, in form (Trinkaus, 2007; Brace, 1979, 2005; Simmons and Smith, 1991). Many have also pointed to the presence of “occipital bunning” in some early modern European remains as indicating a strong Neanderthal influence (Simmons and Smith 1991; Brace, 2005). It is further hypnotized that only a very small amount of admixture would be necessary for the retention these particular Neanderthal genes (Evans et al, 2006).  

Normal D variants of both ‘MCPH1’ and ‘ASPM’ genes have been shown to have mild affects on human brain size with empirical evidence demonstrating the alleles to reduce brain volume, slightly (Woods et al, 2006). For example, each additional ASPM allele, found at rates of 40% in both Europeans and Papua New Guinea highlanders, was associated with a non significant 10.9 cc (or 4.3 cubic inch)decrease in brain volume compared to those without the gene. While For MCPH1 (frequencies of 80% in Europe), each additional allele was associated with a non significant 19.5 cc (7.6 cubic inch) decrease in brain volume (Woods et al, 2006). Both Blacks and Hispanics were included in this study, and did not change the results of the study.

While selective pressure in favor of smaller brain volume might seem counterintuitive, it should be noted that the fossil records show that brain size in humans has decreased over the past 35,000 years, and on through the Neolithic period (Frayer, 1984; Ruff et al, 1997; Woods, et al, 2006; Henneberg, 1998). Interestingly, the selected variant of MCPH1 is thought to have arisen about 37,000 years ago (Evans et al, 2006) making it a candidate gene responsible for this general decline (Woods et al, 2006). These archaeological changes in brain size are paralleled by changes in body size (Ruff et al, 1997; Woods et al., 2006), and it is possible that decreases in brain size may have exerted selective pressure for corresponding decreases in body size (Ruff et al, 1997; Frayer, 1984; see also, Woods et al., 2006).  

The supposed rate of selection for these particular variant MCPH1 and ASPM alleles, although “hotly” challenged, might also indicate that the genes are relatively unexpressed in the human brain outside of causing ‘Autosomal recessive primary microcephaly.’ One recent study has found that genes with maximal expression in the human brain show “little or no” evidence for positive selection (Nielsen et al, 2005). Whereas the microcephaly genes in question have also been implicated in the development of breast cancer (Xu et al, 2004), and other non brain related conditions (Trimborn et al, 2004). Implying that the mild brain volume reductions observed with each additional variant of ASPM and MCPH1 allele may in fact be adaptively unimportant. It should be further noted that one microcephalin gene (CDK5RAP2) has shown evidence of positive selection in West African Yoruba (Voight, 2006; bond et al, 2005). However, this gene at the MCPH3 locus has been least involved in causing a microcephalin phenotype (Hassan et al, 2007), and is not believed to have arisen in an archaic homo species.

Sensory-Motor Functions and Human Brain size

It is known that the largest portions of the human brain are responsible for sensory and motor functions.  This would mean (at least by the logic, ‘bigger is better’) that people with especially acute senses or strong motor skills can be expected to have larger brains than do others (see Allen, 2002). Studies have shown “blacks”, in general, to possess superior motor abilities and development (Super, 1976; Wilson 1978; DiNucci, 1975), olfactory and visual acuity (Gilad et al., 2003; Voight, 2003; Kleinstein et al, 2003) over whites and other ethnic groups. Some researchers believe that the superior motor abilities demonstrated by black children may in fact be the result of environmental and cultural factors (Super, 1976). The overall implications are the same, however, and suggest that blacks should possess larger brains than do whites and others, on average. For example, Cernovsky (1990) reported that American blacks were superior in brain weight when compared with American whites.

Testosterone, Brain size and Penis size…?

Some of the more desperate claims for racial differences in brain size are accompanied by highly unusual arguments suggesting racial differences in “penis size” (i.e. that they are inversely correlated). Thorough investigation of the formal neuroscience, anthropology, paleontology, anatomy, physiology, and ‘sex psychology’ literature reveal that legitimate references to this - ridiculous (?) - notion are not only remote, but in fact, “completely nonexistent.” The development and size of one’s penis is controlled by testosterone levels during puberty; and it is testosterone (and body size) that determine penis size. Testosterone: “Primary male hormone, causes the reproductive organs to grow and develop; responsible for secondary sexual characteristics, and promotes erections and sexual behavior” (1).  

