Sunday, December 09, 2007

All Brains Are the Same Color

One would think it unnecessary to re-hash this "debate" all over again but here goes.... -

December 9, 2007
Op-Ed Contributor
All Brains Are the Same Color

Ann Arbor, Mich.

JAMES WATSON, the 1962 Nobel laureate, recently asserted that he was “inherently gloomy about the prospect of Africa” and its citizens because “all our social policies are based on the fact that their intelligence is the same as ours — whereas all the testing says not really.”

Dr. Watson’s remarks created a huge stir because they implied that blacks were genetically inferior to whites, and the controversy resulted in his resignation as chancellor of Cold Spring Harbor Laboratory. But was he right? Is there a genetic difference between blacks and whites that condemns blacks in perpetuity to be less intelligent?

The first notable public airing of the scientific question came in a 1969 article in The Harvard Educational Review by Arthur Jensen, a psychologist at the University of California, Berkeley. Dr. Jensen maintained that a 15-point difference in I.Q. between blacks and whites was mostly due to a genetic difference between the races that could never be erased. But his argument gave a misleading account of the evidence. And others who later made the same argument — Richard Herrnstein and Charles Murray in “The Bell Curve,” in 1994, for example, and just recently, William Saletan in a series of articles on Slate — have made the same mistake.

In fact, the evidence heavily favors the view that race differences in I.Q. are environmental in origin, not genetic.

The hereditarians begin with the assertion that 60 percent to 80 percent of variation in I.Q. is genetically determined. However, most estimates of heritability have been based almost exclusively on studies of middle-class groups. For the poor, a group that includes a substantial proportion of minorities, heritability of I.Q. is very low, in the range of 10 percent to 20 percent, according to recent research by Eric Turkheimer at the University of Virginia. This means that for the poor, improvements in environment have great potential to bring about increases in I.Q.

In any case, the degree of heritability of a characteristic tells us nothing about how much the environment can affect it. Even when a trait is highly heritable (think of the height of corn plants), modifiability can also be great (think of the difference growing conditions can make).

Nearly all the evidence suggesting a genetic basis for the I.Q. differential is indirect. There is, for example, the evidence that brain size is correlated with intelligence, and that blacks have smaller brains than whites. But the brain size difference between men and women is substantially greater than that between blacks and whites, yet men and women score the same, on average, on I.Q. tests. Likewise, a group of people in a community in Ecuador have a genetic anomaly that produces extremely small head sizes — and hence brain sizes. Yet their intelligence is as high as that of their unaffected relatives.

Why rely on such misleading and indirect findings when we have much more direct evidence about the basis for the I.Q. gap? About 25 percent of the genes in the American black population are European, meaning that the genes of any individual can range from 100 percent African to mostly European. If European intelligence genes are superior, then blacks who have relatively more European genes ought to have higher I.Q.’s than those who have more African genes. But it turns out that skin color and “negroidness” of features — both measures of the degree of a black person’s European ancestry — are only weakly associated with I.Q. (even though we might well expect a moderately high association due to the social advantages of such features).

During World War II, both black and white American soldiers fathered children with German women. Thus some of these children had 100 percent European heritage and some had substantial African heritage. Tested in later childhood, the German children of the white fathers were found to have an average I.Q. of 97, and those of the black fathers had an average of 96.5, a trivial difference.

If European genes conferred an advantage, we would expect that the smartest blacks would have substantial European heritage. But when a group of investigators sought out the very brightest black children in the Chicago school system and asked them about the race of their parents and grandparents, these children were found to have no greater degree of European ancestry than blacks in the population at large.

Most tellingly, blood-typing tests have been used to assess the degree to which black individuals have European genes. The blood group assays show no association between degree of European heritage and I.Q. Similarly, the blood groups most closely associated with high intellectual performance among blacks are no more European in origin than other blood groups.

The closest thing to direct evidence that the hereditarians have is a study from the 1970s showing that black children who had been adopted by white parents had lower I.Q.’s than those of mixed-race children adopted by white parents. But, as the researchers acknowledged, the study had many flaws; for instance, the black children had been adopted at a substantially later age than the mixed-race children, and later age at adoption is associated with lower I.Q.

