In Fisher’s major work, The Genetical Theory of Natural Selection, published in 1929, he developed the argument that genes for mental ability are more frequent among the wealthy, who have fewer children, whereas the poor, who tend to be less intelligent, have more children; therefore natural selection acts against genes that promote intelligence. This aspect of Fisher’s work is not much discussed, because it was used to support the disastrous eugenics policies of the early twentieth century. But in the view of some population geneticists, its theoretical argument has not been refuted: at least in developed countries, people of higher intelligence tend to have fewer children, so it would seem that their genes cannot become more common in the next generation. Others argue that the poor tend to have more children from lack of education, not any lack of intelligence. “Fisher’s empirical observation is correct, that the lower orders have more babies, but that doesn’t mean their genotypes are inferior,” says Pagel.
Human brain size and intelligence have clearly expanded throughout most of evolution, and it would be strange if this trend should suddenly grind to a halt just as societies, and the skills needed to flourish in them, have become more complex than ever. It would be stranger still if humans, selected throughout evolution on the basis of maximum fitness, the propensity to leave as many descendants as possible, should suddenly abandon this deeply ingrained behavior. Nor is there any evidence from IQ tests to suppose that human cognitive ability is falling, as Fisher predicted. Therefore, despite the apparent correctness of Fisher’s premise, that in modern societies the rich and more intelligent tend to have fewer children, his conclusion of inexorable intellectual decline seems somehow to be false.
The reason, evolutionary psychologists suggest, is that the rich are able to invest more in their children—a college education makes a big difference to future success—and thus they may leave more descendants in the long run, even if they have fewer children. The argument assumes that children who are well educated and well endowed will have children of similar quality, generation after generation, whereas at a certain level of destitution fertility will be reduced. So at some level of wealth, the better way for parents to maximize their Darwinian fitness will be to have fewer children in the expectation of leaving many more great-grandchildren.
Whether this is the case in practice is unclear. Teasing out the relationship between wealth and fertility is no easy matter and the demographic data needed to resolve the issue seem to be lacking. “This is a tricky and subtle business,” writes the evolutionary psychologist Bobbi Low, “and most currently available data, gathered to answer other questions, are inadequate.”350
One way in which future human evolution will differ from that of the past is that in larger populations the effect of genetic drift is much diminished. The larger the population, the longer it takes for one version of a gene to supplant all the alternative versions. Since drift is a principal mechanism for reducing the diversity that is constantly introduced by mutation, it follows that human genomes will become more diverse as neutral mutations accumulate. Too much diversity, according to theoretical calculations, could eventually make people infertile unless they mated only with people whose genomes were similar to their own.351 This would make it impossible for all humans to interbreed, as is the case at present, and confine people to seeking partners within genetically similar groups. Such an outcome would be another step in fragmenting the human population into different species.
The weakening of drift and its mutation-reducing effect might be offset, to some extent, by human intervention, in the form of genetic engineering. Biologists may soon learn how to modify eggs, sperm or the early embryo so as to insert corrective genes that remedy future health defects. New genes inserted into the human genome on a widescale basis to replace existing genes might have the same mutation-shedding effect as genetic drift.
Suppose the genetic modification eventually takes the form of adding many new genes, packaged in the form of an extra chromosome that could be introduced into a couple’s eggs and sperm prior to an in vitro fertilization procedure, which a few decades hence has supplanted the quaint and hazardous method of conceiving at random.
This extra chromosome would include a suite of genes for correcting all genetic diseases diagnosed in the prospective parents. It would carry genes to fortify the immune system, to fend off cancer and to combat the cruel degenerative diseases of age. The in vitro fertilization procedure and the individually tailored genetic engineering would be expensive, but critics who claim that only the rich will benefit might be confounded should governments find the procedure to be so cheap, compared with the lifetime of health care costs it averts, that they offer it free to all citizens.
