that Evidence natural selection is still operating on human intelligence
Melissa Harintho BIOS 10162- Belovsky
The defining process in the evolution of primates and especially humans is the expansion of the brain. While many types of genes could potentially contribute to this process, genes that specifically regulate brain size during development are particularly relevant. The ongoing evolution of such genes, as well as the dissimilar evolutionary patterns of intelligence across different racial and cultural groups indicates that natural selection is still operating on human intelligence. In establishing that positive selection is still operating on human intelligence, the nature and measurability of intelligence must first be examined. A primary characteristic of human intelligence is flexibility. While most animals are specialists (i.e. bees are proficient at communicating through their Waggle dances, beavers are adept at building dams), humans have the ability to imitate many different kinds of skills (1). Studies have shown that chimpanzees are also capable of simulating motor acts, which demonstrates a preexisting capacity for the final development that appears solely in humans. While chimpanzees can represent what they perceive, humans can represent what they imagine: humans' ability to recombine mental elements led to developments such as science and art. For example, Galileo's world without friction, where objects set in motion remain in motion, is not a perceived world, but an imagined one (1). In addition, magnetic resonance imaging (MRI) and external head size measures show that brain size is related to IQ (2); thus, the evolutionary expansion of the human brain is believed to be important to advances in human intelligence such the emergence of language. Microcephalin and ASPM are two genes that regulate brain size and experienced strong positive selection in the ape lineage leading to humans. Their impact on brain size has been demonstrated by the fact that people carrying a non-functioning mutant copy of these genes suffer from microcephaly, a
congenital defect characterized by mental retardation and a normally structured brain that is approximately 70% smaller than usual. In 2003, geneticist Andrew P. Jackson examined the role of Microcephalin in primary microcephaly. In the developing cerebral cortex of the fetal brain, Microcephalin is specifically expressed in the control of the proliferation and/ or differentiation of neuroblasts during neurogenesis. As a result, primary microcephaly is the autosomal recessive neurodevelopmental condition in which there is an overall reduction in cerebral cortex volume comparable to that of early hominids. This correlation leads to the compelling implication that Microcephalin evolved under strong positive selection in the primate lineage leading to Homo sapiens (3). In 2004, Scientists Yin-qiu Wang and Bing Su of China further studied the proposition that Microcephalin evolved under positive selection in the lineage leading to humans. Wang and Su discovered that the evolution of Microcephalin's protein sequence was greatly accelerated throughout the lineage from simian ancestors to chimpanzees and humans, with the most prominent acceleration in the early stages of this lineage. Their findings suggest that about 45 advantageous amino acid changes in Microcephalin might have fixed during the 25- 30 million years of evolution from simian ancestors to modern humans. These observations support the notion that the evolution of Microcephalin has contributed to brain expansion in the simian lineage leading to humans. Thus, Wang and Su concluded it is likely that Microcephalin contributed to brain evolution in primates and humans (4). ASPM (abnormal spindle-like microcephaly associated), the other gene of which mutations lead to primary microcephaly, is also likely to have evolved under positive selection in the lineage leading to modern humans. In 2003, Scientist Jianzhi Zhang determined that ASPM went through an episode of accelerated evolution by positive selection after the separation of humans and chimpanzees, but before the division of modern non- Africans from Africans. Because positive selection only acts on a gene when the gene function is altered and the organismal fitness is increased, Zhang's results suggest that adaptive alterations occurred in ASPM, and that it may be a major genetic factor underlying the evolution of the human brain (5). Using the data and results of these studies as a foundation to portray the ongoing evolution of the human brain, geneticist Bruce Lahn and his colleagues at the University of Chicago in Illinois analyzed the
sequences of Microcephalin and ASPM in the brain. First, Lahn and his team sequenced the Microcephalin gene in an amalgam of 89 ethnically diverse people (the Coriell panel). They found several variants, or alleles, of Microcephalin, all of which carry a specific mutation that changes the protein the gene codes for. A particular set, termed haplotype 49, stood out because of its high frequency of 33% (59 out of 178 chromosomes) in comparison to the frequencies of the other 85 haplotypes, which ranged from 0.6% to 6.2%. Indicators of positive selection, such as the higher frequency of haplotype 49 and the simultaneous maintenance of extended linkage disequilibrium (non-random association of alleles at two or more loci) around the allele, are strong signs that Microcephalin was altered through positive selection (6). This particular Microcephalin mutation currently occurs in the brains of about 70% of humans. The data suggests that the mutation occurred recently and spread rapidly through the human species due to selection pressure, as opposed to the accumulation of random changes through impartial genetic drift. The Lahn team estimated that the age of the new Microcephalin variant is about 37,000 years (with a 95% confidence interval of 14,000 to 60,000 years), whereas the