A superior adoption study — and one not discussed by the hereditarians — was carried out at Arizona State University by the psychologist Elsie Moore, who looked at black and mixed-race children adopted by middle-class families, either black or white, and found no difference in I.Q. between the black and mixed-race children. Most telling is Dr. Moore’s finding that children adopted by white families had I.Q.’s 13 points higher than those of children adopted by black families. The environments that even middle-class black children grow up in are not as favorable for the development of I.Q. as those of middle-class whites.

Important recent psychological research helps to pinpoint just what factors shape differences in I.Q. scores. Joseph Fagan of Case Western Reserve University and Cynthia Holland of Cuyahoga Community College tested blacks and whites on their knowledge of, and their ability to learn and reason with, words and concepts. The whites had substantially more knowledge of the various words and concepts, but when participants were tested on their ability to learn new words, either from dictionary definitions or by learning their meaning in context, the blacks did just as well as the whites.

Whites showed better comprehension of sayings, better ability to recognize similarities and better facility with analogies — when solutions required knowledge of words and concepts that were more likely to be known to whites than to blacks. But when these kinds of reasoning were tested with words and concepts known equally well to blacks and whites, there were no differences. Within each race, prior knowledge predicted learning and reasoning, but between the races it was prior knowledge only that differed.

What do we know about the effects of environment?

That environment can markedly influence I.Q. is demonstrated by the so-called Flynn Effect. James Flynn, a philosopher and I.Q. researcher in New Zealand, has established that in the Western world as a whole, I.Q. increased markedly from 1947 to 2002. In the United States alone, it went up by 18 points. Our genes could not have changed enough over such a brief period to account for the shift; it must have been the result of powerful social factors. And if such factors could produce changes over time for the population as a whole, they could also produce big differences between subpopulations at any given time.

In fact, we know that the I.Q. difference between black and white 12-year-olds has dropped to 9.5 points from 15 points in the last 30 years — a period that was more favorable for blacks in many ways than the preceding era. Black progress on the National Assessment of Educational Progress shows equivalent gains. Reading and math improvement has been modest for whites but substantial for blacks.

Most important, we know that interventions at every age from infancy to college can reduce racial gaps in both I.Q. and academic achievement, sometimes by substantial amounts in surprisingly little time. This mutability is further evidence that the I.Q. difference has environmental, not genetic, causes. And it should encourage us, as a society, to see that all children receive ample opportunity to develop their minds.

Richard E. Nisbett, a professor of psychology at the University of Michigan, is the author of “The Geography of Thought: How Asians and Westerners Think Differently and Why.”

Copyright 2007 The New York Times Company


  1. American military excludes those below IQ 85. That group is half of the blacks but only 10% of the whites. So the "US military matings with Germans" study is bogus. If only the smartest half of the white military were involved, the children of whites would have easily excelled. PC types are so driven to condemn the genetic/IQ relationship, they conveniently overlook this huge error in the German study...

  2. Race and Brain size: Blacks have Larger Brains

    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 others. Brain sizes vary considerably within any species, but this variation is not usually related to intelligence. Instead, it correlates (isometrically) with body size: large people tend to have larger brains (Gould, 1981, 1999; Henneberg, 1998). As a result, women on average will have smaller brains than men (Peters, 1991; Gould, 1981). This does not, however, indicate that the level of male intelligence is higher than female intelligence; Neanderthals had on average larger brains than anatomically modern humans (Tattersall, 1995; Gould, 1981) but most would agree that they were considerably less intelligent than Homo sapiens (Tattersal, 1995, 2004; Gould, 1981; Mithen 1998). Paleoanthropological research also argues that brainsize in humans may be the result of the gastrointestinal tract and its musculoskeletal supports; indicating that brain anatomy may have little to do with brain functioning (See Henneberg, 1998).