The early versions of the extra chromosome, to continue the scenario a little further, are allowed only to carry genes that correct threats to health. But when the first generation of humans to carry twenty-four pairs of chromosomes turns out to be entirely normal and robustly healthy, various enhancements of desirable qualities are allowed. The extra chromosomes carry genes that promote longevity, improve the symmetry and beauty of the body, and enhance intelligence, though all within carefully prescribed limits. After various adjustments, the technology is brought to a high level of perfection. The only downside is that the people with twenty-four chromosome pairs cannot interbreed with those carrying the old fashioned number unless the latter agree to genetic modification, which many resist. Once again speciation, the division of the human population into two or more species, is the unintended outcome.
Two choices lie ahead. One is between directed human evolution and the natural kind, the other is whether to allow or promote speciation. The idea of directing human evolution, by modifying the germline, may seem adventurous, but evolution’s method rests on the outcome of two chance-driven processes, mutation and drift. It could be contended that despite the madness of its method, evolution has not done too badly so far. But evolution works with glacial speed. With germline modification, on the other hand, just as in the breeding of domesticated animals, human intervention can reach a desired outcome much more quickly.
The most serious disadvantage of actively managing the human germline probably lies in the risks incurred by unintentionally suppressing evolution’s vast capacity for novelty. By creating mutations at random, and testing each out to see if it works, evolution comes up with innovations that no one would think of. Those in charge of modifying the human germline, on the other hand, doubtless constrained by medical ethics to avoid all risk, would inevitably freight the genome with their conservative preferences.
Speciation, the other major issue in the human evolutionary future, is another powerful way of generating novelty and hence of improving the essentially unfavorable odds that the human species will last a long time. Our previous reaction to kindred species was to exterminate them, but we have mellowed a lot in the last 50,000 years. A bifurcation into land people and sea people—mammals have returned to the sea several times already—might not necessarily lead to conflict, nor would that of separately evolving populations on Mars and Earth. More problematic would be different human species occupying the same environment, especially if one were somehow deemed inferior or bound in helotry to the other.
There is no one human evolutionary future but many possible paths, some to be shaped by chance, some by choice. We have come so far. There is so much farther to go.
NOTES
1 Genesis 3: 7, 21.
2 Ralf Kittler, Manfred Kayser, and Mark Stoneking, “Molecular Evolution of Pediculus Humanus and the Origin of Clothing,” Current Biology 13:1414-1417 (2003). Other researchers have challenged a technical aspect of the paper. The challenge, if sustained, would suggest a considerably older date, perhaps up until 500,000 years ago, for the evolution of the body louse and the invention of clothing. David L. Reed et al., “Genetic Analysis of Lice Supports Direct Contact between Modern and Archaic Humans,” Public Library of Science Biology 2:1972-1983 (2004); Nicholas Wade,
“What a Story Lice Can Tell,” New York Times, October 5, 2004, p. F1.
3 Feng-Chi Chen and Wen-Hsiung Li, “Genomic Divergences between Humans and Other Hominoids and the Effective Population Size of the Common Ancestor of Humans and Chimpanzees,” American Journal of Human Genetics 68:444-456 (2001).
4 Pascal Gagneux et al., “Mitochondrial Sequences Show Diverse Evolutionary Histories of African Hominoids,” Proceedings of the National Academy of Sciences 96:5077-5082 (1999).
5 Richard G. Klein, The Human Career, 2nd edition, University of Chicago Press, 1999, p. 251. Unless otherwise specified, the paleoanthropological and archaeological facts in this chapter are mostly drawn either from this broad and lucid textbook, or from a more popular book that is based on it, The Dawn of Human Culture by Richard G. Klein and Blake Edgar, John Wiley & Sons, 2002.
6 Chen and Li, “Genomic Divergences.” The number of DNA differences between two species depends on the size of the parent population and the number of generations for which the two species have been separate. If the generation time and the number of years since the split are known, geneticists can estimate what they call the “effective” population size. This is a theoretical population, which must be multiplied by a factor of two to five to get the census-size population.
7 P. S. Rodman, in Adaptations for Foraging in Non-human Primates, Columbia University Press 1984, pp. 134-160, cited in Robert Foley, Humans before Humanity, Blackwell, 1995, p. 140.