emergence the of modern human was about 200,000 years ago. Thus, the relatively recent occurrence of the Microcephalin variant indicates that positive selection took place much later than the emergence of the modern human in Africa (6). The Lahn team also sequenced the ASPM gene from the same original group of individuals (the Coriell panel), and found another mutation that alters the protein ASPM codes for. This mutation, termed haplotype 63, has a high frequency of 21%, marking a stark contrast to the other haplotypes, whose frequencies ranged from 0.56% to 3.3%. Furthermore, the researchers estimated that the age of the new ASPM variant, at only about 5,800 years (with a 95% confidence interval of 500 to 14,100 years), is even more recent than the emergence of the new Microcephalin variant. The variant is already present in about a quarter of people alive today, and is more common in Europe and the Middle East than in the rest of the world. The Lahn team indicates a correlation of the emergence of the ASPM mutation with the rapid increase in population associated with the development of cities and written language in the Middle East, but it has not examined the significance of this correlation yet (7). Another approach that has been taken to demonstrate that natural selection still operates on human intelligence has been to examine the evolution patterns of particular groups in society. One such study, conducted by Gregory Cochran and colleagues at the University of Utah in Salt Lake City, tested the
hypothesis that high IQ test scores of Ashkenazi Jews are a product of natural selection, which stem from their occupation of an unusual social niche (in medieval Europe). Specifically, the Cochran team tested the hypothesis that Ashkenazi literacy, economic specialization, and closure to inward gene flow led to a social environment in which there was high fitness payoff to intelligence (specifically verbal and mathematical intelligence). In their study, the researchers found that well-known clusters of Ashkenazi genetic diseases (lipid storage disorders and sphingolipid disorders in particular) increase intelligence in heterozygotes. Cochran and his colleagues determined that the clustering of such disorders (such as Canavan disease, Gaucher disease, and Tay-Sachs disease) in only a few pathways, and the presence at elevated frequency of more than one deleterious allele at many of them, could not have been produced merely by genetic drift. Their findings suggest that high IQ test scores of Ashkenazi Jews are attributable to positive selection (8). In another study, J. Philippe Rushton and Arthur R. Jensen advocated a stronger hereditarian model- 80% genetic-20% environmental- in the discussion of how much human intelligence is due to innate aptitude versus how much is acquired throughout the lifetime of each individual. In their study, the researchers examined the implications of the lack of narrowing of the 15- to 18-point average IQ difference between Blacks and Whites over the past 100 years. Rushton and Jensen declared that the IQ differences are more attributable to differences in brain size than to environmental factors such as racism. Furthermore, the researches claimed that associated differences such as standard of living and level of education lie in factors that are mostly heritable (2). Rushton and Jensen asserted that around the world, mean IQs differ much less within major population groups than between them. They expressed that while Whites have IQs close to 100 whether they live in Europe, Canada, Australia, New Zealand, or South Africa, Blacks in sub-Saharan Africa have IQs closer to 70 regardless of whether they live in East, West, Central, or Southern Africa- or whether the data were collected in the 1920s or the 2000s. The researchers maintained that genetic factors explain this worldwide pattern in a way that culture- only theory has not. For example, the worldwide pattern contradicts the hypothesis that the low IQ of American Blacks is due to racism, because the lower IQs of Blacks in Africa provides evidence against the theory that White racism has been responsible for the low IQ of American Blacks. Moreover, Rushton and Jensen pointed out that racism has had no adverse impact on the intelligence of East Asians and Jews, who average higher IQ scores than do Europeans (2).
Rushton and Jenson also incorporated the study of brain size patterns in their understanding of evolutionary race differences. They found that the three-way pattern of East Asian-White-Black differences in brain size that is found in adulthood (1,364 cm3, 1,356 cm3, and 1,267 cm3, respectively) is also detectable at birth. Such statistics provide further evidence for the researchers' claim that a stronger hereditarian model is more appropriate in the discussion of ongoing natural selection on human intelligence (2). The evolutionary expansion of the brain has led to the unique flexibility and capability of imagination distinct in modern humans today (1). Collectively, several studies offer strong evidence that natural selection is still operating on human intelligence. The recent selective histories of Microcephalin and ASPM in humans continue the trend of positive selection that has operated for millions of years in the hominid lineage (3-7). In addition, the differing evolutionary patterns of intelligence among racial and cultural groups in society contribute to the notion that positive selection is still operating on human intelligence (2, 8).
References and Notes 1. D. Premak, Science 303, 318 (2004). 2. J. P. Rushton et al., Psych. Pub. Pol. and Law 11, 328 (2005). 3. A. P. Jackson et al., Am. J. Hum. Genet. 71, 136 (2002). 4. Y. Q. Wang, B. Su, Hum. Mol. Genet. 13, 1331 (2004). 5. J. Zhang, Genetics 165, 2063 (2003). 6. P. D. Evans et al., Science 309, 1717 (2005). 7. N. Mekel-Bobrov et al., Science 309, 1720 (2005). 8. G. Cochran et. al., J. Biosoc. Sci. 38, 659 (2006).