    Tobias (1970) compared 7 racial and national groups in a study on brain size, in which he reported that the brain size of American blacks was larger than any white group, (which included American, English and French whites) except those from the Swedish sub sample (who had the largest brains of any of the groups measured), and American blacks were also estimated to have some 200 million more neurons than American whites (See Tobias 1970; Weizmann et al. 1990). Gould (1981, 1996) discovered upon recalculating Morton’s skull data that the crania of blacks in his sample were on average larger than those of whites. Morton included in his sample of black crania 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 (See Gould, 1981, 1996). After correcting these errors it was shown that the black sample had larger crania (and presumably, larger brains) than did whites (ibid).

    Interestingly, during the time periods in which the data for the above mentioned studies were collected anthropomorphic research has shown that blacks were on average physically smaller in stature than whites and received poorer nutrition (e.g. Alan, 2006). Indicating that in spite of relatively lower anthropomorphic measurements and poorer nutritional intake, blacks still demonstrated larger brain volume.

    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 produce the largest compilation of data ever assembled, with all items based entirely on his own measurements of skulls for all races. From his extensive tables (38 male African and 101 male Caucasian skulls), Tiedemann concludes that no differences in brain sizes can distinguish human races (See Gould, 1999). In some instances the favor was actually in the direction of blacks.

    Most contemporary evidence shows that there is virtually no correlation between the intensity of different selective force gradients and cranial morphology (Harvati and Weaver, 2006; Keita, 2004; Roseman and Weaver, 2004; Roseman, 2004; Gould, 1981, 1996; Brace, 2001). Research shows that positive geographic selective force correlations relating to craniometric variables are usually only (‘vaguely’) observed when samples from extreme cold (arctic) environments, such as Inuit types and Siberians, are included in analysis (Roseman, 2004; Harvati and Weaver, 2006). For example, Harvati and Weaver (2006) found a weak association between cranial centroid sizes and climatic variables, which approached, but did not reach, significance. This effect disappeared when an Inugsuk (a group from Greenland similar to Eskimos) sample was removed from the analysis (ibid). Roseman (2004) observed similar findings with a Siberian sample – once the Serbian sample was removed from the analysis, there was no indication that environmental temperature or latitude would play ‘any’ role in cranial morphology. In sum, recent studies comparing craniometric and neutral genetic affinity matrices have concluded that, on average, human cranial variation fits a model of neutral expectation.

    Keita (2004) in his principal components analysis on male crania from the northeast quadrant of Africa and selected European and other African series found no consistent ‘size differences’ between regional groups, as all samples showed marked variation in 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 this study was to assess the anatomical basis of patterns of craniofacial variation along an African–European continuum, with special focus on North Africa. There was Interest in whether there was a sharp boundary separating 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 in this study, for most variables (see Keita, 2004).

    Other physical anthropological research also shows the crania of Sub-Saharan Africans to be generally wider, exhibiting greater cranial breath than European and North African samples. For example sub-Saharan specimens show a generalized vertical facial flattening, with consequent widening of the entire structure (Bruner and Manzi, 2004). 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 certain 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. African populations tend to exhibit more cranial variation than do other world populations (Hanihara et al, 2003; Keita, 2004; Roseman and Weaver, 2007). Relethford (1994) and Relethford and Harpending (1994) 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. Manica et al (2007) note a smooth loss of genetic diversity with increasing distance from Africa, and along with this, using a large data set of skull measurements and an analytical framework equivalent to that used for genetic data, also show that the loss in genetic diversity is mirrored by a loss in phenotypic variability.

    Extensive research in human genetics on ‘presumably’ neutral loci has shown that the overwhelming majority of human diversity is found among individuals within local populations. Previous studies of craniometric diversity are similar to these 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).

    Genetic studies of human brainsize have discovered two genes that when mutated can result in severely reduced brain volume, or ‘Autosomal recessive primary microcephaly’. 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 are seen in Europe/Eurasia – while there is contradictory research that shows these genes to also be common among Papua New Guinea Highlanders (Yu et al, 2007). The 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.), with newer D variants showing positive selection arising about 5,800 years ago (Evans et al, 2005; Zhang, 2003), although other research calls seriously into question whether these gene variants are actually being selected for (see Voight 2006; Yu et al, 2007).