8 Richard G. Klein, The Human Career, 2nd edition, University of Chicago Press, 1999, figure 8.3, p. 580.
9 Roger Lewin and Robert A. Foley, Principles of Human Evolution, 2nd ed., Blackwell, 2004, p. 450.
10 Robert Foley, Humans before Humanity, Blackwell, 1995, p. 170.
11 Richard G. Klein, The Human Career, p. 292.
12 Richard Wrangham, “Out of the Pan, Into the Fire,” in Frans B. M. DeWaal, ed., Tree of Origin, Harvard University Press, 2001, p. 137.
13 Richard G. Klein and Blake Edgar, The Dawn of Human Culture, Wiley, 2002, p. 100; Robert A. Foley, “Evolutionary Perspectives,” in W. G. Runciman, ed., The Origin of Human Social Institutions, Oxford University Press, 2001, pp. 171-196.
14 Richard G. Klein, The Human Career, p. 292.
15 Charles Darwin, The Descent of Man and Selection in Relation to Sex, 2nd edition, 1874, p. 58.
16 Mark Pagel and Walter Bodmer, “A Naked Ape Would Have Fewer Parasites,” Proceedings of the Royal Society B (Suppl.) 270:S117-S119 (2003).
17 Rosalind M. Harding et al., “Evidence for Variable Selective Pressures at MC1R,” American Journal of Human Genetics 66:1351-1361 (2000).
18 Nina G. Jablonski and George Chaplin, “The Evolution of Human Skin Coloration,” Journal of Human Evolution 39:57-106 (2000).
19 Alan R. Rogers, David Iltis, and Stephen Wooding, “Genetic Variation at the MC1R Locus and the Time Since Loss of Human Body Hair,” Current Anthropology 45:105-108 (2004).
20 Nina G. Jablonski and George Chaplin, “Skin,” Scientific American 74:72-79 (2002).
21 Arthur H. Neufeld and Glenn C. Conroy, “Human Head Hair Is Not Fur,” Evolutionary Anthropology 13:89 (2004); B. Thierry, “Hair Grows to Be Cut,” Evolutionary Anthropology 14:5 (2005); Alison Jolly, “Hair Signals,” Evolutionary Anthropology 14:5 (2005).
22 Hermelita Winter et al., “Human Type I Hair Keratin Pseudogene phihHaA Has Functional Orthologs in the Chimpanzee and Gorilla: Evidence for Recent Inactivation of the Human Gene After the Pan-Homo Divergence.” Human Genetics 108:37-42 (2001).
23 R. X. Zhu et al., “New Evidence on the Earliest Human Presence at High Northern Latitudes in Northeast Asia,” Nature 431:559-562 (2004).
24 Robert Foley, Humans before Humanity, Blackwell, 1995, p. 75.
25 Richard G. Klein, “Archeology and the Evolution of Human Behavior,” Evolutionary Anthropology 9(1):17-36 (2000).
26 Richard Klein and Blake Edgar, The Dawn of Human Culture, p. 192.
27 Richard Klein, The Human Career, p. 512.
28 Ian McDougall et al., “Stratigraphic Placement and Age of Modern Humans from Kibish, Ethiopia,” Nature 433:733-736 (2005).
29 From a list of fifteen modern behaviors described by Paul Mellars in “The Impossible Coincidence—A Single-Species Model for the Origins of Modern Human Behavior in Europe,” Evolutionary Anthropology 14:12-27 (2005).
30 Richard Klein, The Human Career, p. 492.
31 Sally McBrearty and Alison S. Brooks, “The Revolution That Wasn’t: A New Interpretation of the Origin of Modern Human Behavior,” Journal of Human Evolution 39:453-563 (2000).
32 Christopher Henshilwood et al., “Middle Stone Age Shell Beads from South Africa,” Science 304:404 (2004).
33 James M. Bowler et al., “New Ages for Human Occupation and Climatic Change at Lake Mungo, Australia,” Nature 421:837-840 (2003).
34 Michael C. Corballis, “From Hand to Mouth: The Gestural Origins of Language,” in Morten H. Christiansen and Simon Kirby, Language Evolution, Oxford University Press, 2003, pp. 201-219.