With this in mind; employing elementary logic one may safely arrive at the conclusion that because men tend to have dramatically higher levels of testosterone than do women (about 10 times the level), and on average have larger brains (due mostly to body size); that testosterone not only increases body and penis size, but also brain size! In fact, the relationship between larger brain size and testosterone is one of common knowledge, and is well documented in the literature (e.g. Solms and Turnbull, 2002; Hulshoff Pol et al, 2006; Nottenbohm, 1980; Bloch and Gorski, 1988). Moreover, low testosterone levels have been associated with smaller penis and testes size in humans (McLachlan and Allan, 2005).

Low testosterone is also associated with failure to go through full normal puberty, poor muscle development, reduced muscle strength, low interest in sex (decreased libido), osteoporosis (thinning of bones common in whites and Asians), poor concentration, difficulty getting and keeping erections, low semen volume, longer time to recover from exercise and easy fatigue, “in men” (McLachlan and Allan, 2005). At the other relative extreme, high testosterone has been associated with improved health and longevity, superior motor abilities, increased reproductive success (in men), increased mental focus (sharpens focus and concentration), larger brain volume, and “boldness” (Dabbs and Dabbs, 2000; Solms and Turnbull, 2002; Hulshoff Pol et al, 2006; Fink el al, 2005).   

With respect to brain size, again; it is known that sex hormones (e.g. testosterone, estrogen) induce sexually-dimorphic brain development and organization. Research with cross-sex hormone administration to transsexuals has provided a unique opportunity to study the effects of sex steroids on brain morphology in young adulthood. Hulshoff Pol et al (2006) used magnetic resonance brain images prior to, and during, cross-sex hormone treatment to study the influence of anti-androgen +estrogen treatment on brain morphology in eight young adult male-to-female transsexual subjects and of androgen treatment in six female to- male transsexuals. The team found that compared with controls, anti-androgen (i.e. male sex hormones/testosterone) + estrogen treatment decreased brain volumes of male-to-female subjects towards female proportions, while androgen treatment in female-to-male subjects increased total brain and hypothalamus volumes towards male proportions (Hulshoff Pol et al, 2006 ). These findings have been replicated in animal studies (Nottenbohm, 1980; Bloch and Gorski, 1988).  

The reductions in brain size observed after anti-androgen treatment in male-to-female subjects were also very dramatic (31cc in only a 4 month period). Indeed, the magnitude of change signified a decrease in brain volume, which is at least ten times the average decrease observed a year in healthy adult individuals (Hulshoff Pol et al, 2006). The authors include that it was not surprising that the influences of sex hormones on the brain were not limited to the hypothalamus, but were also expressed as changes in total brain size. Estrogen and androgen receptor mRNA containing neurons are not limited to the hypothalamus, but are distributed throughout the adult human brain (Hulshoff Pol et al, 2006; Simerly et al, 1990).  

Research shows that American blacks possess androgen levels (e.g. male sex hormones) that are about 10% higher than American whites (Ross and Henderson, 1994; Bernstein et al, 1986; Ross et al, 1995). This would mean that white men, on average, possess ‘estrogen to androgen’ levels that are higher than that of black men; while these dynamics have been shown empirically to reduce the size of the male brain toward female proportions. East Asians are shown to have lower androgens levels than even whites (Ross et al, 1995). Other research shows that males with lower androgen levels tend also to have higher pitched voices and are less dominant and more feminine in appearance (Fink el al, 2005; Dabbs and Dabbs, 2000), which is consistent with experiments that investigate the effects of androgen levels, sexual dimorphism and the brain (Hulshoff Pol et al, 2006; Simerly et al, 1990; Nottenbohm, 1980; Bloch and Gorski, 1988). Vegetarians have also been found to have lower androgen levels than do those who eat meat (Dabbs and Dabbs, 2000), while castrated males tend also to have lower androgen levels (King A. et al, 2001).

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