    Microcephaly genetic researchers believe that D alleles may have first arisen in an archaic homo species about 1.1 million years ago before introgression into modern Homo sapien sapiens about 37, 000 years ago; possibly as the result of interspecies breeding (Evans et al, 2006). It is thought that microcephalin shows by far the most compelling evidence of admixture among the human loci examined thus far (Evans et al, 2006). Modern humans arose only 100,000 years ago in Africa (Horan et al, 2005), which would make D alleles more than 1million years “older” than modern humans, and certainly very primitive by any stretch. Much physical anthropological evidence also supports the theory that modern Europeans may share close relationships with European Neanderthals (Brace, 1979, 2005; Trinkaus, 2007; Wolpoff, 2004).

    Normal D variants of both ‘MCPH1’ and ‘ASPM’ genes have been shown to have mild affects on human brainsize with empirical evidence demonstrating the alleles to reduce brain volume, slightly (Woods et al, 2006). For example, each additional ASPM allele was associated with a non significant 10.9 cc decrease in brain volume. For MCPH1, each additional allele was associated with a non significant 19.5 cc decrease in brain volume (Woods et al, 2006).

    While selective pressure in favor of smaller brain volume might seem counterintuitive, it should be noted that the fossil records suggest 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). 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 (‘though hotly challenged’) for these particular variant MCPH1 and ASPM alleles might also indicate that the genes are relatively unexpressed in the human brain, outside of causing ‘Autosomal recessive primary microcephaly.’ In one study it was shown that genes with maximal expression in the human brain tend to show little or no evidence for positive selection (Nielsen et al, 2006). For example, 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 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.

    It is recognized that the largest portions of the human brain are devoted to sensory and motor functions, which would mean that people with especially acute senses or strong motor skills can be expected to have larger brains than do others (Allen, 2002). Studies have shown that blacks in general possess superior motor skills and sensory acuity (e.g. visual acuity) over whites (Super, 1976; Wilson 1978; DiNucci, 1975; Kleinstein et al, 2003). Some believe that the superior motor abilities demonstrated by black children may be the result of environmental and cultural factors (Super, 1976). The overall implications are the same, however, and suggest that blacks should have larger brains than whites, and others. 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, “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 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 has been associated with smaller penis and testes size in humans (McLachlan and Allan, 2005). Low testosterone has also been 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, larger brain volume, longevity 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 over 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).

    American blacks are documented as possessing androgen levels (e.g. Testosterone) that are about 10% higher than American whites (Ross and Henderson, 1994; Bernstein et al, 1986; Ross et al, 1995). This implies that white men in general will possess higher estrogen to androgen levels than do black men, and this has been shown to have significant affects on overall brain volume; with evidence showing a general decrease in male brain volume. East Asians have been shown to possess lower levels of androgens, still (Ross et al, 1995). Although differences in androgen levels between blacks and whites are significant, they are not excessive by any degree, and should also offer a number of genetic, health and other male secondary sexual characteristic benefits to blacks.


    Alan S.A. (2006). African-American and White living standards in the 19th century American south; a biological comparison. CESifo Working Paper No. 1696.

    Allen B.P. (2006). If No “Races,” No Relevance to Brain Size, and No Consensus on Intelligence, Then No Scientific Meaning to Relationships Among These Notions: Reply to Rushton11. General Psychologist, Summer, 2003 Volume 38:2 Pages 31-32.

    Bernstein L, Ross RK, Judd H, et al (1986). Serum testosterone levels in young black and white men. J Natl Cancer Inst 76:45—48, 1986.

    Bloch GJ & Gorski RA. (1988) Estrogen/progesterone treatment in adulthood affects the size of several components of the medial preoptic area in the male rat. Journal of Comparative Neurology 1988 275 613–622.

    Bond J, Roberts E, Springell K, Lizarraga SB, Scott S, et al. (2005) A centrosomal mechanism involving CDK5RAP2 and CENPJ controls brain size. Nat Genet 37: 353–355.

    Bruner E., Manzi G. (2004).Variability in facial size and shape among North and East African human populations. Ital. J. Zool., 71: 51-56 (2004).