35 Marc D. Hauser, The Evolution of Communication, MIT Press, 1996, p. 309.
36 Ibid., p. 38.
37 Steven Pinker, The Language Instinct, William Morrow, 1994, p. 339.
38 Marc D. Hauser, Noam Chomsky, and W. Tecumseh Fitch, “The Faculty of Language: What Is It, Who Has It, and How Did It Evolve?” Science 298:1569-1579 (2002).
39 Derek Bickerton, Language and Species, University of Chicago Press, 1990, p. 105.
40 Ray Jackendoff, Foundations of Language, Oxford University Press, 2002, p. 233.
41 Frederick J. Newmeyer, “What Can the Field of Linguistics Tell Us about the Origins of Language?” in Language Evolution, by Morten H. Christiansen and Simon Kirby, Oxford University Press, 2003, p. 60.
42 Nicholas Wade, “Early Voices: The Leap of Language,” New York Times, July 15, 2003, p. F1.
43 Steven Pinker, e-mail, June 16, 2003, quoted in part in Wade, “Early Voices.”
44 Steven Pinker and Paul Bloom, “Natural Language and Natural Selection,” Behavioral and Brain Sciences 13(4):707-784 (1990).
45 Derek Bickerton, Language and Species, p. 116.
46 Ray Jackendoff, Foundations of Language, p. 240.
47 Ann Senghas, Sogaro Kita, and Asli Özyürek, “Children Creating Core Properties of Language: Evidence from an Emerging Sign Language in Nicaragua,” Science 305:1779-1782 (2004).
48 Wendy Sandler et al., “The Emergence of Grammar: Systematic Structure in a New Language,” Proceedings of the National Academy of Sciences 102:2661-2665 (2005).
49 Nicholas Wade, “Deaf Children’s Ad Hoc Language Evolves and Instructs,” New York Times, September 21, 2004, p. F4.
50 Michael C. Corballis, “From Hand to Mouth,” p. 205.
51 Louise Barrett, Robin Dunbar, and John Lycett, Human Evolutionary Psychology, Princeton University Press, 2002.
52 Geoffrey Miller, The Mating Mind, Random House, 2000.
53 Steven Pinker, “Language as an Adaptation to the Cognitive Niche,” in Morten H. Christiansen and Simon Kirby, Language Evolution, Oxford University Press, 2003, p. 29.
54 Paul Mellars, “Neanderthals, Modern Humans and the Archaeological Evidence for Language,” in Nina G. Jablonski and Leslie C. Aiello, eds., The Origin and Diversification of Language, California Academy of Sciences, 1988, p. 99.
55 Faraneh Vargha-Khadem, interview, October 1, 2001.
56 Faraneh Vargha-Khadem, Kate Watkins, Katie Alcock, Paul Fletcher, and Richard Pass ingham, “Praxic and Nonverbal Cognitive Deficits in a Large Family with a Genetically Transmitted Speech and Language Disorder,” Proceedings of the National Academy of Sciences 92:930-933 (1995).
57 Faveneh Vargha-Khadem et al., “Neural Basis of an Inherited Speech and Language Disorder,” Proceedings of the National Academy of Science 95:12659-12700 (1998).
58 Many genes were first discovered by biologists working with fruit flies, among whom it is a point of pride to give ge
nes colorful names. These odd names are often adopted for the equivalent gene when it is discovered in humans, apart from names like dunce or rutabaga that are deemed too colorful. The forkhead gene was so named because when it is mutated, the fly larvae develop spiky structures on their head. Other genes of similar structure were found, and all turned out to have a signature section of DNA, called the forkhead box, which specified a region in the forkhead protein that binds to specific sequence of DNA. This is because the forkhead proteins control the activity of other genes by binding to regions of DNA just upstream of genes. Humans have turned out to possess a large family of forkhead box genes, the subgroups of which are named by letters of the alphabet. FOXP2 is the second member of the P group of the family of forkhead box genes. Gary F. Marcus and Simon F. Fisher, “FOXP2 in Focus: What Can Genes Tell Us About Speech and Language?” Trends in Cognitive Sciences 7:257-262 (2003).
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