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Matt Ridley is the author of provocative books on evolution, genetics and society. His books have sold over a million copies, been translated into thirty languages, and have won several awards.

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Culture, genes and the human revolution

By Simon Fisher and Matt Ridley

Simon Fisher and I have published a Perspectives article in Science magazine.


From Science magazine:

by Simon E. Fisher and Matt Ridley

(Simon E. Fisher, Department of Language and Genetics, Max Planck Insti- tute for Psycholinguistics, Nijmegen 6525 XD, Netherlands. 2Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen 6525 EN, Netherlands. Matt Ridley, House of Lords, London SW1A 0PW, UK. E-mail:

State-of-the-art DNA sequencing is providing ever more detailed insights into the genomes of humans, extant apes, and even extinct hominins (13), offering unprecedented opportunities to uncover the molecular variants that make us human. A common assumption is that the emergence of behaviorally modern humans after 200,000 years ago required—and followed—a specific biological change triggered by one or more genetic mutations. For example, Klein has argued that the dawn of human culture stemmed from a single genetic change that “fostered the uniquely modern ability to adapt to a remarkable range of natural and social circumstance” (4). But are evolutionary changes in our genome a cause or a consequence of cultural innovation (see the figure)?

Many nuanced accounts of human evolution implicitly assume that biological changes must precede cultural changes. Vallender et al. described how alterations in size, wiring, and physiology of the human brain yielded advanced cognition, and hence a transformation of behavioral repertoires that encompassed everything from language and tool use to science and art. They posited that it is because of complex cognition that human beings are uniquely capable of cultural evolution, rather than vice versa (5). In a recent paper that elegantly emphasizes the importance of gene expression and metabolic changes in human evolution, Somel et al. adopt a similar view. They argue that a small number of mutations, altering the structure or expression of developmental regulators, drove the emergence of human cognitive traits to trigger a cultural explosion around 200,000 years ago (3).

This prevailing logic in the field may put the cart before the horse. The discovery of any genetic mutation that coincided with the “human revolution” (6) must take care to distinguish cause from effect. Supposedly momentous changes in our genome may sometimes be a consequence of cultural innovation. They may be products of culture-driven gene evolution (7).

In certain cases this is obvious. Lactase-persistence mutations did not trigger dairy farming; they spread as an evolutionary response to dairy consumption (8). The higher alcohol tolerance of Europeans relative to Asians did not prompt, but followed, greater alcohol consumption in Europe (9).

Such examples are mostly drawn from after the Neolithic revolution and the invention of agriculture. But culture-driven gene evolution may have also operated earlier in human history and could be key to understanding our origins. Wrangham’s argument (10) that the invention of fire and cooking altered human gut size 2 million years ago is a case in point, positing that genetic change was contingent on prior cultural innovation.

Under the culture-driven view, many critical genomic alterations that facilitated spoken language, for example, might have spread through our ancestors after this trait emerged.

That is, prior behavioral changes of the species provide a permissive environment in which the function- ally relevant genomic changes accumulate. The selective advantage of a genetic change that increased language proficiency would likely be greatest in a population that was already using language.

Take the FOXP2 gene. More than a decade ago, rare FOXP2 mutations were implicated in an unusual inherited disorder: Affected people have problems coordinating sequences of mouth movements that underlie fluent speech, accompanied by difficulties in expressing and under- standing language (11). Sequencing of versions of FOXP2 in other primates revealed that two evolutionary changes in the protein-coding part of the gene occurred in the human lineage after it split from that of the chimpanzees (12). There was also evidence of recent Darwinian selection acting at the locus (12). The findings prompted speculation that alteration of FOXP2 triggered the explosion of creativity marking the emergence of behaviorally modern humans (4). Further studies have suggested that the changes to the human FOXP2 protein pre- dated the splitting of Neandertals and mod- ern humans several hundred thousand years ago (13). Most recently, researchers have pin- pointed intronic noncoding changes at the FOXP2 locus that arose after the split from Neandertals and that might have affected how the gene is regulated (2).

In considering the roles of FOXP2 in human evolution, it is important to recognize that it has a deep evolutionary history. Animal studies indicate ancient conserved roles of this gene in patterning and plasticity of neural circuits, including those involved in integrating incoming sensory information with outgoing motor behaviors (14). The gene has been linked to acquisition of motor skills in mice and to auditory-guided learning of vocal repertoires in songbirds (14, 15). Contributions of FOXP2 to human spoken language must have built on such ancestral functions.

Indeed, further data from mouse models suggest that humanization of the FOXP2 protein may have altered the properties of some of the circuits in which it is expressed, perhaps those closely tied to movement sequencing and/or vocal learning (13).

Given these findings, it seems unlikely that FOXP2 triggered the appearance of spo- ken language in a nonspeaking ancestor. It is more plausible that altered versions of this gene were able to spread through the populations in which they arose because the species was already using a communication system requiring high fidelity and high variety. If, for instance, humanized FOXP2 confers more sophisticated control of vocal sequences, this would most benefit an animal already capable of speech. Alternatively, the spread of the relevant changes may have had nothing to do with emergence of spoken language, but may have conferred selective advantages in another domain.

FOXP2 is not the only gene associated with the human revolution (3). However, it illustrates that when an evolutionary mutation is identified as crucial to the human capacity for cumulative culture, this might be a consequence rather than a cause of cultural change (8). The smallest, most trivial new habit adopted by a hominid species could— if advantageous—have led to selection of genomic variations that sharpened that habit, be it cultural exchange, creativity, technological virtuosity, or heightened empathy.

This viewpoint is in line with recent understanding of the human revolution as a gradual but accelerating process, in which features of behaviorally modern human beings came together piecemeal in Africa over many tens of thousands of years (6). Recognizing the role of culture-driven gene evolution in the origins of modern humans provides a powerful reminder of how easy it is to confuse cause and effect in science.


References and Notes

1. M. Meyer et al., Science 338, 222 (2012).

2. T. Maricic et al., Mol. Biol. Evol. 30, 844 (2013).

3. M. Somel, X. Liu, P. Khaitovich, Nat. Rev. Neurosci. 14, 112 (2013).

4. R. G. Klein, The Dawn of Human Culture (Wiley, New York, 2002).

5. E. J. Vallender et al., Trends Neurosci. 31, 637 (2008). 6. S. McBrearty, in Rethinking the Human Revolution, P. Mellars, K. Boyle, O. Bar-Yosef, C. Stringer, Eds. (McDonald Institute for Archaeological Research, Cambridge, UK, 2007), pp. 133–151.

7. P. J. Richerson, R. Boyd, Not by Genes Alone (Univ. of Chicago Press, Chicago, 2004).

8. K. N. Laland et al., Nat. Rev. Genet. 11, 137 (2010). 9. J. Diamond, Guns, Germs and Steel (Norton, New York, 1997).

10. R.Wrangham, Catching Fire:How Cooking Made Us Human (Basic Books, New York, 2009).

11. C. S. Lai et al., Nature 413, 519 (2001).

12. W. Enard et al., Nature 418, 869 (2002).

13. W.Enard,Curr.Opin.Neurobiol.21,415(2011).

14. S. E. Fisher, C. Scharff, Trends Genet. 25, 166 (2009). 15. C. A. French et al., Mol. Psychiatry 17, 1077 (2012).

Acknowledgments: S.E.F. is supported by the Max Planck Society. We thank D. Dediu for helpful comments.