    Brace C.L, Nelson A.R., Seguchi N, Oe H., Sering L., Qifeng P., Yongyi L., and Tumen D (2001). Old World sources of the first New World human inhabitants: A comparative craniofacial view. PNAS August 14, 2001 u vol. 98 u no. 17 u 10017–10022.

    Cernovsky Z.Z. (1990). Race and Brain Weight: A note on Rushton’s conclusions. Psychological Reports 66:337-38.

    Dabbs,J.M, Dabbs M.G. (2000). Heroes, Rogues and Lovers: Testosterone and Behavior. McGraw-Hill Companies (July 25, 2000).

    DiNucci, James M. (1975). Motor Performance Age and Race Differences between Black and Caucasian Boys Six to Nine Years of Age. The ERIC database, an initiative of the U.S. Department of Education. 1975-02-00.

    Evan P., Mekel-Bobrov N., Vallender E., Hudson R., Lahn B., (2006). Evidence that the adaptive allele of the brain size gene microcephalin introgressed into Homo sapiens from an archaic Homo lineage. 18178–18183, PNAS November 28, 2006, vol. 103, no. 48.

    Erik Trinkaus (1984). Reply. Current anthropology. Vol. 25 . No. 3 June 1984.

    Fink B., Grammer K., Mitteroecker P., Gunz P., Schaefer K.,. Bookstein F.L. and Manning J.T. (2005). Second to fourth digit ratio and face shape Proc. R. Soc. B (2005) 272, 1995–2001.

    Frayer, D.W. (1984). In The Origins of Modern Humans: A world survey of the Fossil Evidence (eds Smith, F.H. & Spencer, f.) 211-250 (Liss, New York, 1984).

    Gould, S. J. (1981). Mismeasure of Man. New York: Norton.

    Gould, S. J. (1996). Mismeasure of Man (2nd edition). New York: Norton.

    Gould S.J. (1999). The Great Physiologist of Heidelberg - Friedrich Tiedemann - Brief Article. Natural History, July, 1999

    Hanihara T, Ishida H., and Dodo Y (2003). Characterization of Biological Diversity through Analysis of Discrete Cranial Traits. American Journal of Physical Anthropology 121:241–251 (2003).

    Hassan M.J., Khurshid M, Azeem Z., John P, Ali G., Chishti M.S. and Ahmad W. Previously described sequence variant in CDK5RAP2 gene in a Pakistani family with autosomal recessive primary microcephaly. BMC Medical Genetics 2007, 8:58.

    Henneberg M. (1998). Evolution of the Human Brain: Is Bigger Better? Clinical and Experimental Pharmacology and Physiology Volume 25 Issue 9 Pages 745-749, September 1998

    Hiernaux J. (1975). The people of Africa. New York: Charles Scribner’s Sons.

    Horan R.D., Bulte E., Shogren J.F. (2005). How trade saved humanity from biological exclusion: an economic theory of Neanderthal extinction. Journal of Economic Behavior & Organization Volume 58, Issue 1, September 2005, Pages 1-29.

    Hulshoff Pol H.E., Cohen-Kettenis P.T., Peper J.S., Cahn W. (2006). Changing your sex changes your brain: influences of testosterone and estrogen on adult human brain structure. European Journal of Endocrinology (2006) 155 S107–S114.

    Mithen, S., 1998 (Ed). Creativity in Human Evolution and Prehistory, London: Routledge.

    Murphy, N. B. (1968). Carotid cerebral angiography in Uganda: review of boo consecutive cases. East African M. 7.,1968,45,47-60.

    Nielsen,R., Bustamante,C., Clark,A.G., Glanowski,S., Sackton,T.B., Hubisz,M.J., Fledel-Alon,A.,

    Nottebohm F. (1980). Testosterone triggers growth of brain vocal control nuclei in adult female canaries. Brain Research 1980 189 429.

    Tanenbaum,D.M., Civello,D., White,T.J., et al. (2005). A scan for positively selected genes in the genomes of humans and chimpanzees. PLoS Biol. 3.

    Relethford JH. 1994. Craniometric variation among modern human populations. Am J Phys Anthropol 95:53–62.

