's Race, Evolution, and Behavior covers a sensitive topic, racial differences, in a lot of detail, and with a heavy hand. Most of the book is overflowing with statistics and citations to an enormous number of references in quite a few fields by quite a few researchers. If the idea was to overwhelm the reader, I'll admit it was successful in my case. I eventually learned that I could skim the statistics, and look for prose summaries of the significance. didn't pay much attention to what it all means until near the end.
's main point is that there are several attributes on which there is systematic variation among the races, and his claim is that the consistency hints at a possible cause. He's mostly interested in convincing us of his pet theory of the cause of the differences. He's weighing us down with evidence to show us how consistent the inter-racial differences are. He mentions exceptions to the trends, but doesn't give them much emphasis, or provide plausible explanations within his framework.
The traits that focuses on include brain size, intelligence (as measured by IQ tests and other tests that correlate with g), maturation rate, personality, social organization, and reproductive effort. Other than intelligence (and brain size which is strongly correlated with it), and arguably social organization, these are not scales with a good end and a bad end, they're just differences. The consistency that focuses on is that whichever of these attributes you measure, you end up with whites in the middle, and orientals and blacks to either side. The story that wants to build out of that data is that the differences line up the way you'd expect if you tried to predict the direction from r/K evolutionary theory. (Basically, differential evolution in environments of scarcity and plenty; in this case, evolution in the tropics versus the northern latitudes in the Ice age.) He makes a fairly good case for the consistency; there appears to be something going on that puts orientals and blacks at two extremes and whites somewhere between them. But his favorite explanation doesn't seem to be strongly supported. It's roughly consistent with the data, but I'd need more explanation for the exceptions before I'll accept the case as demonstrated.
My biggest complaint about the book is about an important point, orthogonal to 's argument, that he doesn't address at all. clearly knows that discussion of racial differences is a hot-button issue, and the reason that people care is not because of the difference the data will make to our beliefs about the evolutionary causes of the difference. It's a hot-button issue because accepting the data seems to tell us something significant about innate differences or tendencies to differ among people on aspects of behavior that matter to social policy. When addressed these issues in The Bell Curve, they were careful to give us the important caveat: the differences between the mean IQs are significant, but the overlap among the curves is large. That means that you can predict the average IQ of a group if you know the racial make-up, but you don't really know much about an individual from that detail. (Wikipedia has a nice graphic showing how much overlap there is among the curves. With the other attributes discusses (aggressiveness, impulsivity, law abidingness, life span), it's much harder to figure out what interventions might be called for if we knew the differences were significant and pervasive, but not knowing how much overlap there is between races on these measurements makes it hard for me to even tell whether they matter other than in discussions about evolutionary causes.
Another factor, relating to intelligence, that was brought up at the reading group, is fascinating and was completely unaddressed. says that American Blacks have an average IQ of 85, while in central Africa, the number is closer to 70. In the US, we have the feeling that we could immediately recognize someone with an IQ of 70 as subnormal, but if that's the average in sub-saharan Africa, then something else is going on, because you have to assume that 90% of the population is functional. So the IQ of 70 must mean something different than what we'd assume here, where it normally implies other deficits than just cognitive. It's not clear what an average IQ of 70 in a functioning population would mean. This casts some doubt in my mind on the usefulness of IQ for cross-cultural or cross-racial comparisons. The Wikipedia article makes similar observations.
As to 's thesis, I remain unconvinced that r/K theory is the best explanation for the differences. r/K theory is well-established from studies of other animals, but isn't careful in marshalling his arguments to convince me that r/K with appropriate caveats for some unexpected cases provides a good enough match to the data. Wikipedia mentions several attacks on 's thesis and methods, but no alternative explanations of note. That's fine; sometimes the facts you need for the right theory aren't at hand when you want them.
3 comments:
RACE and BRAIN SIZE:
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 loosely with body size: large people tend to have larger brains (Gould, 1981). As a result, women on average will have smaller brains than men (Peters, 1991). However, this does not 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). In addition, female brains are structured in a way that would more than make up for any size differences.
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 skulls 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. Also, Morton did some early measurements with seed instead of shot. When he discovered that this method gave inconsistent results, he re did the Caucasian values with shot, but not the blacks (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.
Most empirical evidence shows that there is virtually no correlation between the intensity of different selective force gradients (e.g. latitude/temperature) and cranial morphology (Harvati and Weaver, 2006; Keita, 2004; Roseman and Weaver, 2004; Roseman, 2004; Gould, 1981, 1996; Brace, 2001). Indeed, positive geographic selective force correlations relating to craniometric variables are usually only (vaguely) observed when people 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 played ‘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 also 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 interest 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 Zulu sample appeared to have the largest crania of any group in the analysis, followed by Norse (Norway) and then Teita (Kenya). 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).
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. 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; Brace, 2001).
Other physical anthropological research has also shown that the crania of Sub-Saharan Africans are generally wider than European and North African samples, verbatim. 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; Hiernaux, 1975; 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.
Genetic studies of human brainsize have discovered two genes that when mutated can result in a 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. 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 some research calls into question whether these newer variants are 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). In fact, 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.
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 – particularly in Europe - 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), while the ASPM variant is thought to have arisen only 5,800 years ago. 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 (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 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.
Cernovsky (1990) reports that American blacks were superior in brain weight when compared with American whites. It is also known 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). It has been shown in several studies that blacks in general possess superior motor skills when compared to whites (Super, 1976; Wilson 1978; DiNucci, 1975); some believe that this may be the result of environmental and cultural factors (Super, 1976). The overall implications are the same, however, and suggest that blacks have larger brains.
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).
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 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 also been replicated in animal studies (Nottenbohm, 1980; Bloch and Gorski, 1988).
Brain size decreases after anti-androgen treatment observed in the above mentioned study where 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).
Research has documented that American blacks possess androgen levels (e.g. Testosterone) that are as much as 10% higher than American whites (Ross and Henderson, 1994; Bernstein et al, 1986; Ross et al, 1995). This is indicative that whites also possess higher estrogen to androgen levels than blacks. East Asians have been shown to possess lower levels of androgens than even whites (Ross et al, 1995). Additionally, as the differences in androgen levels between blacks and whites are not excessive, they should also offer a number of genetic and health benefits, as well as increasing overall brain volume, and male sex characteristics.
References:
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)
Douglas B. (2008). Race, Intelligence and IQ: Are People of African Decent More Intelligent? Africaresource: educational, arts and research materials.
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.
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
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
Manica A, Amos W, Balloux F, Hanihara T. (2007). The effect of ancient population bottlenecks on human phenotypic variation. Nature 448:346–349.
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)
Not surprisingly, given the size and formality of the previous comments, I found several other copies of the article around the net. It's not too objectionable, so I won't delete it. But realize that it's a broadcast, and not a comment particular to anything here.
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