    Relethford JH, Harpending HC. 1994. Craniometric variation, genetic theory, and modern human origins. Am J Phys Anthropol 95:249–270.

    Roseman C.C. (2004). Detecting interregionally diversifying natural selection on modern human cranial form by using matched molecular and morphometric data. Proc Natl Acad Sci U S A. 2004 August 31; 101(35): 12824–12829.

    Roseman C.C., Weaver T.D. (2007) Molecules versus morphology? Not for the human cranium. Volume 29, Issue 12 , Pages 1185 – 1188.

    Roseman C.C., Weaver T.D. (2004). Multivariate apportionment of global human craniometric diversity. American Journal of Physical Anthropology. Volume 18, Issue 5, Pages 668 - 675.

    Ross, R.K., Coetzee, G. A., Reichardt, J., Skinner, E, and Henderson, B.E. (1995). Does the Racial-Ethnic Variation in Prostate Cancer Risk Have a Hormonal Basis? Cancer, Volume 75, Issue S7 (p 1778-1782).

    Ross R.K., Henderson B.E. (1994). Do diet and androgens alter prostate cancer risk via a common etiologic pathway? / Natl Cancer lnst 1994; 86:252-4.

    Ruff C.B., Trinkaus E., and Holliday T.W. (1997). Body mass and encephalization in Pleistocene Homo. Nature Vol. 387, 8 May 1997.

    Simerly RB, Chang C, Muramatsu M & Swanson LW. (1990). Distribution of androgen and estrogen receptor mRNA-containing cells in the rat brain: an in situ hybridization study. Journal of Comparative Neurology 1990 294 76–95.

    Solms M. and, Turnbull O. (2002). The brain and the inner world. Other Press, New York

    Keita S. (2004). Exploring Northeast African Metric Craniofacial Variation at the Individual Level: A Comparative Study Using Principal Components Analysis. American Journal of Human Biology 16:679–689 (2004).

    Super, C. M. (1976). Environmental effects on motor development: The case of African infant precocity. Developmental Medicine and Child Neurology, 18, 561–567.

    Tattersall, I. and J.H. Schwartz (2000). Extinct Humans, New York: Westview Press.

    Tattersall (1995) The Fossil Trail (Ev).

    Tobias, T.V. (1970). Brain Size, Grey matter and Race – Fact or Fiction? American Journal of Physical Anthropology 32:3-26.

    Trimborn,M., Bell,S.M., Felix,C., Rashid,Y., Jafri,H., Griffiths,P.D., Neumann,L.M., Krebs,A., Reis,A., Sperling,K., et al. (2004). Mutations in Microcephalin cause aberrant regulation of chromosome condensation. Am. J. Hum. Genet., 75, 261-266.

    Voight BF, Kudaravalli S, Wen X, Pritchard JK (2006) A map of recent positive selection in the human genome. PLoS Biol 4(3): e72.

    Wilson A. (1978). Developmental Psychology of the Black Child. Africana Research Publications (December 1978).

    Woods R., Freimer N., Young J., Fears S, Sicotte N., Service S., Valentino D., Toga A., Mazziotta J. (2006). Normal Variants of Microcephalin and ASPM Do Not Account for Brain Size Variability. Human Molecular Genetics, Volume 15, Number 12, 15 June 2006, pp. 2025-2029(5).

    Xu X., Lee J., and Stern D.F. (2004). Microcephalin Is a DNA Damage Response Protein Involved in Regulation of CHK1 and BRCA1. THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 279, No. 33, Issue of August 13, pp. 34091–34094, 2004.

    Yu F, Hill R.S., Schaffner S.F., Sabeti P.C., Wang E.T. et al (2007).Comment on “Ongoing Adaptive Evolution of ASPM, a Brain Size Determinant in Homo sapiens”. Mignault A.A,1 Ferland RJ. Et al, 20 APRIL 2007 VOL 316 SCIENCE.

    Zhang J. (2003). Evolution of the Human ASPM Gene, a Major Determinant of Brain Size. Genetics 165: 2063–2070 (December 2003).